Academic literature on the topic 'Modulation of cell size'
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Journal articles on the topic "Modulation of cell size"
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Vanoni, M., R. L. Rossi, L. Querin, V. Zinzalla, and L. Alberghina. "Glucose modulation of cell size in yeast." Biochemical Society Transactions 33, no. 1 (February 1, 2005): 294–96. http://dx.doi.org/10.1042/bst0330294.
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Saccharomyces cerevisiae cells grown in glucose have larger average size than cells grown in ethanol. Besides, yeast must reach a carbon source-modulated critical cell size in order to enter S phase at Start. This control is of outmost physiological relevance, since it allows us to coordinate cell growth with cell cycle progression and it is responsible for cell size homeostasis. The cell sizer mechanism requires the overcoming of two sequential thresholds, involving Cln3 and Far1, and Clb5,6 and Sic1, respectively. When both thresholds are non-functional, carbon source modulation of cell size at Start is completely abolished. Since inactivation of extracellular glucose sensing through deletion of either the GPR1 or the GPA2 gene causes a marked, but partial, reduction in the ability to modulate cell size and protein content at Start, it is proposed that both extracellular and intracellular glucose signalling is required for properly setting the cell sizer in glucose media.
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Duncombe, Todd A., Chi-Chih Kang, Santanu Maity, Toby M. Ward, Mark D. Pegram, Niren Murthy, and Amy E. Herr. "Hydrogel Pore-Size Modulation for Enhanced Single-Cell Western Blotting." Advanced Materials 28, no. 2 (November 16, 2015): 327–34. http://dx.doi.org/10.1002/adma.201503939.
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Baroni, M. D., E. Martegani, P. Monti, and L. Alberghina. "Cell size modulation by CDC25 and RAS2 genes in Saccharomyces cerevisiae." Molecular and Cellular Biology 9, no. 6 (June 1989): 2715–23. http://dx.doi.org/10.1128/mcb.9.6.2715-2723.1989.
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A detailed kinetic analysis of the cell cycle of cdc25-1, RAS2Val-19, or cdc25-1/RAS2Val-19 mutants during exponential growth is presented. At the permissive temperature (24 degrees C), cdc25-1 cells show a longer G1/unbudded phase of the cell cycle and have a smaller critical cell size required for budding without changing the growth rate in comparison to an isogenic wild type. The RAS2Val-19 mutation efficiently suppresses the ts growth defect of the cdc25-1 mutant at 36 degrees C and the increase of G1 phase at 24 degrees C. Moreover, it causes a marked increase of the critical cell mass required to enter into a new cell division cycle compared with that of the wild type. Since the critical cell mass is physiologically modulated by nutritional conditions, we have also studied the behavior of these mutants in different media. The increase in cell size caused by the RAS2Val-19 mutation is evident in all tested growth conditions, while the effect of cdc25-1 is apparently more pronounced in rich culture media. CDC25 and RAS2 gene products have been showed to control cell growth by regulating the cyclic AMP metabolic pathway. Experimental evidence reported herein suggests that the modulation of the critical cell size by CDC25 and RAS2 may involve adenylate cyclase.
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Baroni, M. D., E. Martegani, P. Monti, and L. Alberghina. "Cell size modulation by CDC25 and RAS2 genes in Saccharomyces cerevisiae." Molecular and Cellular Biology 9, no. 6 (June 1989): 2715–23. http://dx.doi.org/10.1128/mcb.9.6.2715.
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A detailed kinetic analysis of the cell cycle of cdc25-1, RAS2Val-19, or cdc25-1/RAS2Val-19 mutants during exponential growth is presented. At the permissive temperature (24 degrees C), cdc25-1 cells show a longer G1/unbudded phase of the cell cycle and have a smaller critical cell size required for budding without changing the growth rate in comparison to an isogenic wild type. The RAS2Val-19 mutation efficiently suppresses the ts growth defect of the cdc25-1 mutant at 36 degrees C and the increase of G1 phase at 24 degrees C. Moreover, it causes a marked increase of the critical cell mass required to enter into a new cell division cycle compared with that of the wild type. Since the critical cell mass is physiologically modulated by nutritional conditions, we have also studied the behavior of these mutants in different media. The increase in cell size caused by the RAS2Val-19 mutation is evident in all tested growth conditions, while the effect of cdc25-1 is apparently more pronounced in rich culture media. CDC25 and RAS2 gene products have been showed to control cell growth by regulating the cyclic AMP metabolic pathway. Experimental evidence reported herein suggests that the modulation of the critical cell size by CDC25 and RAS2 may involve adenylate cyclase.
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Marais, A. David. "Therapeutic modulation of low-density lipoprotein size." Current Opinion in Lipidology 11, no. 6 (December 2000): 597–602. http://dx.doi.org/10.1097/00041433-200012000-00005.
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Zhou, Shaoli, Tianquan Yang, Yawen Mao, Ye Liu, Shiqi Guo, Ruoruo Wang, Genwang Fangyue, et al. "The F-box protein MIO1/SLB1 regulates organ size and leaf movement in Medicago truncatula." Journal of Experimental Botany 72, no. 8 (January 28, 2021): 2995–3011. http://dx.doi.org/10.1093/jxb/erab033.
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Abstract The size of leaf and seed organs, determined by the interplay of cell proliferation and expansion, is closely related to the final yield and quality of forage and crops. Yet the cellular and molecular mechanisms underlying organ size modulation remain poorly understood, especially in legumes. Here, MINI ORGAN1 (MIO1), which encodes an F-box protein SMALL LEAF AND BUSHY1 (SLB1) recently reported to control lateral branching in Medicago truncatula, was identified as a key regulator of organ size. We show that loss-of-function of MIO1/SLB1 severely reduced organ size. Conversely, plants overexpressing MIO1/SLB1 had enlarged organs. Cellular analysis revealed that MIO1/SLB1 controlled organ size mainly by modulating primary cell proliferation during the early stages of leaf development. Biochemical analysis revealed that MIO1/SLB1 could form part of SKP1/Cullin/F-box (SCF) E3 ubiquitin ligase complex, to target BIG SEEDS1 (BS1), a repressor of primary cell division, for degradation. Interestingly, we found that MIO1/SLB1 also played a key role in pulvinus development and leaf movement by modulating cell proliferation of the pulvinus as leaves developed. Our study not only demonstrates a conserved role of MIO1/SLB1 in the control of organ size in legumes, but also sheds light on the novel function of MIO1/SLB1 in leaf movement.
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Cipollina, Chiara, Lilia Alberghina, Danilo Porro, and Marina Vai. "SFP1 is involved in cell size modulation in respiro-fermentative growth conditions." Yeast 22, no. 5 (2005): 385–99. http://dx.doi.org/10.1002/yea.1218.
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Mumtaz, Muhammad Ali, Fangman Li, Xingyu Zhang, Jinbao Tao, Pingfei Ge, Ying Wang, Yaru Wang, Wenxian Gai, Haiqiang Dong, and Yuyang Zhang. "Altered brassinolide sensitivity1 Regulates Fruit Size in Association with Phytohormones Modulation in Tomato." Horticulturae 8, no. 11 (October 31, 2022): 1008. http://dx.doi.org/10.3390/horticulturae8111008.
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BRs (Brassinosteroids) regulate many essential pathways related to growth, cell elongation, cell expansion, plant architecture, and fruit development. The potential exogenous application of BR-derivatives has been proven to stimulate plant growth and development, including quality attributes of fruits, whereas its biosynthesis inhibition has shown the opposite effect. In this study, BR-insensitive tomato mutants were used to reveal the potential function of BR signaling in the regulation of fruit development to elaborate the regulatory mechanism of BR signaling in tomato fruits. The BR-signaling mutant exhibited a typical dwarf phenotype and reduced vegetative growth, fruit size, and weight. Microscopic and transcriptional evaluation of the abs1 mutant fruits implies that reduced cell size and number are responsible for the phenotypic variations. Additionally, we also found that the altered content of phytohormones, such as auxin, gibberellin, cytokinin, and ethylene levels, contributed to altered fruit development. Moreover, fruit growth and cell development-specific gene expression levels were downregulated in BR-insensitive plants; culminating in reduced cell size, cell number, and cell layers. These findings provide insight into physio-chemical changes during fruit development in response to BR-insensitivity.
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Jang, Seonghoe, Jwa-Yeong Cho, Gyung-Ran Do, Yeeun Kang, Hsing-Yi Li, Jaeeun Song, Ho-Youn Kim, Beom-Gi Kim, and Yue-Ie Hsing. "Modulation of Rice Leaf Angle and Grain Size by Expressing OsBCL1 and OsBCL2 under the Control of OsBUL1 Promoter." International Journal of Molecular Sciences 22, no. 15 (July 21, 2021): 7792. http://dx.doi.org/10.3390/ijms22157792.
