Relevant bibliographies by topics / Functional reprogramming

Academic literature on the topic 'Functional reprogramming'

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Published: 9 November 2023

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Journal articles on the topic "Functional reprogramming"

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Trakala, Marianna, Sara Rodríguez-Acebes, María Maroto, Catherine E. Symonds, David Santamaría, Sagrario Ortega, Mariano Barbacid, Juan Méndez, and Marcos Malumbres. "Functional Reprogramming of Polyploidization in Megakaryocytes." Developmental Cell 32, no. 2 (January 2015): 155–67. http://dx.doi.org/10.1016/j.devcel.2014.12.015.

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Kubatiev, A. A., and A. A. Pal'tsyn. "INTRACELLULAR BRAIN REGENERATION: A NEW VIEW." Annals of the Russian academy of medical sciences 67, no. 8 (August 11, 2012): 21–25. http://dx.doi.org/10.15690/vramn.v67i8.345.

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Mechanism of neuron regeneration in the cortex was discovered. Heterokaryon, a cell with two distinct nuclei, is formed by the fusion of neuron with oligodendrocyte. We showed that oligodendrocyte nucleus in heterokaryons is exposed to neuron-specific reprogramming. Oligodendrocyte nucleus becomes similar to neuron nucleus and in result of reprogramming is undefined from it according to morphology (size, shape, chromatin structure). Reprogrammed oligodendrocyte nuclei begin to express the neural specific markers NeuN and MAP2. Rate of transcription in the oligodendrocyte nuclei increases as in neurons. After completion of neuron-specific reprogrammin, second nucleus appears in neuron which increases the functional capacity of the cell. We present evidence that this process is the basis of physiological and reparative regeneration of the brain.
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Kumar, Satish, Joanne E. Curran, David C. Glahn, and John Blangero. "Utility of Lymphoblastoid Cell Lines for Induced Pluripotent Stem Cell Generation." Stem Cells International 2016 (2016): 1–20. http://dx.doi.org/10.1155/2016/2349261.

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A large number of EBV immortalized LCLs have been generated and maintained in genetic/epidemiological studies as a perpetual source of DNA and as a surrogatein vitrocell model. Recent successes in reprograming LCLs into iPSCs have paved the way for generating more relevantin vitrodisease models using this existing bioresource. However, the overall reprogramming efficiency and success rate remain poor and very little is known about the mechanistic changes that take place at the transcriptome and cellular functional level during LCL-to-iPSC reprogramming. Here, we report a new optimized LCL-to-iPSC reprogramming protocol using episomal plasmids encoding pluripotency transcription factors and mouse p53DD (p53 carboxy-terminal dominant-negative fragment) and commercially available reprogramming media. We achieved a consistently high reprogramming efficiency and 100% success rate using this optimized protocol. Further, we investigated the transcriptional changes in mRNA and miRNA levels, using FC-abs ≥ 2.0 and FDR ≤ 0.05 cutoffs; 5,228 mRNAs and 77 miRNAs were differentially expressed during LCL-to-iPSC reprogramming. The functional enrichment analysis of the upregulated genes and activation of human pluripotency pathways in the reprogrammed iPSCs showed that the generated iPSCs possess transcriptional and functional profiles very similar to those of human ESCs.
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Paoletti, Camilla, Carla Divieto, and Valeria Chiono. "Impact of Biomaterials on Differentiation and Reprogramming Approaches for the Generation of Functional Cardiomyocytes." Cells 7, no. 9 (August 21, 2018): 114. http://dx.doi.org/10.3390/cells7090114.

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The irreversible loss of functional cardiomyocytes (CMs) after myocardial infarction (MI) represents one major barrier to heart regeneration and functional recovery. The combination of different cell sources and different biomaterials have been investigated to generate CMs by differentiation or reprogramming approaches although at low efficiency. This critical review article discusses the role of biomaterial platforms integrating biochemical instructive cues as a tool for the effective generation of functional CMs. The report firstly introduces MI and the main cardiac regenerative medicine strategies under investigation. Then, it describes the main stem cell populations and indirect and direct reprogramming approaches for cardiac regenerative medicine. A third section discusses the main techniques for the characterization of stem cell differentiation and fibroblast reprogramming into CMs. Another section describes the main biomaterials investigated for stem cell differentiation and fibroblast reprogramming into CMs. Finally, a critical analysis of the scientific literature is presented for an efficient generation of functional CMs. The authors underline the need for biomimetic, reproducible and scalable biomaterial platforms and their integration with external physical stimuli in controlled culture microenvironments for the generation of functional CMs.
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Özcan, Ismail, and Baris Tursun. "Identifying Molecular Roadblocks for Transcription Factor-Induced Cellular Reprogramming In Vivo by Using C. elegans as a Model Organism." Journal of Developmental Biology 11, no. 3 (August 31, 2023): 37. http://dx.doi.org/10.3390/jdb11030037.

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Generating specialized cell types via cellular transcription factor (TF)-mediated reprogramming has gained high interest in regenerative medicine due to its therapeutic potential to repair tissues and organs damaged by diseases or trauma. Organ dysfunction or improper tissue functioning might be restored by producing functional cells via direct reprogramming, also known as transdifferentiation. Regeneration by converting the identity of available cells in vivo to the desired cell fate could be a strategy for future cell replacement therapies. However, the generation of specific cell types via reprogramming is often restricted due to cell fate-safeguarding mechanisms that limit or even block the reprogramming of the starting cell type. Nevertheless, efficient reprogramming to generate homogeneous cell populations with the required cell type’s proper molecular and functional identity is critical. Incomplete reprogramming will lack therapeutic potential and can be detrimental as partially reprogrammed cells may acquire undesired properties and develop into tumors. Identifying and evaluating molecular barriers will improve reprogramming efficiency to reliably establish the target cell identity. In this review, we summarize how using the nematode C. elegans as an in vivo model organism identified molecular barriers of TF-mediated reprogramming. Notably, many identified molecular factors have a high degree of conservation and were subsequently shown to block TF-induced reprogramming of mammalian cells.
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Kalo, Eric, Scott Read, and Golo Ahlenstiel. "Reprogramming—Evolving Path to Functional Surrogate β-Cells." Cells 11, no. 18 (September 8, 2022): 2813. http://dx.doi.org/10.3390/cells11182813.

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Numerous cell sources are being explored to replenish functional β-cell mass since the proof-of -concept for cell therapy of diabetes was laid down by transplantation of islets. Many of these cell sources have been shown to possess a degree of plasticity permitting differentiation along new lineages into insulin-secreting β-cells. In this review, we explore emerging reprograming pathways that aim to generate bone fide insulin producing cells. We focus on small molecules and key transcriptional regulators that orchestrate phenotypic conversion and maintenance of engineered cells.
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Peng, Bo, Hui Li, and Xuan-Xian Peng. "Functional metabolomics: from biomarker discovery to metabolome reprogramming." Protein & Cell 6, no. 9 (July 2, 2015): 628–37. http://dx.doi.org/10.1007/s13238-015-0185-x.

