Relevant bibliographies by topics / Developmental biology/pattern formation

Academic literature on the topic 'Developmental biology/pattern formation'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Developmental biology/pattern formation"

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GREEN, P. B. "Developmental Biology: Pattern Formation." Science 229, no. 4709 (July 12, 1985): 156. http://dx.doi.org/10.1126/science.229.4709.156.

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Pas, Kristofor, Samantha Laboy-Segarra, and Juhyun Lee. "Systems of pattern formation within developmental biology." Progress in Biophysics and Molecular Biology 167 (December 2021): 18–25. http://dx.doi.org/10.1016/j.pbiomolbio.2021.09.005.

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Pas, Kristofor, Samantha Laboy-Segarra, and Juhyun Lee. "Systems of pattern formation within developmental biology." Progress in Biophysics and Molecular Biology 167 (December 2021): 18–25. http://dx.doi.org/10.1016/j.pbiomolbio.2021.09.005.

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Swanson, GavinJ. "Pattern formation. A primer in developmental biology." FEBS Letters 186, no. 1 (July 1, 1985): 124. http://dx.doi.org/10.1016/0014-5793(85)81359-4.

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Kicheva, A., M. Cohen, and J. Briscoe. "Developmental Pattern Formation: Insights from Physics and Biology." Science 338, no. 6104 (October 11, 2012): 210–12. http://dx.doi.org/10.1126/science.1225182.

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Akam, Michael, and John Gerhart. "Pattern formation and developmental mechanisms." Current Opinion in Genetics & Development 2, no. 4 (January 1992): 541–42. http://dx.doi.org/10.1016/s0959-437x(05)80168-6.

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Stemple, Derek L., and Jean-Paul Vincent. "Pattern formation and developmental mechanisms." Current Opinion in Genetics & Development 14, no. 4 (August 2004): 325–27. http://dx.doi.org/10.1016/j.gde.2004.06.016.

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McGinnis, William, and Cheryll Tickle. "Pattern formation and developmental mechanisms." Current Opinion in Genetics & Development 15, no. 4 (August 2005): 355–57. http://dx.doi.org/10.1016/j.gde.2005.06.005.

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Firtel, Rick, and Magdalena Zernicka-Goetz. "Pattern formation and developmental mechanisms." Current Opinion in Genetics & Development 16, no. 4 (August 2006): 331–32. http://dx.doi.org/10.1016/j.gde.2006.06.014.

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Hartmann, Christine, and Ross Cagan. "Pattern formation and developmental mechanisms." Current Opinion in Genetics & Development 17, no. 4 (August 2007): 261–63. http://dx.doi.org/10.1016/j.gde.2007.07.002.

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Dissertations / Theses on the topic "Developmental biology/pattern formation"

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Hunt, Gordon S. "Mathematical modelling of pattern formation in developmental biology." Thesis, Heriot-Watt University, 2013. http://hdl.handle.net/10399/2706.

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The transformation from a single cell to the adult form is one of the remarkable wonders of nature. However, the fundamental mechanisms and interactions involved in this metamorphic change still remain elusive. Due to the complexity of the process, researchers have attempted to exploit simpler systems and, in particular, have focussed on the emergence of varied and spectacular patterns in nature. A number of mathematical models have been proposed to study this problem with one of the most well studied and prominent being the novel concept provided by A.M. Turing in 1952. Turing's simple yet elegant idea consisted of a system of interacting chemicals that reacted and di used such that, under certain conditions, spatial patterns can arise from near homogeneity. However, the implicit assumption that cells respond to respective chemical levels, di erentiating accordingly, is an oversimpli cation and may not capture the true extent of the biology. Here, we propose mathematical models that explicitly introduce cell dynamics into pattern formation mechanisms. The models presented are formulated based on Turing's classical mechanism and are used to gain insight into the signi cance and impact that cells may have in biological phenomena. The rst part of this work considers cell di erentiation and incorporates two conceptually di erent cell commitment processes: asymmetric precursor di erentiation and precursor speci cation. A variety of possible feedback mechanisms are considered with the results of direct activator upregulation suggesting a relaxation of the two species Turing Instability requirement of long range inhibition, short range activation. Moreover, the results also suggest that the type of feedback mechanism should be considered to explain observed biological results. In a separate model, cell signalling is investigated using a discrete mathematical model that is derived from Turing's classical continuous framework. Within this, two types of cell signalling are considered, namely autocrine and juxtacrine signalling, with both showing the attainability of a variety of wavelength patterns that are illustrated and explainable through individual cell activity levels of receptor, ligand and inhibitor. Together with the full system, a reduced two species system is investigated that permits a direct comparison to the classical activator-inhibitor model and the results produce pattern formation in systems considering both one and two di usible species together with an autocrine and/or juxtacrine signalling mechanism. Formulating the model in this way shows a greater applicability to biology with fundamental cell signalling and the interactions involved in Turing type patterning described using clear and concise variables.
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Cruywagen, Gerhard C. "Tissue interaction and spatial pattern formation." Thesis, University of Oxford, 1992. http://ora.ox.ac.uk/objects/uuid:f242b785-9b46-4c21-a789-477b025ce4b3.