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Leaf angle and grain size are important agronomic traits affecting rice productivity directly and/or indirectly through modulating crop architecture. OsBC1, as a typical bHLH transcription factor, is one of the components comprising a complex formed with LO9-177 and OsBUL1 contributing to modulation of rice leaf inclination and grain size. In the current study, two homologues of OsBC1, OsBCL1 and OsBCL2 were functionally characterized by expressing them under the control of OsBUL1 promoter, which is preferentially expressed in the lamina joint and the spikelet of rice. Increased leaf angle and grain length with elongated cells in the lamina joint and the grain hull were observed in transgenic rice containing much greater gibberellin A3 (GA3) levels than WT, demonstrating that both OsBCL1 and OsBCL2 are positive regulators of cell elongation at least partially through increased GA biosynthesis. Moreover, the cell elongation was likely due to cell expansion rather than cell division based on the related gene expression and, the cell elongation-promoting activities of OsBCL1 and OsBCL2 were functional in a dicot species, Arabidopsis.
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Mitra, Mautusi, Henning Kirst, David Dewez, and Anastasios Melis. "Modulation of the light-harvesting chlorophyll antenna size in Chlamydomonas reinhardtii by TLA1 gene over-expression and RNA interference." Philosophical Transactions of the Royal Society B: Biological Sciences 367, no. 1608 (December 19, 2012): 3430–43. http://dx.doi.org/10.1098/rstb.2012.0229.
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Truncated light-harvesting antenna 1 ( TLA1 ) is a nuclear gene proposed to regulate the chlorophyll (Chl) antenna size in Chlamydomonas reinhardtii . The Chl antenna size of the photosystems and the chloroplast ultrastructure were manipulated upon TLA1 gene over-expression and RNAi downregulation. The TLA1 over-expressing lines possessed a larger chlorophyll antenna size for both photosystems and contained greater levels of Chl b per cell relative to the wild type. Conversely, TLA1 RNAi transformants had a smaller Chl antenna size for both photosystems and lower levels of Chl b per cell. Western blot analyses of the TLA1 over-expressing and RNAi transformants showed that modulation of TLA1 gene expression was paralleled by modulation in the expression of light-harvesting protein, reaction centre D1 and D2, and VIPP1 genes. Transmission electron microscopy showed that modulation of TLA1 gene expression impacts the organization of thylakoid membranes in the chloroplast. Over-expressing lines showed well-defined grana, whereas RNAi transformants possessed loosely held together and more stroma-exposed thylakoids. Cell fractionation suggested localization of the TLA1 protein in the inner chloroplast envelope and potentially in association with nascent thylakoid membranes, indicating a role in Chl antenna assembly and thylakoid membrane biogenesis. The results provide a mechanistic understanding of the Chl antenna size regulation by the TLA1 gene.
Dissertations / Theses on the topic "Modulation of cell size"
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GOTTI, LAURA. "Nutritional modulation of cell size at s phase initiation in the buddine yeast saccharomyces cerevisiae: a role for glucose sensing and the cyclin dependent kinase inhibitor." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/19573.
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The budding yeast Saccharomyces cerevisiae is a model organism for studies on cell cycle. For the survival of this cells a tight coordination of cell growth and division occurs at Start, a regulatory area of the cell cycle positioned immediately before beginning of S phase, at the G1-S boundary. Start is the event, or set of events, that commits a cell to a round of division.
This mechanism is based on achieving of a critical cell size (protein content per cell at the onset of DNA replication, Ps) to enter into S phase. Ps increases in proportion with ploidy and is modulated by nutrients. In fact, in bach cultures, the average cell size remains at low levels during growth on non-fermentable substrates, while the average size of cells increases in a linear way with the specific growth rate only during growth on fermentable substrates.
A genome-wide genetic analysis has suggested that cell size control could be due to ribosome biogenesis rate, one of the most energetic demanding processes in a cell and it is modulated according to nutrient availability. Indeed, a large cluster of genes involved in ribosome biogenesis, have been identified in a screen for small size (whi) mutants. This includes SFP1 and SCH9 genes. The first encode a zinc finger protein, promoting the transcription of a large cluster of genes involved in ribosome biogenesis, where the latter is serine threonine protein kinase involved in stress response and nutrient-sensing signaling pathway.
Recent work from our laboratory allowed to identify that Far1, a cyclin kinase dependent inhibitor, and Cln3, a G1 phase cyclin, may form a nutritional modulated threshold controlling the entrance into S phase. Two parallel pathways downstream from the TORC1 complex regulate expression of genes encoding ribosomal proteins (RP) and the so-called RiBi regulon, composed by genes involved in ribosome biogenesis. The two pathways involve Sfp1, and Sch9. Therefore it was of interest to see whether the increase in size (RNA and protein) brought about by FAR1 overexpression was mediated by Sfp1 and Sch9.
The effect of FAR1 overexpression on cell size parameters in the wild type BY4741 strain (isogenic to the sch9Δ and sfp1Δ mutants), grown in synthetic complete media supplemented with either ethanol or glucose as a carbon source, was similar to that reported in the W303 background. sfp1Δ and sch9Δ mutants were much smaller than wild type both in glucose - confirming previous data (Jorgensen et al., 2002; Jorgensen et al., 2004) - and ethanol-supplemented media. As observed in wild type cells, in both mutant strains FAR1 overexpression had only minor effects on cell cycle and cell size related parameters on glucose-grown cells. FAR1 overexpression did not affect duplication time in ethanol-grown sch9Δ cells, while sfp1Δ mutants overexpressing the FAR1 gene product were quite unhealthy with a large increase in duplication time.
Overall increase in cell size was dramatic in ethanol-grown cells: however, while in wild type cells and sch9Δ mutants the increase in cell size derived from a balanced increase in RNA and protein content, in the sfp1Δ mutant the increase in protein content was not accompanied by an increase in RNA content, as shown by both FACS and chemical analysis, indicating that the Sfp1 is required to maintain proper coupling of RNA and protein syntheses when the Far1 protein is overexpressed in ethanol-grown-cells.
The observation that FAR1 overexpression has different effects in sfp1Δ cells grown in ethanol and glucose media was not entirely unexpected. First, in untransformed cells, the Far1 level of glucose-grown cells is larger than in ethanol-grown cells, while ectopically expressed Far1 accumulates to a similar level regardless of the carbon source: as a result, Far1 overexpression is more dramatic in ethanol-grown cells than in glucose-grown cells (Alberghina et al., 2004). Accordingly, the effect of Far1 overexpression on cell size are minor on cells grown in glucose-supplemented media and much more dramatic in ethanol-grown cells.
In the second part of this study we try to determine whether (and possibly, to which extent) the regulatory function of glucose can be separated from its nutrient function. To this aim, we characterized yeast strains in which glucose sensing is strongly reduced. An essential requisite for the survival of free living microorganism like the budding yeast Saccharomyces cerevisiae is the capacity to regulate growth and cell cycle progression according to the frequent changes in the nutrient status, so that proliferation is rapid when large supplies of nutrients are available and ceases when these becomes exhausted. Nutrients like glucose must therefore generate signals that are somehow received and elaborated by the complex machinery governing growth and cell cycle progression. Besides being the favorite carbon and energy source for S. cerevisiae, glucose can act as a signaling molecule (“hormone”) to regulate multiple aspects of yeast physiology: addition of glucose to quiescent or ethanol growing cells triggers a fast and massive reconfiguration of the transcriptional program, which enables the switch to fermentative metabolism and promotes an outstanding increase of the cell biosynthetic capacity. Yeast cells evolved several mechanisms for monitoring glucose level in their habitat: the cAMP-PKA pathways (with its two branches comprising Ras and the Gpr1-Gpa2 module), the Rgt2/Snf3-Rgt1 pathway and the main repression pathway involving the kinase Snf1.
In order to investigate whether the glucose effect on cell size was due to its function as nutrient, that require metabolism of the sugar, or to sensing of extracellular glucose levels, yeast strains in which one or more of the glucose sensing pathway was impaired, due to gene deletion of glucose receptors (GPR1, SNF3, RGT2), were analyzed. These mutants show only a partial nutritional modulation of cell size and/or of duplication time.
The gpa2Δ gpr1Δ strain does not show substantial changes in duplication time compared to its isogenic wild type grown in the same conditions, while its protein content is consistently lower. In the snf3Δ rgt2Δ and in the snf3Δ rgt2Δ gpa2Δ gpr1Δ strains a lower protein content is accompanied by an increase in duplication time, when compared to wild type strain. Furthermore, in all glucose sensing mutants the variation of protein content, as function of glucose levels, is less than the wild type. In the presence of ethanol, the kinetic parameters of mutants strain analyzed are comparable to wild type: there is only a strong increase in the duplication time, while there isn’t a further decrease in protein content compared to 0.05% glucose concentration. Data obtained show that the Gpa2-Gpr1 pathway specifically modulates Ps setting, while the Snf3-Rgt2 pathway plays an important role in Ps and growth rate setting of the cells.