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Tian, E., Guoqiang Sun, Guihua Sun, Jianfei Chao, Peng Ye, Charles Warden, Arthur D. Riggs, and Yanhong Shi. "Small-Molecule-Based Lineage Reprogramming Creates Functional Astrocytes." Cell Reports 16, no. 3 (July 2016): 781–92. http://dx.doi.org/10.1016/j.celrep.2016.06.042.

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Zhu, Hui, Srilatha Swami, Pinglin Yang, Frederic Shapiro, and Joy Y. Wu. "Direct Reprogramming of Mouse Fibroblasts into Functional Osteoblasts." Journal of Bone and Mineral Research 35, no. 4 (December 30, 2019): 698–713. http://dx.doi.org/10.1002/jbmr.3929.

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Zhou, Huanyu, Matthew E. Dickson, Min Soo Kim, Rhonda Bassel-Duby, and Eric N. Olson. "Akt1/protein kinase B enhances transcriptional reprogramming of fibroblasts to functional cardiomyocytes." Proceedings of the National Academy of Sciences 112, no. 38 (September 9, 2015): 11864–69. http://dx.doi.org/10.1073/pnas.1516237112.

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Conversion of fibroblasts to functional cardiomyocytes represents a potential approach for restoring cardiac function after myocardial injury, but the technique thus far has been slow and inefficient. To improve the efficiency of reprogramming fibroblasts to cardiac-like myocytes (iCMs) by cardiac transcription factors [Gata4, Hand2, Mef2c, and Tbx5 (GHMT)], we screened 192 protein kinases and discovered that Akt/protein kinase B dramatically accelerates and amplifies this process in three different types of fibroblasts (mouse embryo, adult cardiac, and tail tip). Approximately 50% of reprogrammed mouse embryo fibroblasts displayed spontaneous beating after 3 wk of induction by Akt plus GHMT. Furthermore, addition of Akt1 to GHMT evoked a more mature cardiac phenotype for iCMs, as seen by enhanced polynucleation, cellular hypertrophy, gene expression, and metabolic reprogramming. Insulin-like growth factor 1 (IGF1) and phosphoinositol 3-kinase (PI3K) acted upstream of Akt whereas the mitochondrial target of rapamycin complex 1 (mTORC1) and forkhead box o3 (Foxo3a) acted downstream of Akt to influence fibroblast-to-cardiomyocyte reprogramming. These findings provide insights into the molecular basis of cardiac reprogramming and represent an important step toward further application of this technique.
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Dissertations / Theses on the topic "Functional reprogramming"

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Hoffmann, Daniel [Verfasser], and Hans-Ulrich [Akademischer Betreuer] Mösch. "Functional reprogramming of Candida glabrata epithelial adhesins by exchange of variable structural motifs / Daniel Hoffmann ; Betreuer: Hans-Ulrich Mösch." Marburg : Philipps-Universität Marburg, 2021. http://d-nb.info/1227580169/34.

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FARIA, PEREIRA MARLENE CRISTINA. "EPIGENETIC AND FUNCTIONAL ASSESSMENT OF ENHANCEROPATHIES ACROSS HUMAN MODELS: FOCUS ON GABRIELE-DE VRIES SYNDROME." Doctoral thesis, Università degli Studi di Milano, 2022. https://hdl.handle.net/2434/945230.

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Yin Yang 1 (YY1) is a ubiquitous zinc finger transcription factor (TF) that occupies active enhancers and promoters contributing to physical interactions between these regions via DNA looping. Increasing evidence shows that disruption of non-coding regions such as enhancers is prevalent across different neurodevelopmental disorders (NDDs) with intellectual disability (ID) features. Indeed, YY1 haploinsufficiency causes a NDD with ID, named Gabriele-de Vries syndrome (GADEVS). Although it is known that YY1 controls the expression of a dazzling list of genes and influences various cellular processes in numerous cell types, the impact of this TF in the neurodevelopment of the human cortex is yet to be unraveled. By taking advantage of disease-modeling as a tool to investigate the pathogenesis of GADEVS across different time points and tissues we gathered new insights about how YY1 haploinsufficiency exerts such a dramatic phenotype in individuals carrying mutations. We reprogrammed patient-derived and healthy somatic cells into induced-pluripotent stem cells (iPSCs) and observed, already at the pluripotent stage, a major transcriptional dysregulation. Moreover, since YY1-mutated patients exhibit ID features, we differentiated our cohort of iPSCs into cortical neurons as well organoids and were able to capture stage-specific striking features, not only at the transcriptomic level, but also structural and compartmentalization impairments. Of note, YY1-mutated neurons displayed synaptic disparities, sufficient to induce astrogliosis-like features in surrounding astrocytes, both shown to be critical for proper brain function and plasticity forms in the CNS. Instead, in cortical organoids we recapitulated features of abnormal ventricle formation, pathological hallmarks observed in GADEVS patients and mice models followed by ID and developmental delay. This study showed, for the first time, the molecular signatures that possibly lead to cognitive defects in human patients and provide the first solid foundation for the development of therapeutic strategies and drug screening in the future.
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Jing, Chenzhi. "Characterisation of the effect and functional significance of Fcγ receptor crosslinking on metabolic processes in macrophages." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/280316.

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The metabolic state of an immune cell directly influences its ability to function and differentiate, ultimately affecting immunity, inflammation and tolerance. Different immune cell subsets have differing metabolic requirements. Macrophages, as the frontline, tissue-resident cells of the innate immune system, undergo profound metabolic reprogramming in response to environmental stimuli. To date, there has been little consideration how macrophage metabolism might be affected by humoral immunity. IgG antibodies are the soluble effector molecules of the adaptive humoral immune system. Fcγ receptors (FcγRs) mediate the cellular functions of IgG antibodies and are expressed on most immune cells including macrophages. FcγR cross-linking induced by IgG immune complexes (ICs) is important for defence against some infections but can also play a pathogenic role in autoimmunity. Here, I studied the metabolic reprogramming induced in macrophages by IgG IC ligation of FcγRs. I first investigated how FcγRs cross-linking might impact glucose metabolism. We show that macrophages undergo a switch to glycolysis in response to IgG IC stimulation. FcγR-associated glycolysis was dependent on the mammalian target of rapamycin (mTOR) and hypoxia-inducible factor (HIF)1α. Moreover, this glycolytic switch was required to generate a number of pro-inflammatory mediators and cytokines. Inhibition of glycolysis, or genetic depletion of HIF1α in macrophages resulted in the attenuation of IL1β and other inflammatory mediators produced in response to IgG IC in vitro. To determine the relevance of these observations to responses to IgG IC in vivo and, in particular, to IC-associated tissue inflammation in autoimmune diseases such as system lupus erythematosus (SLE), I developed three models to interrogate tissue macrophages. Following administration of IC to peritoneal macrophages, I observed IL1β-associated neutrophil recruitment that was abrogated by inhibiting glycolysis, or in the presence of HIF-1a deficiency. Similarly, following administration of intravenous IC, or nephrotoxic serum, kidney macrophage activation was abrogated by glycolysis inhibition or by myeloid HIF-1a deficiency. Together my data reveal the cellular molecular mechanisms required for FcγR-mediated metabolic reprogramming in macrophages and define a novel therapeutic strategy in autoantibody-induced inflammation. In the final part of the thesis I identified additional metabolic pathways that were altered by FcγR ligation, including cholesterol biosynthesis and fatty acid biosynthesis. This has important implications for protective immune responses and autoimmune susceptibility, since a number of intermediates in these pathways can directly regulate and contribute to immune responses. In summary, I have demonstrated the metabolic alterations triggered by FcγR ligation, reveal the cellular molecular mechanisms required for FcγR-mediated cellular respiration reprogramming in macrophages and define a potential therapeutic target in autoimmunity.
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Lo, Presti Caroline. "Reprogrammation métabolique dans les leucémies aigues myéloblastiques (LAM) : Impact clinique et mécanismes oncogéniques De novo adult acute myeloid leukemia patients display at diagnosis functional deregulation of redox balance correlated with molecular subtypes and overall survival." Thesis, Université Grenoble Alpes, 2020. http://www.theses.fr/2020GRALV017.