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The development of spatial structure and form on vertebrate skin is a complex and poorly understood phenomenon. We consider here a new mechanochemical tissue interaction model for generating vertebrate skin patterns. Tissue interaction, which plays a crucial role in vertebrate skin morphogenesis, is modelled by reacting and diffusing signal morphogens. The model consists of seven coupled partial differential equations, one each for dermal and epidermal cell densities, four for the signal morphogen concentrations and one for describing epithelial mechanics. Because of its complexity, we reduce the full model to a small strain quasi-steady-state model, by making several simplifying assumptions. A steady state analysis demonstrates that our reduced system possesses stable time-independent steady state solutions on one-dimensional spatial domains. A linear analysis combined with a multiple time-scale perturbation procedure and numerical simulations are used to examine the range of patterns that the model can exhibit on both one- and two-dimensions domains. Spatial patterns, such as rolls, squares, rhombi and hexagons, which are remarkably similar to those observed on vertebrate skin, are obtained. Although much of the work on pattern formation is concerned with synchronous spatial patterning, many structures on vertebrate skin are laid down in a sequential fashion. Our tissue interaction model can account for such sequential pattern formation. A linear analysis and a regular perturbation analysis is used to examine propagating epithelial contraction waves coupled to dermal cell invasion waves. The results compare favourably with those obtained from numerical simulations of the model. Furthermore, sequential pattern formation on one-dimensional domains is analysed; first by an asymptotic technique, and then by a new method involving the envelopes of the spatio-temporal propagating solutions. Both methods provide analytical estimates for the speeds of the wave of propagating pattern which are in close agreement with those obtained numerically. Finally, by numerical simulations, we show that our tissue interaction model can account for two-dimensional sequential pattern formation. In particular, we show that complex two-dimensional patterns can be determined by simple quasi-one-dimensional patterns.
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Baker, Ruth E. "Periodic pattern formation in developmental biology : a study of the mechanisms underlying somitogenesis." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418815.

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Somitogenesis, the sequential formation of a periodic pattern along the antero-posterior axis of vertebrate embryos, is one of the most obvious examples of the segmental patterning processes that take place during embryogenesis and also one of the major unresolved events in developmental biology. The principal aim of this thesis is to develop a series of mathematical models for somite formation. We begin by reviewing the current models for somitogenesis in the light of new experimental evidence regarding the presence of a segmentation clock and graded expression of FGF8. We conduct a preliminary investigation into the wavefront of FGF8 along the antero-posterior axis and integrate this model into the framework of an existing model for a signalling process. We demonstrate that this new “Clock and Wavefront” model can produce coherent series’ of somites in a manner that is tightly regulated in both space and time, and that it can also mimic the effects seen when FGF8 expression is perturbed locally. We then use the model to make some experimentally testable predictions. The latter part of the thesis concentrates on building more biologically accurate model for the FGF8 gradient. We move to consider a model for the FGF8 gradient which involves a complex network of biochemical interactions with negative feedback between FGF8 and retinoic acid. The resulting system of seven coupled non-linear equations, including both ordinary and partial differential equations, is difficult to analyse. To facilitate our understanding of the non-linear interactions between FGF8 and retinoic acid, we finally consider a reduced model which can display travelling wavefronts of opposing FGF8 and retinoic acid concentrations moving down the antero-posterior axis. The model allowed us to calculate a minimum wave speed for the wavefronts as a function of key model parameters such as the rate of FGF8 and retinoic acid decay; strong dependence on the values of these parameters is a result that is hypothesised to occur in vivo.
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Williamson, Carly Zoe. "A Computational Model of Divergent Pattern Formation in Caenorhabditis elegans and Caenorhabditis briggsae Vulval Development." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1460574181.