In conclusion, this work highlighted that the elements involved in the cell size determination are multiple and interconnected. A strong alteration in cell size and protein content could originate not only from alteration in the dosage of genes involved in the molecular mechanism of the threshold which controls Ps, but also from environmental conditions. Of particular relevance seems to be that glucose effect is largely acting as a signaling molecule, rather than as an energy source. Further studies are necessary in order to clarify the molecular mechanism that link the glucose sensing to the molecular machinery responsible of G1-S transition.
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Hubatsch, Lars. "Interplay between cell size and cell polarity." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10055636/.
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Cell polarity is a fundamental phenomenon underlying processes such as asymmetric cell division, tissue homeostasis and directed cell migration. In metazoans, the conserved PAR (-titioning defective) protein network polarizes cells with different shapes and sizes. Here, I investigate whether cell size influences the polarity pattern set up by the PARs. PAR polarity is typically achieved by localizing different sets of antagonizing proteins to opposing membrane domains. Antagonism ensures that mixing of the two species is restricted to a region between the two domains. Theoretically, this can be described using reaction-diffusion models, in which abstract biochemical agents are able to exchange between membrane and cytosol, and are subjected to cytosolic and membrane diffusion. Under suitable conditions, their interactions give rise to a stable pattern. In such a system, the interplay between diffusion and reaction rates determines the pattern by setting key length scales, for example, the extent of the boundary region between the two opposing domains. Using computer simulations, I first show that current reaction-diffusion models fail to adapt such pattern length scales to cell size. Second, this results in pattern breakdown below a certain minimum size, producing completely uniform protein distributions across the membrane. We term this size critical polarizable system size (CPSS). To test the first prediction - failure to adapt to cell size - I measured kinetic parameters and the resulting pattern length scales in differently sized cells, using the early C. elegans embryo as a model. The results suggest a moderate, if any, adaptation, prompting me to examine the second prediction - failure to maintain polarity at small sizes. By combining novel computational methods for 3D membrane reconstruction with cell size mutants, I then show that small cells are indeed unable to maintain polarity, thus establishing a lower size limit for polarity in vivo.
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Maguire, Sharon Marie. "Germ cell modulation of Sertoli cell function." Thesis, University of Edinburgh, 1994. http://hdl.handle.net/1842/20662.
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The aim of this work was to assess the influence of germ cells on the expression of selected Sertoli cell mRNAs. To this end, adult rats were treated with 650mg/kg methoxyacetic acid (MAA) to induce the specific depletion of >80% of pachytene and later spermatocytes from most tubules, and expression of selected Sertoli cell mRNAs was then assessed at various times after treatment when particular germ cell types were depleted selectively (see Bartlett et al. 1988; Allenby et al., 1991). Studies on the expression of cyclic protein 2(CP-2) mRNA supported the hypothesis that germ cells can influence the cyclic function of Sertoli cells. Expression of CP-2 mRNA was shown by Northern blot analysis to decrease significantly 21 days after MAA treatment. In situ hybridisation showed that CP-2 mRNA expression was decreased or absent from tubules at stages at which CP-2 mRNA is normally expressed (stages IV-VII) when elongate spermatids were depleted selectively from these tubules. This decrease was reflected in loss of CP-2 protein production. These observations lead us to hypothesise that elongate spermatids positively modulate CP-2 expression in the Sertoli cell, with this modulation occurring at the level of transcription. In conclusion, this study demonstrated that germ cells do appear to influence Sertoli cell gene expression. This can occur at the level of transcription as was demonstrated by the effect of elongate spermatids on CP-2 mRNA expression, or may occur post-transcriptionally, as would appear to be the case with ABP.
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Cadart, Clotilde. "Cell size homeostasis in animal cells." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS103/document.
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Le mécanisme d’homéostasie de taille chez les cellules animales est très peu compris actuellement. Cette question est pourtant d’un intérêt majeur car le maintien de l’homéostasie de taille dans une population de cellules prolifératives doit se faire par une coordination entre la croissance et la division. Chez la levure S. pombe, il a ainsi été montré que la taille est une information cruciale pour déclencher l’entrée en mitose (Fantes, 1977). Chez plusieurs bactéries et les cellules filles de la levure S. cerevisiae au contraire, de récentes études ont au contraire montré que l’homéostasie de taille était le résultat d’une addition constante de volume, indépendamment de la taille initiale des cellules (Campos et al., 2014; Soifer et al., 2016; Taheri-Araghi et al., 2015). Ce mécanisme est appelé « adder » et génère une régression des tailles à la moyenne, génération après génération. Ces résultats ont été possibles grâce au développement de techniques permettant la mesure dynamique du volume à l’échelle de la cellule unique et sur plusieurs générations. Une telle mesure est cependant très difficile chez les cellules de mammifère dont le volume fluctue constamment et qui cyclent sur des temps plus longs (environ 20 heures). Pour cette raison, la plupart des approches proposées sont indirectes (Kafri et al., 2013; Sung et al., 2013; Tzur et al., 2009) ou reposent sur une mesure de la masse plutôt que du volume (Mir et al. 2014; Son et al., 2012). Ensemble, ces études ont montré que les cellules de mammifère croissaient de manière exponentielle. Elles ont aussi remis en cause le modèle traditionnel qui proposait que l’homéostasie de taille reposait sur l’adaptation de la durée du cycle et mis en avant un rôle de la régulation de la vitesse de croissance. Cependant, aucun modèle n’a réellement été proposé ou démontré. La nature et l’existence même d’un mécanisme maintenant l’homéostasie de taille des cellules de mammifère est en fait discutée (Lloyd, 2013).Pour caractériser l’homéostasie de taille des cellules de mammifères, nous avons développé une technique permettant pour la première fois la mesure du volume de ces cellules sur des cycles complets (Cadart et al., 2017; Zlotek-Zlotkiewicz et al. 2015). Nous montrons que plusieurs types cellulaires (HT29, MDCK et HeLa) se comportent d’une manière similaire à celle d’un « adder ». Pour tester davantage cette observation, nous induisons artificiellement des divisions asymétriques en confinant les cellules dans des micro-canaux. Nous observons que les asymétries de tailles sont réduites mais pas complètement corrigées au cours du cycle suivant, à la manière d’un « adder ». Pour comprendre comment la croissance et la progression dans le cycle sont coordonnées et génère cet « adder », nous combinons notre méthode de mesure de volume avec un suivi de la progression dans les différentes phases du cycle. Nous montrons que la durée de la phase G1 est inversement corrélée au volume initial des cellules. Cependant, cette corrélation semble contrainte par une durée minimale de G1 mise en évidence lors de l’étude de cellules artificiellement poussées à atteindre de grandes tailles. Néanmoins, même dans cette condition où la modulation de la durée du cycle est perdue, l’observation du « adder » est maintenue. Ceci suggère un rôle complémentaire de la régulation de la vitesse de croissance des cellules. Nous proposons donc une méthode pour estimer théoriquement la contribution relative de l’adaptation de la vitesse de croissance et de la durée du cycle dans le contrôle de la taille. Nous utilisons cette méthode pour proposer un cadre général où comparer le processus homéostatique des bactéries et de nos cellules. En conclusion, notre travail apporte pour la première fois la démonstration que les cellules de mammifères maintiennent l’homéostasie grâce à un mécanisme similaire au « adder ». Ce mécanisme semble impliquer à la fois une modulation de la durée du cycle et du taux de croissanceThe way proliferating mammalian cells maintain a constant size through generations is still unknown. This question is however central because size homeostasis is thought to occur through the coordination of growth and cell cycle progression. In the yeast S. pombe for example, the trigger for cell division is the reach of a target size (Fantes, 1977). This mechanism is referred to as ‘sizer’. The homeostatic behavior of bacteria and daughter cells of the yeast S. cerevisiae on the contrary was recently characterized as an ‘adder’ where all cells grow by the same absolute amount of volume at each cell cycle. This leads to a passive regression towards the mean generation after generation (Campos et al., 2014; Soifer et al., 2016; Taheri-Araghi et al., 2015). These findings were made possible by the development of new technologies enabling direct and dynamic measurement of volume over full cell cycle trajectories. Such measurement is extremely challenging in mammalian cells whose shape constantly fluctuate over time and cycle over 20 hours long periods. Studies therefore privileged indirect approaches (Kafri et al., 2013; Sung et al., 2013; Tzur et al., 2009) or indirect measurement of cell mass rather than cell volume (Mir et al. 2014; Son et al., 2012). These studies showed that cells overall grew exponentially and challenged the classical view that cell cycle duration was adapted to size and instead proposed a role for growth rate regulation. To date however, no clear model was reached. In fact, the nature and even the existence of the size homeostasis behavior of mammalian cells is still debated (Lloyd, 2013).In order to characterize the homeostatic process of mammalian cells, we developed a technique that enable measuring, for the first time, single cell volume over full cell cycle trajectories (Cadart et al., 2017; Zlotek-Zlotkiewicz et al. 2015). We found that several cell types, HT29, HeLa and MDCK cells behaved in an adder-like manner. To further test the existence of homeostasis, we artificially induced asymmetrical divisions through confinement in micro-channels. We observed that asymmetries of sizes were reduced within the following cell cycle through an ‘adder’-like behavior. To then understand how growth and cell cycle progression were coordinated in way that generates the ‘adder’, we combined our volume measurement method with cell cycle tracking. We showed that G1 phase duration is negatively correlated with initial size. This adaptation is however limited by a minimum duration of G1, unraveled by the study of artificially-induced very large cells. Nevertheless, the adder behavior is maintained even in the absence of time modulation, thus suggesting a complementary growth regulatory mechanism. Finally, we propose a method to estimate theoretically the relative contribution of growth and timing modulation in the overall size control and use this framework to compare our results with that of bacteria. Overall, our work provides the first evidence that proliferating mammalian cells behave in an adder-like manner and suggests that both growth and cell cycle duration are involved in size control
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Ricolo, Delia. "Cytoskeletal modulation of single-cell branching." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/404782.