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Le métabolisme des cellules cancéreuses est fortement perturbé et dérégulé dans les cancers. Plusieurs exemples illustrent ce phénomène, notamment la reprogrammation métabolique décrite dans l’effet Warburg, les dérégulations fonctionnelles de certaines voies métaboliques telles que l’augmentation de la production de ROS dans les cellules cancéreuses, ou la mise en évidence d’oncométabolites liés à des mutations acquises telles que les mutations IDH1/2 qui entraînent la production d’un métabolite directement associé au processus leucémique dans les LAM. Afin de caractériser les reprogrammations métaboliques associées au processus leucémique, nous avons analysé par une approche HRMAS les métabolites produits par différentes lignées cellulaires leucémiques représentant différents sous types de LAM (génotype et phénotype différents). Dans ce modèle, nous avons montré que chaque type de lignée présentait un métabolisme particulier à l’état basal, témoin d’une signature métabolique différente selon la nature de la lignée. En situation de stress métabolique (culture en milieu sans sérum), toutes ces lignées développent des mécanismes d’adaptation de leur métabolisme à la carence en nutriments. En particulier, il existe une signature commune caractérisée par la surexpression de métabolites de la voie des phospholipides et de régulation du stress oxydant au bout de 24h de culture en milieu sans sérum. Grâce à ces mécanismes d’adaptation les cellules leucémiques retrouvent au bout de 48h, une viabilité supérieure à 95% et un profil métabolique quasi-identique aux conditions normales. Ces résultats montrent que les cellules leucémiques développent des mécanismes communs de survie, impliquant notamment des dérégulations du métabolisme des lipides, qui leur permettent de continuer à proliférer en situation de stress métabolique. D’autres conditions expérimentales ont été testées, notamment en condition de carence en glucose afin d’explorer la piste de la dérégulation de certains acides aminés comme l’alanine dans ces lignées. De plus, l’étude quantitative et qualitative des acides gras dans les LAM via une approche lipidomique révèle une adaptation similaire des profils lipidomiques des lignées dans les mêmes conditions de privation en sérum précédemment testées. En parallèle, dans une étude sur 54 patients au diagnostic de LAM, nous avons confirmé par l’approche HRMAS qu’il existait chez les patients LAM des différences de profil métabolique en fonction du sous-type de LAM. Nous avons également montré que ces signatures métaboliques étaient significativement corrélées aux sous-groupes pronostiques cytogénétiques, à la réponse au traitement par chimiothérapie et à la survie des patients. Nous montrons notamment que les métabolites surexprimés chez les patients de mauvais pronostic sont retrouvés surexprimés également chez les patients réfractaires au traitement. L’analyse de ces métabolites montrent le rôle particulier de plusieurs voies métaboliques dans le pronostic des LAM : i) la dérégulation de la synthèse de 2-hydroxyglutarate associée aux mutations de l’enzyme IDH1/2, ii) la dérégulation du métabolisme des phospholipides, retrouvant une surexpression de phospholipides dans les plasmas de patients de pronostic défavorable, et iii) la surexpression de la synthèse de certains acides aminés chez les patients chimiorésistants, suggérant une implication de la voie de signalisation LKB1/AMPK
Cells metabolism is strongly disturbed and deregulated in cancers. Several examples reflect this phenomenon, including metabolic reprogramming described in the Warburg effect, functional deregulations of particular metabolic pathways such as the increase of the ROS production in cancer cells, or the identification of oncometabolites linked to acquired mutations such as IDH1/2 mutations, which lead to the production of a metabolite directly linked to the leukemic process in AML. In order to characterize the metabolic reprogramming associated with the leukemic process, we analyzed by an HRMAS approach the metabolites produced by different leukemic cell lines representing different subtypes of AML (different genotype and phenotype). In this model, we have shown that each type of cell line exhibited a particular metabolism in the basal state, witnessing a different metabolic signature depending on the nature of the cell line. In condition of metabolic stress (culture in a serum-free environment), all these cell lines develop mechanisms to adapt their metabolism to nutrient deficiency. Particularly, there is a common signature characterized by the overexpression of metabolites of the phospholipid pathway and of regulation of oxidative stress after 24 hours of culture in a medium without serum. Thanks to these adaptation mechanisms, the leukemic cells find after 48 hours a viability higher than 95% and a metabolic profile almost identical to normal conditions. These results show that leukemic cells develop common survival mechanisms, notably involving deregulations of lipid metabolism, which allow them to continue to proliferate in condition of metabolic stress. Other experimental conditions have been tested, in particular in glucose deficiency conditions in order to explore the path of deregulation of some amino acids such as alanine in these cell lines. Moreover, the quantitative and qualitative study of fatty acids in AMLs through a lipidomic approach reveals a similar adaptation of the lipidomic profiles of the cell lines in the same serum-free conditions previously tested. In parallel, in a study on 54 patients diagnosed with AML, we confirmed by the HRMAS approach that there were differences in metabolic profile in AML patients according to the AML subtype. We also showed that these metabolic signatures were significantly correlated with cytogenetic prognostic subgroups, response to chemotherapy treatment and patient survival. We show in particular that the metabolites overexpressed in patients with poor prognosis are found overexpressed also in patients refractory to treatment. The analysis of these metabolites shows the particular role of several metabolic pathways in the prognosis of AML: i) deregulation of the synthesis of 2-hydroxyglutarate associated with mutations in the IDH1/2 enzyme, ii) deregulation of the metabolism of phospholipids, showing an overexpression of phospholipids in adverse prognosis patients plasmas, and iii) overexpression of the synthesis of some amino acids in chemoresistant patients, suggesting an involvement of the LKB1/AMPK signaling pathway
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Deva, Nathan Aurélia. "Caractérisation des bases moléculaires et cellulaires de la reprogrammation fonctionnelle radio-induite des macrophages dans le cadre du traitement du cancer." Electronic Thesis or Diss., université Paris-Saclay, 2023. http://www.theses.fr/2023UPASL079.