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Sadeghi, Nazlie. "The N-cadherin prodomain: regulation of synpase formation «in vivo» and developmental expression pattern in the zebrafish central nervous system." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19229.

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The formation of neuronal connections in the central nervous system (CNS) occurs as nascent pre- and postsynaptic membranes are primed to generate a mature synaptic junctional complex. Although the precise sequence of events leading to synapse assembly is not well understood, the presence and adhesive capacity of a limited number of highly specialized molecules on the pre and post-synaptic membranes are thought to determine where and when synapses will form (Sperry et al, 1963; Fannon and Colman 1996; Craig et al, 2001). According to recent models of synaptogenesis, signaling through adhesion molecules at cell-cell contact sites leads to the progressive recruitment of pre- and postsynaptic constituents to these sites, resulting in synapse maturation. Presynaptic transport packets (also known as piccolo-bassoon transport packets or active zone precursor vesicles) are thought to deliver proteins en masse to nascent synapses (Zhai et al., 2001; Ziv and Garner 2004). Since N-cadherin is a prominent synaptic adhesion molecule and a significant constituent of these presynaptic transport packets, we hypothesized that it would play an important role in early synaptic development. Using time-lapse confocal microscopy on living embryonic zebrafish Rohon-Beard neurons, we found that modifying N-cadherin to contain an uncleavable prodomain prevents its targeting to microdomains and transiently suppresses synapse formation. Because neurogenesis and synapse formation continue to occur in defined areas of the adult fish brain, we performed an immunohistological survey of the expression pattern of the N-cadherin prodomain in adult zebrafish. The highest levels of expression were in areas believed to have elevated levels of synaptic plasticity
Le pro-domaine de la N-cadherin: Rôle dans la régulation de la synaptogenèse in vivo et expression pendant le développement du système nerveux central chez le poisson zébré. La formation de connections neuronales dans le système nerveux central (SNC) se produit lorsque des membranes pré et post-synaptiques nouvellement formées sont conditionnées à générer un complexe synaptique mature. Malgré notre compréhension limitée de la séquence précise d'évènements conduisant à la formation d'une synapse, la présence et le potentiel adhésif d'un petit nombre de molécules hautement spécialisées retrouvées sur certains sites pré et post-synaptiques semblent déterminer où et quand des synapses seront formées (Sperry et al, 1963; Fannon and Colman 1996; Craig et al, 2001). Selon les théories actuelles sur la synaptogenèse, un signalement intercellulaire par le biais de molécules adhésives présentes à certains sites de contact cellulaire conduit au recrutement graduel de constituants pré et post-synaptiques à ces sites, résultant ainsi en une maturation de la synapse. Dans la neurone pré-synaptique, il est conçu que les colis cellulaires (connus sous le nom de "piccolo-bassoon transport packets", "active zone precursor vesicles" ou tout simplement "transport packets" en anglais) livrent de grandes quantités de protéines aux synapses nouvellement générées (Zhai et al., 2001; Ziv and Garner 2004). Parce que la N-cadherin est une molécule adhésive prééminente de même qu'une constituante principale de ces colis cellulaires, nous avons émis l'hypothèse qu'elle pouvait jouer un rôle important aux origines du développement nerveux. En imageant des neurones "Rohon-Beard" de poissons zébrés à
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Srivastava, Vinit. "Pattern formation in the mammalian striatum, the development of the thalamostriatal projection in the rodent." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0023/MQ50884.pdf.

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Saavedra, Pedro Almeida Dias Guedes. "Pattern formation and planar cell polarity in Drosophila larval development : insights from the ventral epidermis." Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708010.

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Cheesman, Sarah Emily. "Dorsal ventral patterning of the central nervous system : lessons from flies and fish /." view abstract or download file of text, 2003. http://wwwlib.umi.com/cr/uoregon/fullcit?p3113005.