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The embryonic tracheal system of Drosophila melanogaster consists of a network of interconnected epithelial tubes of different size and architecture characterized by different cellular mechanisms of tube formation. The main branches of the Drosophila tracheal system have an extracellular lumen because their cells fold to form a tube. However, terminal cells (TCs), specialized cells designed to connect the tracheal system to target tissues, form unicellular branches by generating of a subcellular lumen. This topology of unicellular tubes is a good model to clarify the mechanisms that orchestrate single-cell branching, a process parallel to capillary sprouting in blood vessels. During tracheal embryonic development, TCs produce seamless tubes, generating a cytoplasmic extension, by cell elongation, and a concurrent intracellular luminal space surrounded by an apical membrane. Cell elongation and subcellular lumen formation are very much dependent on cytoskeleton reorganization.
The main aim of this thesis was to understand new aspects of cytoskeletal modulation that orchestrate subcellular lumen formation. In particular, we have addressed this aim analysing mutants displaying an increase in subcellular lumen branching and mutants characterized by the absence of the subcellular lumen.
We found that mutations in Regulator of Cyclin A (Rca1) and Cyclin A (CycA) affect subcellular branching, causing TCs to form more than one subcellular lumen. The effect of Rca1 is post-mitotic in the tracheal system, and depends on an amplification of centrosome number. Other mutant conditions, characterized by the increase of centrosome number, such as Slimb (slmb) and the overexpression of SAK also show excess of subcellular lumen branching. Furthermore, we showed that de novo lumen formation is impaired in mutant embryos with low centrosome numbers such as sas4 and is restored in the double mutant Rca1; sas4.
The data presented here define a requirement for the centrosome as a microtubule organizing center (MTOC) for the initiation of subcellular lumen formation. We propose that in wt condition two centrosomes are needed to arrange the specific intracellular TC organization necessary to generate a subcellular lumen, and that an excess of centrosome numbers allows for an increase in single- cell branching.
We also analysed the involvement of the spectraplakin Short-stop (Shot) in the cytoskeletal organization of the TCs. Shot is a multifunctional protein involved in many aspects of cytoskeletal organization in different tissues, which can operate as a single cytoskeleton component as well as coordinating cytoskeletal elements between them. This functional versatility of Shot is probably reflected by the abundant generation of isoforms and by the modulation of its numerous domains.
We found that the overexpression of shot in the tracheal system induces extra-branching of the subcellular lumen and this effect depends mainly on the C-tail domain at the C- terminus and its involvement in the stabilization/polimerization of MTs. On the other hand, by examining loss of function alleles, analysing its structural function and visualizing Shot accumulation, we suggest that Shot is not just involved in MT organization in the TC but it also acts as a crosslinker between MTs and the actin network. The first calponin domain (CH1) of the acting binding domain (ABD) at the N-terminal is involved in this cross-linking activity.
Finally, we provide some data indicating a functional overlap between the spectraplakin and the microtubule associated protein (MAP) Tau during subcellular lumen formation.Las células terminales (TCs) de la tráquea del embrión de Drosophila melanogaster son capaces de generar un lumen subcelular y son utilizadas como modelo para la formación de tubos unicelulares de tipo “seamless”. La generación de dicho lumen depende estrictamente de una especifica organización del citoesqueleto que permite la formación de una nueva membrana apical en el interior de la TC. El objetivo del trabajo aquí presentado ha sido lo de aclarar nuevos aspectos de la modulación del citoesqueleto en el contexto de la formación del lumen sub-celular. Los mutantes de Regulator of Cyclin A (Rca1) y CycA (Cyclin A) están caracterizados por TC con mas de un lumen subcelular. El efecto de Rca1 es post-mitótico y esta causado por un aumento del numero de centrosomas. Reportamos, atraves el estudio de Rca1 y otros mutantes afectados en el numero de centrosomas, una estricta asociación entre centrosomas y formación del lumen sub-celular. Nuestros datos revelan, por primer vez, la función de los centrosomas como centros de organización de microtubulos (MTOC) en la TC y que un exceso de centrosomas puede causar un aumento en la capacidad de ramificación del lumen. En este trabajo también hemos analizado la función de la spectraplakina Short-stop (Shot). A través de experimentos de sobre-expresión y falta de función de shot, integrados con estudios estructura-función y de localización de sus productos proteicos hemos concluido que la spectraplakina actúa el la TC acudiendo a diferentes grados de organización citosqueletrica; en nuestro modelo Shot es capaz de promover la estabilización/polymerizacion de microtubulos, y un exceso de esta función puede causar extra ramificación en la TC. Por otro lado, Shot esta implicado en la correcta conexión entre la red de microtubulos y la actina y su falta influye negativamente la formación del lumen sub-celular. También reportamos datos preliminares que indican una superposición funcional entre Shot y la proteína asociada a microtulos (MAP) Tau durante el desarrollo del la TC.
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Forsythe, Paul. "The modulation of mast cell activity." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388087.
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Watt, A. P. "The modulation of mast cell activity." Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368527.
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Luizet, Jean-Baptiste. "Host Cell modulation by Brucella effectors." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1157.