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Les macrophages associés aux tumeurs (TAMs) sont d'importants composants cellulaires du microenvironnement tumoral, qui présentent des fonctions immunosuppressives et sont associés à un mauvais pronostic dans la plupart des cancers. La reprogrammation fonctionnelle de ces macrophages aux propriétés pro-tumorales vers un phénotype pro-inflammatoire aux propriétés anti-tumorales favorise le développement d'une réponse anti-tumorale. Notre équipe a récemment étudié la capacité des radiations ionisantes à reprogrammer les TAMs vers un phénotype pro-inflammatoire. L'augmentation de la capacité des rayonnements ionisants à reprogrammer les TAMs en macrophages pro-inflammatoires est un objectif à atteindre pour améliorer l'efficacité des traitements du cancer.C'est dans ce contexte que mes travaux de thèse ont permis (i) de poursuivre la caractérisation des mécanismes moléculaires impliqués dans la reprogrammation radio-induite des macrophages, (ii) d'identifier le rôle du récepteur purinergique P2Y2 comme un modulateur négatif de la reprogrammation pro-inflammatoire des macrophages ; (ii) de caractériser les bases moléculaires de ce processus biologique et (iii) de proposer d'inhiber l'activité biologique du récepteur purinergique P2Y2, afin d'augmenter la capacité des rayonnements ionisants à déclencher l'activation pro-inflammatoire des macrophages
Tumor-associated macrophages (TAMs) are key components of the tumor microenvironment that display immunosuppressive functions and are associated with poor prognosis in most cancers. The functional reprogramming of these macrophages with pro-tumor properties towards a proinflammatory phenotype with anti-tumor properties promotes the development of an anti-tumor response. Our team recently studied how ionizing radiation modulates macrophage reprogramming towards a proinflammatory phenotype. Increasing the ability of ionizing radiation to reprogram TAMs into proinflammatory macrophages is a key objective to improve the effectiveness of cancer treatments.In this context, my thesis work enabled (i) to further characterize the molecular mechanisms involved in the radiation-induced macrophage reprogramming, (ii) to identify the role of the purinergic receptor P2Y2 as a negative modulator of the proinflammatory reprogramming of macrophages; (ii) to characterize the molecular bases of this biological process, and (iii) to propose the inhibition of the biological activity of P2Y2 receptor, to increase the ability of ionizing radiation, triggering the pro-inflammatory activation of macrophages
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Ozmadenci, Duygu. "Netrin-1 function in somatic cell reprogramming and pluripotency." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1254/document.

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La pluripotence est la capacité d'une cellule à s'auto-renouveler et à donner toutes les cellules somatiques ainsi que les cellules germinales. Les cellules pluripotentes peuvent être aussi reprogrammées à partir de cellules somatiques, ouvrant ainsi de nouvelles opportunités pour l'utilisation thérapeutique des cellules souches dans le traitement des maladies dégénératives. La connaissance des mécanismes moléculaires, en particulier des voix de signalisation qui contrôlent la pluripotence, est cruciale pour l'amélioration de notre compréhension de l'embryogenèse précoce et l'utilisation des iPSC (cellules souches pluripotentes induites) dans la médicine régénérative. Ici, je donne la première description de la Nétrine-1 en tant que régulateur de la reprogrammation et de la pluripotence. La Nétrine-1 et ses récepteurs ont été initialement caractérisés dans le système neuronal, mais il a aussi été montré qu'ils étaient exprimés dans différents types cellulaires et impliqués dans divers processus. Dans la première partie, j'ai contribué à explorer comment Nétrine-1 empêche l'apoptose médiée par son récepteur à dépendance DCC (Deleted in Colon Carcinoma) pendant la reprogrammation. Dans la deuxième partie, j'ai disséqué les fonctions et la régulation de cette voie dans le maintien de la pluripotence et dans l'engagement des lignages
Pluripotency is the ability of embryonic epiblast cells to self-renew and to give rise to all somatic cells as well as germ cells. Somatic cells can also be reprogrammed toward pluripotency, opening new avenues for stem cell based therapies in the treatment of degenerative diseases. Deciphering the molecular mechanisms, and in particular signaling pathways that control pluripotency is crucial to improve our understanding of early embryogenesis and the use of iPSC (inducible Pluripotent Stem Cell) in regenerative medicine.Herein, I provide the first description of Netrin-1 as a regulator of reprogramming and pluripotency. Netrin-1 and its receptors are present in many cell types and are engaged in a variety of cellular processes beyond its initial characterization in the neuronal system. In the first part, I contributed to explore how Netrin-1 prevents apoptosis mediated by its dependence receptor DCC (Deleted in Colon Carcinoma) during reprogramming. In the second part, I dissected the functions and regulation of this pathway in pluripotency maintenance and in lineage commitment
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Cao, Lu. "A genome wide approach to stress response and chronological ageing in yeast." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/285995.

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Caloric restriction (CR) extends lifespan from yeast to mammals. In budding yeast, inhibition of the conserved TOR and/or PKA pathways has been shown to mediate lifespan extension by CR partly through the activation of stress response. However, how the stress response is regulated at the systems level is poorly understood. In this study, by using fluorescent reporters whose expression is dependent on the transcription factors Msn2/4 and Gis1, two separate screenings were conducted to reveal novel regulators of the stress response induced by starvation. A 'focused' screening on the 272 'signalling' mutants revealed that, apart from the previously identified Rim15, Yak1 and Mck1 kinases, the SNF1/AMPK complex, the cell wall integrity (CWI) pathway and a number of cell cycle regulators are necessary to elicit appropriate stress response. The chronological lifespan (CLS) of these signalling mutants correlates well with the amount of accumulated storage carbohydrates but poorly with transition-phase cell cycle status. Subsequent analyses reveal that the levels of intracellular reactive oxygen species are controlled by Rim15, Yak1 and Mck1. Furthermore, CLS extension enabled by tor1 deletion is dependent on the above three kinases. These data suggest that the signalling pathways (SNF1 and CWI) and the kinases downstream of TOR/PKA (Rim15, Yak1 and Mck1) coordinate the metabolic reprogramming (to accumulate storage carbohydrates) and the activation of anti-oxidant defence systems (to control ROS levels) to extend chronological lifespan. A 'genome-wide' screening of a haploid deletion library indicates that less than 10% of the non-essential genes are implicated in the regulation of starvation-induced stress response. Gene ontology analysis suggests that they can be grouped into major clusters including mitochondrial function, r-RNA processing, DNA damage and repair, transcription from RNA polymerase and cell cycle regulation. Further phenotypic assays confirm the previous observation that CLS extension is mostly correlated with the accumulation of storage carbohydrates. Compromised expression of stress response reporters is confirmed by FACS in a variety of mitochondrial mutants, suggesting that mitochondrial respiration also plays a key role in the activation of stress response. Put together, the above findings indicate that stress response and metabolic reprogramming induced by glucose starvation are coordinated by multiple signalling pathways and the activation of mitochondrial respiration is essential to both cellular processes and to CLS extension.
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Kaemena, Daniel Fraser. "CRISPR/Cas9 genome-wide loss of function screening identifies novel regulators of reprogramming to pluripotency." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31184.