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Thesis (Ph. D.)--University of Oregon, 2003.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 95-102). Also available for download via the World Wide Web; free to University of Oregon users.
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Schweickart, Robert Allen. "FRAZZLED PLAYS A ROLE IN THE FORMATION OF CELL DENSITY PATTERNS IN THE EARLY DROSOPHILA EMBRYO." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1545181299374722.

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Marín, de Mas Igor Bartolomé. "Development and application of novel model-driven and data-driven approaches to study metabolism in the framework of systems medicine." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/296313.

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The general aim of this thesis is to develop and apply new computational tools to overcome existing limitations in the analysis of metabolism. This thesis is focused on developing new computational strategies to overcome the following identified limitations: i) The existing metabolic flux analysis tools does not account for the existence of metabolic channeling: Here we developed a new computational tool based on non-stationary 13 C-FBA to evaluate different models reflecting different topologies of intracellular metabolism, using the channeling in hepatocytes as case of concep ii) Metabolic drug-target discovery based on GSMM does not consider the different cell subpopulations existing within the tumor: Here we develope a method that integrate trancriptomic data into a comparative genome-scale metabolic network reconstruction analysis in the context of intra-tumoral heterogeneity . We determined subpopulation-specific drug targets . Additionally we determined a metabolic gene signature associated to tumor progression in pc that was correlated with other types of cancer. Iii) Current mechanistic and probabilistic computational approaches are not suitable to study the complexity of the crosstalk between metabolic and gene regulatory networks.: Here we developed a novel computational method combining probabilistic and mechanistic approaches to integrate multi-level omic data into a discrete model-based analysis. This method allowed to analyze the mechanism underlying the crosstalk between metabolism and gene regulation, using as case of concept the study of the abnormal adaptation to training in COPD patients.
La presente tesis doctoral se centra en el desarrollo de herramientas computacionales que permitan el estudio de los mecanismos moleculares que ocurren dentro de la célula. Mas específicamente estudia el metabolismo celular desde diferentes puntos de vista usando y desarrollando métodos computacionales basados en diversas metodologías. Así pues en un primer capitulo se desarrolla un método basado en el analista de los flujos metabólicos en estado no estacional isotópico utilizando modelos cinéticos para estudiar el fenómeno de la canalización metabólica en hepatocitos. Este fenómeno modifica la topología metabólica alterando el fenotipo. Nuestro método nos permitió discriminar varios modelos con distintas topología prediciendo la existencia de canalización metabólica en la glucólisis. En el segundo capitulo se desarrolló un método para analizar el metabolismo tumoral teniendo en cuenta la heterogeneidad de poblaciones. En concreto estudiamos dos subpoblaciones extraídas de una linea celular de cáncer de próstata. Para ello utilizamos un modelo a gran escala de todo el metabolismo celular humano. El análisis reflejó la existencia de diferencias notables a nivel de vías metabólicas concretas, confiriendo a cada subpoblacion sensibilidades distintas a diferentes fármacos. En esta linea se demostró que mientras las células PC-3M eran sensibles al etomoxir e insensibles al calcitriol, las PC-3S presentaban una sensibilidad opuesta. En el tercero y ultimo capitulo de la tesis desarrollamos un nuevo método computacional que integra aproximaciones probabilísticas y mecanicistas para integrar diferentes tipos de datos en un análisis basado en modelos discretos. Para ello utilizamos como caso de concepto el estudio de la adaptación anómala al entrenamiento de pacientes con EPOC. El análisis reveló diferencias importantes a nivel de metabolismo energético en comparación con el grupo control.
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Books on the topic "Developmental biology/pattern formation"

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Laboratory, Cold Spring Harbor, ed. Pattern formation during development. Plainview, N.Y: Cold Spring Harbor Laboratory Press, 1997.

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Pattern formation: Ciliate studies and models. New York: Oxford University Press, 1989.

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The shaping of life: The generation of biological pattern. Cambridge, UK: Cambridge University Press, 2011.

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Society for Developmental Biology. Symposium. Genetics of pattern formation and growth control. Edited by Mahowald Anthony P. New York: Wiley-Liss, 1990.

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Frederik, Nijhout H., Nadel Lynn, and Stein Daniel L, eds. Pattern formation in the physical and biological sciences. Reading, Mass: Addison-Wesley, 1997.

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Held, Lewis I. Models for embryonic periodicity. Basel: Karger, 1992.