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Brucella abortus est une bactérie pathogène responsable d’une zoonose ré-émergente causant plus de 500 000 décès par an. Brucella est une bactérie à Gram négative facultative intracellulaire capable d’infecter un grand spectre de cellules différents en entrant par phagocytose ou macropinocytose. Une fois à l’intérieur de la cellule, Brucella est retrouvée dans une vacuole doublement membranée appelée Brucella-containing vacuole (BCV). Brucella va alors interagir partiellement avec les différents compartiments endosomaux et lysosomaux afin d’établir sa niche réplicative au sein du réticulum endoplasmique est un aspect clé de sa virulence. Pour cela il a été démontré que Brucella abortus possède le système de sécrétion de type IV (SST4) démontré pour être un facteur de virulence majeur très répandu chez de nombreuses bactéries pathogènes. Mon projet de thèse consiste à caractériser un effecteur identifié pour être secrété par ce SST4. Nous avons appelé cet effecteur Brucella secreted protein L (BspL). Nous avons pu par différentes approches biologiques déterminer son mode d’action chez les cellules hôtes infectées ainsi que son importance pour le cycle intracellulaire de la bactérie. Nous avons en effet vu que cet effecteur localisait au sein du réticulum endoplasmique, organelle majeure de la cellule eucaryote, et induisait du stress. Ce stress est ressenti par la cellule grâce à différents senseurs cellulaires qui vont converger vers l’activation d’une réponse cellulaire appelée «UnfoldedProtein Response». Cette voie cellulaire va par différents mécanismes moléculaires tenter de contrer ce désordre induit au sein du réticulum afin de restaurer une homéostasie cellulaire. Cependant en recherchant de potentielles de notre effecteur BspL nous avons identifié Homocysteine-responsive endoplasmic reticulum-resident ubiquitin-like domain member 1 (Herp) une protéine impliquée dans de nombreux processus de régulations physiologiques du réticulum en cas de stress comme la dégradation associée au réticulum (ERAD). Nous avons donc par la suite démontré que l’action de BspL n’était pas uniquement d’induire du stress mais d’augmenter la capacité d’action de l’ERAD au sein de la cellule. Par ailleurs nous avons vu que BspL était important pour Brucella dans le contrôle de la cinétique de formations de ses vésicules de sortie de la cellule afin de pouvoir faire son cycle sans sortir prématurément. Ainsi l’identification de cet effecteur a permis de mettre en évidence l’importance de l’ERAD pour la première fois dans la pathogénie de Brucella. De plus cet effecteur est le premier à être identifié pour participer dans la régulation des vacuoles de sortie de Brucella. En parallèle nous avons vu que BspL impactait d’autres organites qui sont les mitochondries en fragmentant la connectivité de ce réseau mitochondrial. Aujourd’hui nous savons que les mitochondries et le réticulum sont étroitement connectés notamment avec l’implication du réticulum dans le processus de fission mitochondriale. Par ailleurs il est également connu que l’induction de stress par des agents physiques ou chimiques également fragmente le réseau mitochondrial. Nous avons néanmoins vu que le processus de fragmentation mitochondriale des mitochondries étaient indépendants du stress induit par BspL. Ces résultats ont été également confirmés en infection avec la comparaison d’une souche sauvage et mutante pour le gène codant pour BspL. En conclusion nous avons identifié un effecteur de Brucella associé au détournement de diverses fonctions au sein de la cellule. Il a permis de mettre en évidence l’importance du contrôle de l’ERAD pour contrôler la cinétique de réplication de la bactérie. Par ailleurs le fait que BspL soit également associé aux mitochondries semblent indiquer que l’effecteur pourrait avoir un rôle différentiel au cours du temps pendant l’infectionThis work provides new insights not only into Brucella pathogenesis, but also places effector targeting of the endoplasmic reticulum quality control machinery at the center of bacterial intracellular trafficking, a completely novel research topic that could be of relevance for other bacterial pathogens. The endoplasmic reticulum-associated degradation (ERAD) pathway plays a vital role in this quality control process, co-regulated with protein folding, stress responses and degradation pathways. Dysfunction of these processes can lead to severe diseases due to either the accumulation of misfolded proteins, namely neurodegenerative diseases; or due to the destruction of the entire pool of a given protein, such as the case of cystic fibrosis transmembrane conductance regulator (CFTR). Certain viruses have been shown in the past to directly hijack ERAD components to control immune responses and viral assembly. However, little is known on the control of ERAD during bacterial infections. In addition, insights into ERAD modulation could have an important impact in clinical research, for example, by providing new clues on how to boost the cell’s capacity to handle misfolded proteins. Brucella is an excellent model intracellular pathogen, with a well characterized cellular cycle that relies on a type IV secretion system to establish a replicative niche derived from the endoplasmic reticulum. It is then able to modify this vacuole by a currently unknown mechanism, induce autophagy and form vacuoles that will enable bacterial escape from the cell (Starr et al Cell Host and Microbe 2011). The effector proteins that mediate the formation of these Brucella replicative and autophagy vacuoles remain unknown. Here we identify a new type IV secretion effector that interacts with Herp to facilitate ERAD and delay the formation of autophagic Brucella-containing vacuoles to prevent premature bacterial dissemination. Intriguingly, we also show that ERAD is fine-tuned during infection as at early stages blocking of ERAD is beneficial whereas at late stages of the infection it results in premature egress. The work is obviously of interest for the Brucella community with the characterization of a novel type IV secretion system effector and, in addition, the identification of the first effector implicated in control of the formation of autophagic Brucella-containing vacuoles. However, our study will also appeal to a broader audience as it identifies an eukaryotic target not previously implicated in bacterial pathogenesis, Herp a key modulator of ERAD highlighting a novel mechanism of bacterial regulation of the endoplasmic reticulum quality control machinery for intracellular trafficking
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Brown, Marena Dessette. "Sickle cell-endothelial interactions : modulation of cell adhesion molecule expression." Diss., Georgia Institute of Technology, 1995. http://hdl.handle.net/1853/11306.
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Wu, Chia-Yung. "Control of gene expression by cell size." Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/57564.
Full textAbstract:
Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2010.This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student submitted PDF version of thesis.
Includes bibliographical references.
Polyploidy, increased copy number of whole chromosome sets in the genome, is a common cellular state in evolution, development and disease. Polyploidy enlarges cell size and alters gene expression, producing novel phenotypes and functions. Although many polyploid cell types have been discovered, it is not clear how polyploidy changes physiology. Specifically, whether the enlarged cell size of polyploids causes differential gene regulation has not been investigated. In this thesis, I present the evidence for a size-sensing mechanism that alters gene expression in yeast. My results indicate a causal relationship between cell size and gene expression. Ploidy-associated changes in the transcriptome therefore reflect transcriptional adjustment to a larger cell size. The causal and regulatory connection between cell size and transcription suggests that the physical features of a cell (such as size and shape) are a systematic factor in gene regulation. In addition, cell size homeostasis may have a critical function - maintenance of transcriptional homeostasis.
by Chia-Yung Wu.
Ph.D.
Books on the topic "Modulation of cell size"
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Young-Joon, Surh, ed. Dietary modulation of cell signaling pathways. Boca Raton: Taylor & Francis, 2008.
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Rabinovich, Peter M., ed. Synthetic Messenger RNA and Cell Metabolism Modulation. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-260-5.
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Martin, Ashley Diane. Modulation of endothelial cell characteristics by pericytes. [s.l: The Author], 1998.
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Seo, Jeong Taeg. Modulation of intracellular pH and cell volume in salivary glands. Manchester: University of Manchester, 1995.
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Rabinovich, Peter M. Synthetic messenger RNA and cell metabolism modulation: Methods and protocols. New York: Humana Press, 2013.
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Pan, Kally Zhang. Cell Size Control in Fission Yeast. [New York, N.Y.?]: [publisher not identified], 2013.
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Somogyi, Roland. Modulation of gap junction channels in exocrine cells of the pancrea: Interactions with intracellular signal transduction mechanisms = Modulation von Zell-Zellkanälen in exokrinen Zellen des Pankreas : Interaktionen mit intrazellulären Signaltansduktionsmechanismen. Konstanz: Universitätsverlag Konstanz, 1989.
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McQuaid, Karen E. Acute modulation of endothelial cell barrier function by reactive oxygen and nitrogen species. Dublin: University College Dublin, 1997.
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Fox, Gerard B. Behavioural, functional and pharmacological modulation of rodent neural cell adhesion molecule mediated neuroplasticity. Dublin: University College Dublin, 1995.
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Florian, Lang, ed. Cell volume regulation. Basel: Karger, 1998.
Find full textBook chapters on the topic "Modulation of cell size"
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Kumar Das, Susanta, and Madhusweta Das. "Size Modulation Operations." In Fundamentals and Operations in Food Process Engineering, 279–318. Boca Raton : Taylor & Francis, CRC Press, 2019.: CRC Press, 2019. http://dx.doi.org/10.1201/9780429058769-7.
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De Mello, Walmor C. "Modulation of Junctional Permeability." In Cell-to-Cell Communication, 29–64. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1917-7_2.
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Mencía Castaño, Irene, Rosanne M. Raftery, Caroline M. Curtin, Johannes Grillari, Heinz Redl, and Fergal J. O’Brien. "microRNA Modulation." In Cell Engineering and Regeneration, 511–76. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-08831-0_34.
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Castaño, Irene Mencía, Rosanne M. Raftery, Caroline M. Curtin, Johannes Grillari, Heinz Redl, and Fergal J. O’Brien. "microRNA Modulation." In Cell Engineering and Regeneration, 1–66. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-37076-7_34-1.
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Sveiczer, Ákos, and Anna Rácz-Mónus. "Cell Cycle, Cell Size Regulation." In Encyclopedia of Systems Biology, 343–46. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_8.
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Hong, Keelung, Nejat Düzgüneş, Paul R. Meers, and Demetrios Papahadjopoulos. "Protein Modulation of Liposome Fusion." In Cell Fusion, 269–84. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-9598-1_12.
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Haselton, F. R., J. S. Alexander, S. N. Mueller, and A. P. Fishman. "Modulation of Endothelial Paracellular Permeability." In Endothelial Cell Dysfunctions, 103–26. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-0721-9_6.
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Rogosa, Morrison, Micah I. Krichevsky, and Rita R. Colwell. "Individual Vegetative Cell Size." In Springer Series in Microbiology, 58–59. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4986-3_6.
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Okhamafe, Augustine O., and Mattheus F. A. Goosen. "Modulation of Membrane Permeability." In Cell Encapsulation Technology and Therapeutics, 53–62. Boston, MA: Birkhäuser Boston, 1999. http://dx.doi.org/10.1007/978-1-4612-1586-8_5.