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In 2006, Kazutoshi Takahashi and Shinya Yamanaka demonstrated the ability of four transcription factors; Oct4, Sox2, Klf4 and c-Myc to 'reprogram' differentiated somatic cells to a pluripotent state. This technology holds huge potential in the field of regenerative medicine, but reprogramming also a model system by which to the common regulators of all forced cell identity changes, for example, transdifferentiation. Despite this, the mechanism underlying reprogramming remains poorly understood and the efficiency of induced pluripotent stem cell (iPSC) generation, inefficient. One powerful method for elucidating the gene components influencing a biological process, such as reprogramming, is screening for a phenotype of interest using genome-wide mutant libraries. Historically, large-scale knockout screens have been challenging to perform in diploid mammalian genomes, while other screening technologies such as RNAi can be disadvantaged by variable knockdown of target transcripts and off-target effects. Components of clustered regularly interspaced short palindromic repeats and associated Cas proteins (CRISPR-Cas) prokaryote adaptive immunity systems have recently been adapted to edit genomic sequences at high efficiency in mammalian systems. Furthermore, the application of CRISPR-Cas components to perform proofof- principle genome-wide KO screens has been successfully demonstrated. I have utilised the CRISPR-Cas9 system to perform genome-wide loss-of-function screening in the context of murine iPSC reprogramming, identifying 18 novel inhibitors of reprogramming, in addition to four known inhibitors, Trp53, Cdkn1a, Jun, Dot1l and Gtf2i. Understanding how these novel reprogramming roadblocks function to inhibit the reprogramming process will provide insight into the molecular mechanisms underpinning forced cell identity changes.
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Chidiac, Mounia. "A study of apolipoprotein L1 patho-physiological functions." Doctoral thesis, Universite Libre de Bruxelles, 2015. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/217789.

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Apolipoprotéines L est une famille nouvellement caractérisée en humain sans une fonction patho- physiologique définitive. Ces protéines sont classiquement considérées être impliquées dans le transport et métabolisme des lipides, principalement due à l'association de son premier membre de la famille sécrétée l’apolipoprotéine L1 aux particules des lipoprotéines de haute densité. Néanmoins, le reste des membres sont des protéines intracellulaires (absence de domaine de peptide signal). Apolipoprotéine L1 a été initialement identifiée comme l'élément clé du facteur trypanolytique dans le sérum humain. L'exploration de la séquence des différents apolipoprotéines L a révélé un domaine distinct «B cell lymphoma-2 homology domain 3» ayant des similitudes structurelles et fonctionnelles avec le domaine B cell lymphoma-2 homology domain 3 des protéines de la famille B cell lymphoma-2. Ainsi la découverte de ce domaine peut contribuer à la compréhension de la fonction et rôle des apoLs dans différents mécanismes et processus tels que la mort cellulaire programmée, la prolifération cellulaire, le métabolisme cellulaire .Notre étude visait à caractériser les fonctions de patho- physiologique du premier membre de la famille «apolipoprotéine L1 ». L’expression de l’apolipoprotéine L1 ARNm, à partir de 48 carcinomes papillaires de la thyroïde, a été évaluée par des études à haut débit et normalisée à un pool de tissus normal de la thyroïde. Une confirmation de PCR en temps réel valide ainsi la surexpression d’apoL1 dans 91,67 % des cas testés. Le niveau élevé de l’apolipoprotéine L1 ARNm est en corrélation avec une expression protéique élevée dans les échantillons histologiques (70%), et détermine que les cellules folliculaires de la thyroïde dans la zone de la tumeur sont les cellules principales responsables de l’expression spécifique de l’apolipoprotéine L1. Nous avons étudié l'expression apolipoprotéine L1 dans le modèle de cancer pour approfondir notre compréhension des relations reliant cette expression distincte dans le cancer papillaire de la thyroïde et son rôle et fonction concernant le métabolisme du cancer (de reprogrammation métabolique :effet Warburg).7En outre, la localisation de l’apolipoprotéine L1 dans la mitochondrie des cellules cancéreuses de la thyroïde ainsi que dans la mitochondrie de levure, a été le point de départ de la recherche dans ce nouveau modèle, il nous a permis de révéler et d'introduire de nouvelles hypothèses pour expliquer l'effet inhibiteur de l’apolipoprotéine L1 en fonction des conditions métabolique variantes et l’effet pléotropiques de l’apolipoprotéine L1 sur la levure (dommages des mitochondries et vacuoles). Dans ce manuscrit, nous avons décrit nos efforts à mettre en évidence la spécificité d'expression de l’apolipoprotéine L1 dans le cancer papillaire thyroïdien notamment au niveau de la transcription ainsi que la localisation mitochondriale et l'interférence probable avec les voies métaboliques.
Option Biologie moléculaire du Doctorat en Sciences
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Vasiliauskaite, Lina [Verfasser], and Ramesh [Akademischer Betreuer] Pillai. "EMBRYONIC FUNCTIONS OF REPROGRAMMING MUTANTS MIWI2, MILI AND DNMT3L INFLUENCE ADULT MALE GERMLINE MAINTENANCE / Lina Vasiliauskaite ; Betreuer: Ramesh Pillai." Heidelberg : Universitätsbibliothek Heidelberg, 2017. http://d-nb.info/1180985400/34.

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Books on the topic "Functional reprogramming"

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Venet, Fabienne, and Alain Lepape. Immunoparesis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0313.

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In parallel with an exaggerated pro-inflammatory response, critically-ill patients develop an immunosuppressive phase, termed immunoparesis/immunoparalysis or immune reprogramming. Innate and adaptive immune responses are affected. In particular, impaired neutrophil recruitment to injury sites and abnormal accumulation in remote sites; monocyte deactivation with preferential anti-inflammatory cytokine production and altered antigen presentation capacity; and a dramatic lymphopenia associated with major induction of apoptosis, functional, and phenotypic alterations have been described. The intensity and duration of this injury-induced immune dysfunction have been associated with an increased risk of death and secondary nosocomial infections. Innovative therapeutic strategies aiming at restoring immunological functions are currently being tested. GM-CSF appears to be an interesting candidate while IFN-γ‎ and IL-7 represent novel future therapeutic approaches. There is thus an urgent need for further clinical trials of such immunoadjuvant therapies that should include large cohorts of critically-ill patients stratified by relevant markers of immune dysfunction.
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Wang, Xiao-Dong, and Mathias V. Schmidt, eds. Molecular Mechanisms for Reprogramming Hippocampal Development and Function by Early-Life Stress. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-806-1.