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Rahmann, H., and H. Wiegandt. "Gangliosides and Modulation of Neuronal Functions." In Cell to Cell Signals in Plants and Animals, 212–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76470-7_15.
Full textConference papers on the topic "Modulation of cell size"
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Tang, Lingling, and Tomoyuki Yoshie. "Three-dimensional photonic crystal waveguides and resonators by unit cell size modulation." In Integrated Optoelectronic Devices 2008, edited by Ali Adibi, Shawn-Yu Lin, and Axel Scherer. SPIE, 2008. http://dx.doi.org/10.1117/12.763273.
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Stern, David M., Sara Rimon, Todd Scott, and Peter P. Nawroth. "MODULATION OF ENDOTHELIAL CELL COAGULANT PROPERTIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642946.
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As the cells forming the luminal vascular surface, endothelium is strategically located to play a role in the regulation of coagulation. Participation of endothelium in coagulation involves specific receptors on the cell surface functioning at the level of initiation and propagation of hemostatic reactions. In the anticoagulant protein C pathway, for example, the receptor thrombomodulin initiates thrombin-mediated activation of protein C and a binding site for protein S on bovine endothelium promotes assembly of the functional activated protein C/protein S complex. Endothelium also synthesizes, stores and releases functional protein S constitutively and in response to specific stimuli such as norepinephrine.Since activation of protein C requires thrombin formation in proximity to the vessel wall, we have examined procoagulant reactions on the endothelial cell surface. Endothelium provides a receptor for Factor IX/IXa which is relatively selective for the enzyme form and facilitates Factor IXa-VIII-mediated activation of Factor X. Half-maximal Factor Xa formation occurs at a Factor IXa concentration of 0.4nM on endothelium, whereas lOnM is required on liposomes. This concentration of Factor IXa corresponds to that which results in half-maximal occupancy of endothelial cell Factor IXa binding sites in the presence of Factors VIII and X, thus correlating kinetics and binding measurements. Crosslinking and ligand blotting studies have shown that the receptor is a protein with a molecular weight of ∼160,000. The clinical significance of this receptor is suggested by the moderately severe bleeding disorder observed in a patient with hemophilia B due to an abnormal Factor IX molecule, Factor IXalabama (Factor IXala). Although the coagulant activity of Factor IXala is only mildly decreased on phospholipids, it is severely impaired on endothelium. The affinity of Factor IXala for the endothelial cell Factor X activation complex is decreased by 20-fold compared with the normal enzyme and the binding affinity is similarly decreased. Since the molecular defect in Factor IXala has been previously shown to consist of a single point mutation in the growth factor domain, this indicates a role for the growth factor domain in receptor, recognition.The picture of endothelial cell coagulant properties which emerges from these and other studies is one in which endothelium has either an anticoagulant or procoagulant potential, depending on modulation of receptor expression and release of secreted products. In the quiescent state, anticoagulant mechanisms predominate with only limited amounts of procoagulant activity: there is little tissue factor activity and only a basal level of receptors for Factor IX/lXa. Activation of endothelium by Tumor Necrosis Factor (TNF) or Interleukin 1 can shift this balance. Tissue factor synthesis and expression occurs in a dose-dependent manner, being half-maximal at a TNF concentration of about 150pM. TNF also increases the number of Factor IX/lXa binding sites. Concomitant with enhancement of endothelial cell procoagulant properties is a suppression of cell surface cofactor activity for the anticoagulant protein C pathway. Endothelial cell-dependent, thrombin-mediated activated protein C formation is decreased by 70-80% and activated protein C-protein S-mediated Factor Va inactivation decreases by over 90%. Following the in vivo infusion of Interleukin 1, similar changes in endothelial cell coagulant properties were observed on aortic segments with fibrin deposition occurring on the functionally altered, but morphologically intact endothelium. This modulation of endothelial cell coagulant properties could underlie the prothrombotic state associated with inflammatory disorders and could also explain the recently observed selective intravascular thrombosis of tumor vasculature seen in vivo in meth A sarcomas after administration of TNF.Thus, although endothelium was initially felt to be hemostatically inert, this apparent lack of activity actually masks a delicate balance of procoagulant and anticoagulant mechanisms. The balance can be effectively shifted by physiologic mediators, such as monokines, which alter receptor expression on the endothelial cell surface. Changes in endothelial cell hemostatic properties may be an early indicator of vessel wall disease and underlie the pathogenesis of localized thrombotic processes.
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Young, Richard A., Hans Von Blanckensee, Richard T. Marrocco, and Russell De Valois. "Spatial and temporal tuning differences between broadband and opponent cells in monkey lateral geniculate nucleus." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1987. http://dx.doi.org/10.1364/oam.1987.tuo1.
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The responses of macaque monkey lateral geniculate neurons to full-field temporal achromatic flicker and drifting sine-wave gratings (mean luminance 17 cd/m2) were studied using single-unit recording methods. Cells were also classified into spectrally opponent or broadband on the basis of their responses to diffuse narrowband spectral luminance increments, using principal-component analysis1 and cross-point techniques. The results showed that the mean peak temporal frequency response of broadband cells (10.8 ± 3.2 Hz, n = 12) was significantly greater than that of opponent cells (4.0 ± 0.3 Hz, n = 36) regardless of stimulus modulation level, electrode depth, or whether a cell was the on-or off-center type. Also, the mean response amplitude to the optimum temporal frequency stimulus was significantly larger for broadband cells than opponent cells, again for all conditions tested. Finally, broadband cells responded to lower spatial frequencies of drifting gratings than did opponent cells at all stimulus modulations (e.g., 1.1 ± 0.1 cycles/deg, n = 14 for broadband cells; 1.9 ± 0.2 cycles/deg, n = 45 for opponent cells, 95% stimulus modulation). These spatiotemporal differences between opponent and broadband cell groups in the monkey LGN are consistent with differences between opponent and broadband chromatic channels as inferred from human psychophysical studies.
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Seiple, William, Karen Holopigian, and Monica Lorenzo. "ERG Flicker Sensitivity as a Function of Retinal Eccentricity and Adaptation Level." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1993. http://dx.doi.org/10.1364/navs.1993.nmd.1.
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Both temporal modulation sensitivity and flicker fusion frequency (CFF) increase with increasing eccentricity. Based upon correlations between temporal sensitivity and cone outer segment diameter, it has been proposed that these temporal frequency changes may be due to differences in receptor morphology.1,2 Alternatively, CFF can be made independent of retinal eccentricity by M-scaling (scaling for the number of ganglion cells) and F-scaling (scaling for the luminous flux per ganglion cell). These findings suggested that changes in sensitivity may be correlated with post-receptoral factors such as the number of ganglion cells stimulated, their average receptive field size, and cortical magnification.3,4,5
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Wang, Weizhong, and Matthias Preindl. "Extended ZVS Modulation for a Dual Cell Link in the Demand of Faster Balancing." In 2019 IEEE/SICE International Symposium on System Integration (SII). IEEE, 2019. http://dx.doi.org/10.1109/sii.2019.8700460.
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Cau, Giorgio, Daniele Cocco, and Fabio Serra. "Energy and Cost Analysis of Small Size CHP Coal Gasification Plants Integrated With Syngas Storage Systems." In ASME Turbo Expo 2012: Turbine Technical Conference and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/gt2012-68976.
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This study evaluates the load modulation capabilities of small and medium size CHP systems based on integrated coal gasification and syngas storage (ICGSS) power plants. ICGSS systems can perform a load-following service since a portion of the produced syngas is stored during periods of low energy demand and used to increase power output during periods of peaking demand. In particular, the main energy and economic performance of ICGSS power generation plants were evaluated with reference to three different prime movers (gas turbines, internal combustion engines and hybrid fuel cell systems) and as a function of the required electrical load curve. Moreover, a preliminary economic analysis was also carried out to evaluate the energy production cost in comparison with base-load energy production cost. The results of the study show that ICGSS power plants offer considerable scope for enhancing operating flexibility and load modulation capabilities of CHP systems based on coal gasification. In comparison to coal gasification power plants designed to produce only base-load energy, ICGSS systems require a more powerful prime mover and a larger coal gasification section. In the field of duty-cycles of more likely interest, the coal gasification section needs to be enlarged by 5–50% and a fraction from 2% to 16% of the produced syngas needs to be stored. ICGSS plants based on hybrid fuel cells performed better in terms of electrical efficiency. Moreover, with respect to the corresponding base-load systems, electrical efficiency decreases by about 2–3 percentage points for ICGSS-GT and ICGSS-ICE, while it increases by about 1–2 percentage points for ICGSS-HFC. Finally, syngas storage can reduce energy costs in CHP systems, especially in the case high peaking electricity requirements, large useful heat productions and by using ICGSS based on ICE as prime movers.