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Book chapters on the topic "Functional reprogramming"

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Salts, Nuphar, and Eran Meshorer. "Epigenetics in Development, Differentiation and Reprogramming." In The Functional Nucleus, 421–48. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-38882-3_18.

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Perry, John M., and Linheng Li. "Functional Assays for Hematopoietic Stem Cell Self-Renewal." In Cellular Programming and Reprogramming, 45–54. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-691-7_3.

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Shi, Yan. "Generation of Functional Insulin-Producing Cells from Human Embryonic Stem Cells In Vitro." In Cellular Programming and Reprogramming, 79–85. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-691-7_5.

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Heinrich, Christophe, Magdalena Götz, and Benedikt Berninger. "Reprogramming of Postnatal Astroglia of the Mouse Neocortex into Functional, Synapse-Forming Neurons." In Methods in Molecular Biology, 485–98. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-452-0_32.

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Zhang, Zhonghui, and Wen-Shu Wu. "Application of TALE-Based Approach for Dissecting Functional MicroRNA-302/367 in Cellular Reprogramming." In MicroRNA Protocols, 255–63. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7601-0_21.

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Robinson, Meghan, Oliver McKee-Reed, Keiran Letwin, and Stephanie Michelle Willerth. "Direct Reprogramming Somatic Cells into Functional Neurons: A New Approach to Engineering Neural Tissue In Vitro and In Vivo." In Regenerative Medicine and Plastic Surgery, 447–62. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-19962-3_31.

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Qiu, Boning, Ruben J. de Vries, and Massimiliano Caiazzo. "Direct Cell Reprogramming of Mouse Fibroblasts into Functional Astrocytes Using Lentiviral Overexpression of the Transcription Factors NFIA, NFIB, and SOX9." In Methods in Molecular Biology, 31–43. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1601-7_3.

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Mullin, Nicholas, and Ian Chambers. "The Function of Nanog in Pluripotency." In Nuclear Reprogramming and Stem Cells, 99–112. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-225-0_9.

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Masui, Shinji. "Function of Oct3/4 and Sox2 in Pluripotency." In Nuclear Reprogramming and Stem Cells, 113–25. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-225-0_10.

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Osakada, Fumitaka, and Masayo Takahashi. "Toward Regeneration of Retinal Function Using Pluripotent Stem Cells." In Nuclear Reprogramming and Stem Cells, 155–75. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-225-0_13.

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Conference papers on the topic "Functional reprogramming"

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Möbus, S., J. Markovic, MP Manns, M. Ott, T. Cantz, and AD Sharma. "Functional microRNA screening to improve hepatocyte formation via direct reprogramming." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677090.

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Arnold, F., Mahaddalkar PU, W. Bergmann, J. Gout, Kraus JM, E. Roger, L. Perkhofer, T. Seufferlein, Hermann PC, and A. Kleger. "Functional genomic screening during somatic cell reprogramming identifies Dkk3 as a roadblock of organ regeneration." In DGVS Digital: BEST OF DGVS. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1716151.

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Imianowski, Charlotte, Paula Kuo, Edmund Poon, Matthew Lakins, Michelle Morrow, and Rahul Roychoudhuri. "1069 OX40/CD137 dual agonism potentiates anti-tumour immunity by driving functional reprogramming and instability of regulatory T (Treg) cells." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1069.

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Mandula, J., Rosa Sierra-Mondragon, Darwin Chang, Rachel Jimenez, Eslam Mohamed, Jimena Trillo, Alyssa Obermayer, et al. "944 Targeting of notch ligand Jagged2 in lung cancer cells drives anti-tumor immunity via notch-induced functional reprogramming of tumor-associated macrophages." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0944.

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Jensen, Helle, Rachel Fukuda, Megan Murt, Xiao Wang, Lora Zhao, Sheila Lou, Purnima Sundar, et al. "232 Increased potency and functional persistencein vitroof a next-generation NY-ESO-1-specific TCR therapy incorporating Gen-R™ genetic reprogramming technology." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0232.

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Wu, Sihan, Kai Zheng, and Xin Huang. "Model Checking PV Energy System with Remote Reprogramming Function." In 2016 8th International Conference on Information Technology in Medicine and Education (ITME). IEEE, 2016. http://dx.doi.org/10.1109/itme.2016.0143.

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Kim, Seung-Ku, Jae-Ho Lee, Kyeong Hur, and Doo-Seop Eom. "Tiny Function-Linking for Energy-Efficient Reprogramming in Wireless Sensor Networks." In 2009 Third International Conference on Mobile Ubiquitous Computing, Systems, Services and Technologies (UBICOMM). IEEE, 2009. http://dx.doi.org/10.1109/ubicomm.2009.22.

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Scherz-Shouval, Ruth, Marc L. Mendillo, Giorgio Gaglia, Irit Ben-Aharon, Andrew H. Beck, Luke Whitesell, and Susan Lindquist. "Abstract PR07: Mechanisms of stromal reprogramming mediated by heat shock factor 1." In Abstracts: AACR Special Conference: The Function of Tumor Microenvironment in Cancer Progression; January 7-10, 2016; San Diego, CA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tme16-pr07.

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Johnson, Kelly E., Kellie R. Machlus, Jodi A. Forward, Mason D. Tippy, Saleh A. El-Husayni, Joseph E. Italiano, and Elisabeth M. Battinelli. "Abstract C12: Platelets promote breast cancer metastasis by reprogramming tumor cells to produce IL-8." In Abstracts: AACR Special Conference: The Function of Tumor Microenvironment in Cancer Progression; January 7-10, 2016; San Diego, CA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tme16-c12.

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Jacq, Xavier, Anamarija Jurisic, Julien Daubriac, Ian T. Lobb, Mark Wappett, Aaron Cranston, Peggy Sung, Gerald Gavory, Colin O'Dowd, and Tim Harisson. "Abstract 6057: Discovery of a novel function for USP7 inhibitors: Reprogramming the tumor microenvironment." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-6057.

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Reports on the topic "Functional reprogramming"

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Or, Etti, David Galbraith, and Anne Fennell. Exploring mechanisms involved in grape bud dormancy: Large-scale analysis of expression reprogramming following controlled dormancy induction and dormancy release. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7587232.bard.

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The timing of dormancy induction and release is very important to the economic production of table grape. Advances in manipulation of dormancy induction and dormancy release are dependent on the establishment of a comprehensive understanding of biological mechanisms involved in bud dormancy. To gain insight into these mechanisms we initiated the research that had two main objectives: A. Analyzing the expression profiles of large subsets of genes, following controlled dormancy induction and dormancy release, and assessing the role of known metabolic pathways, known regulatory genes and novel sequences involved in these processes B. Comparing expression profiles following the perception of various artificial as well as natural signals known to induce dormancy release, and searching for gene showing similar expression patterns, as candidates for further study of pathways having potential to play a central role in dormancy release. We first created targeted EST collections from V. vinifera and V. riparia mature buds. Clones were randomly selected from cDNA libraries prepared following controlled dormancy release and controlled dormancy induction and from respective controls. The entire collection (7920 vinifera and 1194 riparia clones) was sequenced and subjected to bioinformatics analysis, including clustering, annotations and GO classifications. PCR products from the entire collection were used for printing of cDNA microarrays. Bud tissue in general, and the dormant bud in particular, are under-represented within the grape EST database. Accordingly, 59% of the our vinifera EST collection, composed of 5516 unigenes, are not included within the current Vitis TIGR collection and about 22% of these transcripts bear no resemblance to any known plant transcript, corroborating the current need for our targeted EST collection and the bud specific cDNA array. Analysis of the V. riparia sequences yielded 814 unigenes, of which 140 are unique (keilin et al., manuscript, Appendix B). Results from computational expression profiling of the vinifera collection suggest that oxidative stress, calcium signaling, intracellular vesicle trafficking and anaerobic mode of carbohydrate metabolism play a role in the regulation and execution of grape-bud dormancy release. A comprehensive analysis confirmed the induction of transcription from several calcium–signaling related genes following HC treatment, and detected an inhibiting effect of calcium channel blocker and calcium chelator on HC-induced and chilling-induced bud break. It also detected the existence of HC-induced and calcium dependent protein phosphorylation activity. These data suggest, for the first time, that calcium signaling is involved in the mechanism of dormancy release (Pang et al., in preparation). We compared the effects of heat shock (HS) to those detected in buds following HC application and found that HS lead to earlier and higher bud break. We also demonstrated similar temporary reduction in catalase expression and temporary induction of ascorbate peroxidase, glutathione reductase, thioredoxin and glutathione S transferase expression following both treatments. These findings further support the assumption that temporary oxidative stress is part of the mechanism leading to bud break. The temporary induction of sucrose syntase, pyruvate decarboxylase and alcohol dehydrogenase indicate that temporary respiratory stress is developed and suggest that mitochondrial function may be of central importance for that mechanism. These finding, suggesting triggering of identical mechanisms by HS and HC, justified the comparison of expression profiles of HC and HS treated buds, as a tool for the identification of pathways with a central role in dormancy release (Halaly et al., in preparation). RNA samples from buds treated with HS, HC and water were hybridized with the cDNA arrays in an interconnected loop design. Differentially expressed genes from the were selected using R-language package from Bioconductor project called LIMMA and clones showing a significant change following both HS and HC treatments, compared to control, were selected for further analysis. A total of 1541 clones show significant induction, of which 37% have no hit or unknown function and the rest represent 661 genes with identified function. Similarly, out of 1452 clones showing significant reduction, only 53% of the clones have identified function and they represent 573 genes. The 661 induced genes are involved in 445 different molecular functions. About 90% of those functions were classified to 20 categories based on careful survey of the literature. Among other things, it appears that carbohydrate metabolism and mitochondrial function may be of central importance in the mechanism of dormancy release and studies in this direction are ongoing. Analysis of the reduced function is ongoing (Appendix A). A second set of hybridizations was carried out with RNA samples from buds exposed to short photoperiod, leading to induction of bud dormancy, and long photoperiod treatment, as control. Analysis indicated that 42 genes were significant difference between LD and SD and 11 of these were unique.
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Miller, Gad, and Jeffrey F. Harper. Pollen fertility and the role of ROS and Ca signaling in heat stress tolerance. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7598150.bard.

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The long-term goal of this research is to understand how pollen cope with stress, and identify genes that can be manipulated in crop plants to improve reproductive success during heat stress. The specific aims were to: 1) Compare heat stress dependent changes in gene expression between wild type pollen, and mutants in which pollen are heat sensitive (cngc16) or heat tolerant (apx2-1). 2) Compare cngc16 and apx2 mutants for differences in heat-stress triggered changes in ROS, cNMP, and Ca²⁺ transients. 3) Expand a mutant screen for pollen with increased or decreased thermo-tolerance. These aims were designed to provide novel and fundamental advances to our understanding of stress tolerance in pollen reproductive development, and enable research aimed at improving crop plants to be more productive under conditions of heat stress. Background: Each year crop yields are severely impacted by a variety of stress conditions, including heat, cold, drought, hypoxia, and salt. Reproductive development in flowering plants is highly sensitive to hot or cold temperatures, with even a single hot day or cold night sometimes being fatal to reproductive success. In many plants, pollen tube development and fertilization is often the weakest link. Current speculation about global climate change is that most agricultural regions will experience more extreme environmental fluctuations. With the human food supply largely dependent on seeds, it is critical that we consider ways to improve stress tolerance during fertilization. The heat stress response (HSR) has been intensively studied in vegetative tissues, but is poorly understood during reproductive development. A general paradigm is that HS is accompanied by increased production of reactive oxygen species (ROS) and induction of ROS-scavenging enzymes to protect cells from excess oxidative damage. The activation of the HSR has been linked to cytosolic Ca²⁺ signals, and transcriptional and translational responses, including the increased expression of heat shock proteins (HSPs) and antioxidative pathways. The focus of the proposed research was on two mutations, which have been discovered in a collaboration between the Harper and Miller labs, that either increase or decrease reproductive stress tolerance in a model plant, Arabidopsis thaliana (i.e., cngc16--cyclic nucleotide gated channel 16, apx2-1--ascorbate peroxidase 2,). Major conclusions, solutions, achievements. Using RNA-seq technology, the expression profiles of cngc16 and apx2 pollen grains were independently compared to wild type under favourable conditions and following HS. In comparison to a wild type HSR, there were 2,776 differences in the transcriptome response in cngc16 pollen, consistent with a model in which this heat-sensitive mutant fails to enact or maintain a normal wild-type HSR. In a comparison with apx2 pollen, there were 900 differences in the HSR. Some portion of these 900 differences might contribute to an improved HSR in apx2 pollen. Twenty-seven and 42 transcription factor changes, in cngc16 and apx2-1, respectively, were identified that could provide unique contributions to a pollen HSR. While we found that the functional HS-dependent reprogramming of the pollen transcriptome requires specific activity of CNGC16, we identified in apx2 specific activation of flavonol-biosynthesis pathway and auxin signalling that support a role in pollen thermotolerance. Results from this study have identified metabolic pathways and candidate genes of potential use in improving HS tolerance in pollen. Additionally, we developed new FACS-based methodology that can quantify the stress response for individual pollen in a high-throughput fashion. This technology is being adapted for biological screening of crop plant’s pollen to identify novel thermotolerance traits. Implications, both scientific and agricultural. This study has provided a reference data on the pollen HSR from a model plant, and supports a model that the HSR in pollen has many differences compared to vegetative cells. This provides an important foundation for understanding and improving the pollen HSR, and therefor contributes to the long-term goal of improving productivity in crop plants subjected to temperature stress conditions. A specific hypothesis that has emerged from this study is that pollen thermotolerance can be improved by increasing flavonol accumulation before or during a stress response. Efforts to test this hypothesis have been initiated, and if successful have the potential for application with major seed crops such as maize and rice.
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Brown Horowitz, Sigal, Eric L. Davis, and Axel Elling. Dissecting interactions between root-knot nematode effectors and lipid signaling involved in plant defense. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598167.bard.