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Abbatiello, Amar, and Md Ahasan Habib. "Development of an In-House Customized Perfusion-Based Bioreactor for 3D Cell Culture." In ASME 2022 17th International Manufacturing Science and Engineering Conference. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/msec2022-85374.
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Abstract Bio-fabrication in the modern age is moving closer to creating viable three-dimensional scaffolds. Both cell-encapsulated and cell-seeded scaffolds need to be cultured to allow for proper cell viability and proliferation. Typical cell culturing methods, due to the three-dimensional nature of the scaffolds, are ineffective as stagnant or even moving mediums cannot enter or pass through the scaffold to reach all the areas inside. To compensate, perfusion bioreactors were developed where a systematic modification of this dynamic culture setup can improve the in vivo stimuli and conditions, and eventually, the overall performance of tissue regeneration. To do this, a set of design modifications were implemented expecting better performance. During operation, the success of an experiment can be difficult without the dynamic feedback due to the fully enclosed nature of a cell-seeded and cell-encapsulated scaffold. To compensate, oxygen sensors have been implemented before and after the perfusion chamber to track the oxygen being used by the cells during the incubation period, giving us a window into the cell’s proliferation. The prototype takes advantage of a dual medium tank design which allowed us to replace the medium without stopping or interrupting perfusion. A cyclical pressure modulation device has been implemented to better simulate in vivo conditions by modulating the pressure within the chamber, mimicking the natural pressure cues within the body such as the heartbeat and movement. The bioreactor will also take advantage of a newly designed perfusion chamber that can accommodate an array of cassettes allowing for a wide assortment of scaffold shapes and sizes.
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Xu, Dongyan, Yuejun Kang, Dongqing Li, Deyu Li, Manoj Sridhar, Anthony B. Hmelo, and Leonard C. Feldman. "Ultra-Sensitive Fluidic Sensors by Integrating Fluidic Circuits and MOSFETs." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-42518.
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Nanofluidic sensors have been developed over the past decade and demonstrated the capability of sensing single DNA molecules. One important and promising class of nanofluidic devices detects single molecules by inserting a nanopore or nanochannel between two fluid cells and inducing an ionic current by applying an electric bias across the nanopore or nanochannel. When molecules are translocated through the nanopore/nanochannel, a modulation of the baseline ionic current can be observed. In this scheme, the ionic current modulation is approximately the same as the channel resistance modulation, requiring the channel size to be comparable to the molecules to be detected. Here we report on a new sensing scheme to detect the translocation of particles through a fluidic channel, which amplifies the resistance modulation by up to 75 times. In this scheme, the device connects the gate of a MOSFET with a fluidic circuit and monitors the modulation of MOSFET’s drain current to detect particles. We demonstrate that amplification can be achieved from both the fluidic circuit and the MOSFET. For a 9.86 μm diameter polystyrene bead that occupies 0.7% of the total volume of the sensing channel, results show that the drain current of the MOSFET is blocked by 30–46%. We also demonstrate the capability of this device to distinguish particles with similar sizes but different surface charges as they translocate through the sensing channel. More interestingly, the experiments with CD4+ T lymphocyte cells show another modulation pattern: the MOSFET’s drain current is first enhanced and then blocked, which is not fully understood and needs further investigation. Although at this moment the device is based on microchannels and the particles detected are micron-size beads and cells, we expect that the same scheme can be applied to nanofluidic circuits for single molecule detection.
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Müller, T. H., K. Rühr, H. H. Callisen, and W. G. Eisert. "MODULATION OF ANTITHROMBOTIC EFFECTS OF CULTURED HUMAN ENDOTHELIAL CELLS BY INHIBITORS OF CYCLOOXIGENASE OR PHOSPHODIESTERASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643364.
Full textAbstract:
Intact endothelial cells are known to form a non-thrombogenic surface and to actively restrict the extent of thrombus formation on denuded vessel walls via such mechanisms as the binding of thrombin and activation of protein C, or the synthesis and release of prostacyclin. In an in vitro system, we have investigated how platelet inhibitors modulate the antithrombotic effects of human endothelial cells. Human endothelial cells isolated from umbilical veins were plated on one half of a subendothelial matrix (SEM) harvested from bovine cornea endothelial cells. The endothelial cells were preincubated with a drug and then exposed to anticoagulated whole blood from human donors in the presence or absence of the same drug and agitated for 15 min. The number and size of platelets interacting with the SEM were quantified by morphometric analysis.In our in vitro system, platelet aggregates on SEM that was partially covered with human endothelial cells were significantly smaller than on uncovered SEM. No difference in platelet adhesion was observed. In the absence of endothelial cells, the cyclooxigenase inhibitors acetylsalicylic acid (ASA) and flurbiprofen strongly reduced the size of aggregates formed on the SEM. Pretreatment of only the endothelial cells with ASA increased the size of the aggregates, while ASA treatment of endothelial cells as well as the whole blood did not reduce the mean aggregate size below that of controls. in contrast, the platelet phosphodiesterase inhibitors AHP 719 and UDCG 212 strongly decreased platelet aggregation without reducing platelet adhesion not only in the absence but also in the presence of endothelial cells pretreated with the inhibitors.Our results demonstrate that this in vitro model of a partially injured vessel wall is well suited to study the effects of endothelial cells on platelet function. Moreover, inhibitors of phosphodiesterase in contrast to ASA have profound antithrombotic effects in this model.
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Mazumder, Sudip K., and Rajni K. Burra. "Fuel Cell Power Conditioner for Stationary Power System: Towards Optimal Design From Reliability, Efficiency, and Cost Standpoint." In ASME 2005 3rd International Conference on Fuel Cell Science, Engineering and Technology. ASMEDC, 2005. http://dx.doi.org/10.1115/fuelcell2005-74178.
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We describe an energy-efficient, fuel cell (FC) powerconditioning system (PCS) for stationary application, which draws practically zero switching-ripple current from the FC and can potentially meet the $40/kW cost target. The PCS consists of a zero-ripple boost converter (ZRBC) followed by a soft-switched and multi-level high-frequency (HF) inverter and a single-phase cycloconverter. The zero-ripple input inductor significantly reduces the input current ripple which may be necessary to enhance the long-term durability of the fuel cell. A new phase-shifted sine-wave modulation of the multi-level high frequency inverter is proposed which results in the zero voltage turn-on (ZVS) of all four switches (without the use of any auxiliary circuit components). For such a sine-wave modulation technique a > 90 % ZVS range is obtained from 25% of the full load to full load. Further, the line-frequency switching of the cycloconverter (at close to unity power factor) results in extremely low switching losses. The intermediate high voltage DC (HVDC) bus facilitates the inclusion of power systems based on other forms of alternative-energy techniques. A cost effective 1 kW prototype of the proposed PCS is built, which achieved a high overall efficiency. We present a detailed description of the operation of the PCS along with its key features and advantages. Finally, experimental results showing the performance and operation of the PCS are demonstrated.
Reports on the topic "Modulation of cell size"
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Paran, Ilan, and Allen Van Deynze. Regulation of pepper fruit color, chloroplasts development and their importance in fruit quality. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598173.bard.
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Pepper exhibits large natural variation in chlorophyll content in the immature fruit. To dissect the genetic and molecular basis of this variation, we conducted QTL mapping for chlorophyll content in a cross between light and dark green-fruited parents, PI 152225 and 1154. Two major QTLs, pc1 and pc10, that control chlorophyll content by modulation of chloroplast compartment size in a fruit-specific manner were detected in chromosomes 1 and 10, respectively. The pepper homolog of GOLDEN2- LIKE transcription factor (CaGLK2) was found as underlying pc10, similar to its effect on tomato fruit chloroplast development. A candidate gene for pc1was found as controlling chlorophyll content in pepper by the modulation of chloroplast size and number. Fine mapping of pc1 aided by bulked DNA and RNA-seq analyses enabled the identification of a zinc finger transcription factor LOL1 (LSD-One-Like 1) as a candidate gene underlying pc1. LOL1 is a positive regulator of oxidative stress- induced cell death in Arabidopsis. However, over expression of the rice ortholog resulted in an increase of chlorophyll content. Interestingly, CaAPRR2 that is linked to the QTL and was found to affect immature pepper fruit color in a previous study, did not have a significant effect on chlorophyll content in the present study. Verification of the candidate's function was done by generating CRISPR/Cas9 knockout mutants of the orthologues tomato gene, while its knockout experiment in pepper by genome editing is under progress. Phenotypic similarity as a consequence of disrupting the transcription factor in both pepper and tomato indicated its functional conservation in controlling chlorophyll content in the Solanaceae. A limited sequence diversity study indicated that null mutations in CaLOL1 and its putative interactorCaMIP1 are present in C. chinensebut not in C. annuum. Combinations of mutations in CaLOL1, CaMIP1, CaGLK2 and CaAPRR2 are required for the creation of the extreme variation in chlorophyll content in Capsicum.