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Root-knot nematodes, Meloidogynespp., are extremely destructive pathogens with a cosmopolitan distribution and a host range that affects most crops. Safety and environmental concerns related to the toxicity of nematicides along with a lack of natural resistance sources threaten most crops in Israel and the U.S. This emphasizes the need to identify genes and signal mechanisms that could provide novel nematode control tactics and resistance breeding targets. The sedentary root-knot nematode (RKN) Meloidogynespp. secrete effectors in a spatial and temporal manner to interfere with and mimic multiple physiological and morphological mechanisms, leading to modifications and reprogramming of the host cells' functions, resulted in construction and maintenance of nematodes' feeding sites. For successful parasitism, many effectors act as immunomodulators, aimed to manipulate and suppress immune defense signaling triggered upon nematode invasion. Plant development and defense rely mainly on hormone regulation. Herein, a metabolomic profiling of oxylipins and hormones composition of tomato roots were performed using LC-MS/MS, indicating a fluctuation in oxylipins profile in a compatible interaction. Moreover, further attention was given to uncover the implication of WRKYs transcription factors in regulating nematode development. In addition, in order to identify genes that might interact with the lipidomic defense pathway induced by oxylipins, a RNAseq was performed by exposing M. javanicasecond-stage juveniles to tomato protoplast, 9-HOT and 13-KOD oxylipins. This transcriptome generated a total of 4682 differentially expressed genes (DEGs). Being interested in effectors, we seek for DEGs carrying a predicted secretion signal peptide. Among the DEGs including signal peptide, several had homology with known effectors in other nematode species, other unknown potentially secreted proteins may have a role as root-knot nematodes' effectors which might interact with lipid signaling. The molecular interaction of LOX proteins with the Cyst nematode effectors illustrate the nematode strategy in manipulating plant lipid signals. The function of several other effectors in manipulating plant defense signals, as well as lipids signals, weakening cell walls, attenuating feeding site function and development are still being studied in depth for several novel effectors. As direct outcome of this project, the accumulating findings will be utilized to improve our understanding of the mechanisms governing critical life-cycle phases of the parasitic M. incognita RKN, thereby facilitating design of effective controls based on perturbation of nematode behavior—without producing harmful side effects. The knowledge from this study will promote genome editing strategies aimed at developing nematode resistance in tomato and other nematode-susceptible crop species in Israel and the United States.
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Sessa, Guido, and Gregory Martin. Role of GRAS Transcription Factors in Tomato Disease Resistance and Basal Defense. United States Department of Agriculture, 2005. http://dx.doi.org/10.32747/2005.7696520.bard.

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The research problem: Bacterial spot and bacterial speck diseases of tomato are causedby strains of Xanthomonas campestris pv. vesicatoria (Xcv) and Pseudomonas syringae pv.tomato (Pst), respectively. These bacteria colonize aerial parts of the plant and causesignificant losses in tomato production worldwide. Protection against Xcv and Pst bycultural practices or chemical control has been unsuccessful and there are only limitedsources of genetic resistance to these pathogens. In previous research supported in part byBARD IS-3237-01, we extensively characterized changes in tomato gene expression uponthe onset of spot and speck disease resistance. A remarkable finding of these studies wasthe inducibility in tomato leaves by both Xcv and Pst strains of genes encodingtranscriptional activator of the GRAS family, which has not been previously linked todisease resistance. Goals: Central goals of this research were to investigate the role of GRAS genes in tomatoinnate immunity and to assess their potential use for disease control.Specific objectives were to: 1. Identify GRAS genes that are induced in tomato during thedefense response and analyze their role in disease resistance by loss-of-function experiments.2. Overexpress GRAS genes in tomato and characterize plants for possible broad-spectrumresistance. 3. Identify genes whose transcription is regulated by GRAS family. Our main achievements during this research program are in three major areas:1. Identification of tomato GRAS family members induced in defense responses andanalysis of their role in disease resistance. Genes encoding tomato GRAS family memberswere retrieved from databases and analyzed for their inducibility by Pst avirulent bacteria.Real-time RT-PCR analysis revealed that six SlGRAS transcripts are induced during theonset of disease resistance to Pst. Further expression analysis of two selected GRAS genesshowed that they accumulate in tomato plants in response to different avirulent bacteria orto the fungal elicitor EIX. In addition, eight SlGRAS genes, including the Pst-induciblefamily members, were induced by mechanical stress in part in a jasmonic acid-dependentmanner. Remarkably, SlGRAS6 gene was found to be required for tomato resistance to Pstin virus-induced gene silencing (VIGS) experiments.2. Molecular analysis of pathogen-induced GRAS transcriptional activators. In aheterologous yeast system, Pst-inducible GRAS genes were shown to have the ability toactivate transcription in agreement with their putative function of transcription factors. Inaddition, deletion analysis demonstrated that short sequences at the amino-terminus ofSlGRAS2, SlGRAS4 and SlGRAS6 are sufficient for transcriptional activation. Finally,defense-related SlGRAS proteins were found to localize to the cell nucleus. 3. Disease resistance and expression profiles of transgenic plants overexpressing SlGRASgenes. Transgenic plants overexpressing SlGRAS3 or SlGRAS6 were generated. Diseasesusceptibility tests revealed that these plants are not more resistant to Pst than wild-typeplants. Gene expression profiles of the overexpressing plants identified putative direct orindirect target genes regulated by SlGRAS3 and SlGRAS6. Scientific and agricultural significance: Our research activities established a novel linkbetween the GRAS family of transcription factors, plant disease resistance and mechanicalstress response. SlGRAS6 was found to be required for disease resistance to Pstsuggesting that this and possibly other GRAS family members are involved in thetranscriptional reprogramming that takes place during the onset of disease resistance.Their nuclear localization and transcriptional activation ability support their proposed roleas transcription factors or co-activators. However, the potential of utilizing GRAS familymembers for the improvement of plant disease resistance in agriculture has yet to bedemonstrated.
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