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Barg, Rivka, Erich Grotewold, and Yechiam Salts. Regulation of Tomato Fruit Development by Interacting MYB Proteins. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7592647.bard.
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Background to the topic: Early tomato fruit development is executed via extensive cell divisions followed by cell expansion concomitantly with endoreduplication. The signals involved in activating the different modes of growth during fruit development are still inadequately understood. Addressing this developmental process, we identified SlFSM1 as a gene expressed specifically during the cell-division dependent stages of fruit development. SlFSM1 is the founder of a class of small plant specific proteins containing a divergent SANT/MYB domain (Barg et al 2005). Before initiating this project, we found that low ectopic over-expression (OEX) of SlFSM1 leads to a significant decrease in the final size of the cells in mature leaves and fruits, and the outer pericarp is substantially narrower, suggesting a role in determining cell size and shape. We also found the interacting partners of the Arabidopsis homologs of FSM1 (two, belonging to the same family), and cloned their tomato single homolog, which we named SlFSB1 (Fruit SANT/MYB–Binding1). SlFSB1 is a novel plant specific single MYB-like protein, which function was unknown. The present project aimed at elucidating the function and mode of action of these two single MYB proteins in regulating tomato fruit development. The specific objectives were: 1. Functional analysis of SlFSM1 and its interacting protein SlFSB1 in relation to fruit development. 2. Identification of the SlFSM1 and/or SlFSB1 cellular targets. The plan of work included: 1) Detailed phenotypic, histological and cellular analyses of plants ectopically expressing FSM1, and plants either ectopically over-expressing or silenced for FSB1. 2) Extensive SELEX analysis, which did not reveal any specific DNA target of SlFSM1 binding, hence the originally offered ChIP analysis was omitted. 3) Genome-wide transcriptional impact of gain- and loss- of SlFSM1 and SlFSB1 function by Affymetrix microarray analyses. This part is still in progress and therefore results are not reported, 4) Search for additional candidate partners of SlFSB1 revealed SlMYBI to be an alternative partner of FSB1, and 5) Study of the physical basis of the interaction between SlFSM1 and SlFSB1 and between FSB1 and MYBI. Major conclusions, solutions, achievements: We established that FSM1 negatively affects cell expansion, particularly of those cells with the highest potential to expand, such as the ones residing inner to the vascular bundles in the fruit pericarp. On the other hand, FSB1 which is expressed throughout fruit development acts as a positive regulator of cell expansion. It was also established that besides interacting with FSM1, FSB1 interacts also with the transcription factor MYBI, and that the formation of the FSB1-MYBI complex is competed by FSM1, which recognizes in FSB1 the same region as MYBI does. Based on these findings a model was developed explaining the role of this novel network of the three different MYB containing proteins FSM1/FSB1/MYBI in the control of tomato cell expansion, particularly during fruit development. In short, during early stages of fruit development (Phase II), the formation of the FSM1-FSB1 complex serves to restrict the expansion of the cells with the greatest expansion potential, those non-dividing cells residing in the inner mesocarp layers of the pericarp. Alternatively, during growth phase III, after transcription of FSM1 sharply declines, FSB1, possibly through complexing with the transcription factor MYBI serves as a positive regulator of the differential cell expansion which drives fruit enlargement during this phase. Additionally, a novel mechanism was revealed by which competing MYB-MYB interactions could participate in the control of gene expression. Implications, both scientific and agricultural: The demonstrated role of the FSM1/FSB1/MYBI complex in controlling differential cell growth in the developing tomato fruit highlights potential exploitations of these genes for improving fruit quality characteristics. Modulation of expression of these genes or their paralogs in other organs could serve to modify leaf and canopy architecture in various crops.
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Locy, Robert D., Hillel Fromm, Joe H. Cherry, and Narendra K. Singh. Regulation of Arabidopsis Glutamate Decarboxylase in Response to Heat Stress: Modulation of Enzyme Activity and Gene Expression. United States Department of Agriculture, January 2001. http://dx.doi.org/10.32747/2001.7575288.bard.
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Most plants accumulate the nonprotein amino acid, g-aminobutyric acid (GABA), in response to heat stress. GABA is made from glutamate in a reaction catalyzed by glutamate decarboxylase (GAD), an enzyme that has been shown by the Israeli PI to be a calmodulin (CaM) binding protein whose activity is regulated in vitro by calcium and CaM. In Arabidopsis there are at least 5 GAD genes, two isoforms of GAD, GAD1 and GAD2, are known to be expressed, both of which appear to be calmodulin-binding proteins. The role of GABA accumulation in stress tolerance remains unclear, and thus the objectives of the proposed work are intended to clarify the possible roles of GABA in stress tolerance by studying the factors which regulate the activity of GAD in vivo. Our intent was to demonstrate the factors that mediate the expression of GAD activity by analyzing the promoters of the GAD1 and GAD2 genes, to determine the role of stress induced calcium signaling in the regulation of GAD activity, to investigate the role of phosphorylation of the CaM-binding domain in the regulation of GAD activity, and to investigate whether ABA signaling could be involved in GAD regulation via the following set of original Project Objectives: 1. Construction of chimeric GAD1 and GAD2 promoter/reporter gene fusions and their utilization for determining cell-specific expression of GAD genes in Arabidopsis. 2. Utilizing transgenic plants harboring chimeric GAD1 promoter-luciferase constructs for isolating mutants in genes controlling GAD1 gene activation in response to heat shock. 3. Assess the role of Ca2+/CaM in the regulation of GAD activity in vivo in Arabidopsis. 4. Study the possible phosphorylation of GAD as a means of regulation of GAD activity. 5. Utilize ABA mutants of Arabidopsis to assess the involvement of this phytohormone in GAD activation by stress stimuli. The major conclusions of Objective 1 was that GAD1 was strongly expressed in the elongating region of the root, while GAD2 was mainly expressed along the phloem in both roots and shoots. In addition, GAD activity was found not to be transcriptionally regulated in response to heat stress. Subsequently, The Israeli side obtained a GAD1 knockout mutation, and in light of the objective 1 results it was determined that characterization of this knockout mutation would contribute more to the project than the proposed Objective 2. The major conclusion of Objective 3 is that heat-stress-induced changes in GAD activity can be explained by heat-stress-induced changes in cytosolic calcium levels. No evidence that GAD activity was transcriptionally or translationally regulated or that protein phosphorylation was involved in GAD regulation (objective 4) was obtained. Previously published data by others showing that in wheat roots ABA regulated GABA accumulation proved not to be the case in Arabidopsis (Objective 5). Consequently, we put the remaining effort in the project into the selection of mutants related to temperature adaptation and GABA utilization and attempting to characterize events resulting from GABA accumulation. A set of 3 heat sensitive mutants that appear to have GABA related mutations have been isolated and partially characterized, and a study linking GABA accumulation to growth stimulation and altered nitrate assimilation were conducted. By providing a better understanding of how GAD activity was and was not regulated in vivo, we have ruled out the use of certain genes for genetically engineering thermotolerance, and suggested other areas of endeavor related to the thrust of the project that may be more likely approaches to genetically engineering thermotolerance.
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Baker, Nicholas E. Cell Proliferation, Cell Death, and Size Regulation. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/adb248354.
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Baar, Joseph. Dendritic Cell-Based Immunotherapy of Breast Cancer: Modulation by CpG. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada431640.
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Baar, Joseph. Dendritic Cell-Based Immunotherapy of Breast Cancer: Modulation by CpG DNA. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412155.
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Sacchi, Nicoletta. Modulation of Breast Tumor Cell Response to Retinoids by Histone Deacetylase Inhibitors. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada417781.
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Cook-Mills, Joan M., Hidayatulla G. Munshi, Robert L. Perlman, and Donald A. Chambers. Mouse Hepatitis Virus Infection Suppresses Modulation of Mouse Spleen T- Cell Activation. Fort Belvoir, VA: Defense Technical Information Center, January 1988. http://dx.doi.org/10.21236/ada237464.
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Hurwitz, Arthur A. Modulation of T Cell Tolerance in a Murine Model for Immunotherapy of Prostatic Adenocarcinoma. Addendum. Fort Belvoir, VA: Defense Technical Information Center, September 2007. http://dx.doi.org/10.21236/ada475839.
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Mignatti, Paolo. Modulation of Breast Cancer Cell Function by Intracellular Signaling Through the Membrane-Type I Matrix Metalloproteinase. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada392922.
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