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Ball, Philip. Nature's patterns: A tapestry in three parts. Oxford: Oxford University Press, 2009.

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Grimes, Gary W. Cellular aspects of pattern formation: The problem of assembly. Basel: Karger, 1991.

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R, Hinchliffe J., Hurle Juan M, Summerbell Dennis, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. Developmental patterning of the vertebrate limb. New York: Plenum Press, 1991.

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Stephen, Childress, ed. Mathematical models in developmental biology. New York, New York: Courant Institute of Mathematical Sciences, New York University, 2015.

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Book chapters on the topic "Developmental biology/pattern formation"

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Müller, Werner A. "Epigenetic Pattern Formation: New Patterns Are Created During Development." In Developmental Biology, 165–201. New York, NY: Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4612-2248-4_9.

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Salazar-Ciudad, Isaac. "Mechanisms of Pattern Formation, Morphogenesis, and Evolution." In Evolutionary Developmental Biology, 1–16. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-33038-9_51-1.

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Salazar-Ciudad, Isaac. "Mechanisms of Pattern Formation, Morphogenesis, and Evolution." In Evolutionary Developmental Biology, 555–70. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-32979-6_51.

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Scott, Matthew P. "The Molecular Biology of Pattern Formation in the Early Embryonic Development of Drosophila." In The Molecular Biology of Cell Determination and Cell Differentiation, 151–85. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-6817-9_5.

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Jost, Jürgen. "Pattern Formation." In Mathematical Methods in Biology and Neurobiology, 89–173. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6353-4_4.

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Deutsch, Andreas. "Spatiotemporal Pattern Formation." In Encyclopedia of Systems Biology, 1963. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_1141.

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Murray, James D. "Neural Models of Pattern Formation." In Mathematical Biology, 481–524. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-08539-4_16.

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Murray, James D. "Neural Models of Pattern Formation." In Mathematical Biology, 481–524. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-08542-4_16.

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Raghavan, V. "Formation of Floral Organs." In Developmental Biology of Flowering Plants, 169–85. New York, NY: Springer New York, 2000. http://dx.doi.org/10.1007/978-1-4612-1234-8_8.

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Kunz, Yvette W. "Cleavage and formation of periblast." In Developmental Biology of Teleost Fishes, 185–206. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/978-1-4020-2997-4_10.

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Conference papers on the topic "Developmental biology/pattern formation"

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Sutantyo, Daniel, Christopher Walker, Nicholas deBono, Jarryd Vargas, Anil Wipat, and Jennifer S. Hallinan. "Engineering bacterial populations for pattern formation." In 2016 IEEE Conference on Computational Intelligence in Bioinformatics and Computational Biology (CIBCB). IEEE, 2016. http://dx.doi.org/10.1109/cibcb.2016.7758116.

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Hoyer, D., S. Nowack, and U. Schneider. "Multi-scale characteristics of resampled fetal heart rate pattern provide novel fetal developmental indices." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090336.

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"Mathematical modeling of robust pattern formation in the Drosophila eye disc." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-122.

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Saleh, Sana, Mukhtar Ullah, and Hammad Naveed. "Role of Cell Morphology in Classical Delta-Notch Pattern Formation." In 2021 43rd Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2021. http://dx.doi.org/10.1109/embc46164.2021.9630053.

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Lee, Hyeyoon, Seong-Moon Cheong, and Jin-Kwan Han. "Abstract B12: March E3 ubiquitin ligase is required for head formation by mediating Dishevelled degradation during Xenopus development." In Abstracts: AACR Special Conference on Developmental Biology and Cancer; November 30 - December 3, 2015; Boston, Massachusetts. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.devbiolca15-b12.

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"Analysis of robust pattern formation in the developing Drosophila eye using two mathematical models." In Bioinformatics of Genome Regulation and Structure/Systems Biology (BGRS/SB-2022) :. Institute of Cytology and Genetics, the Siberian Branch of the Russian Academy of Sciences, 2022. http://dx.doi.org/10.18699/sbb-2022-395.

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Jieling Zhao, Hammad Naveed, Sema Kachalo, Youfang Cao, Wei Tian, and Jie Liang. "Dynamic mechanical finite element model of biological cells for studying cellular pattern formation." In 2013 35th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2013. http://dx.doi.org/10.1109/embc.2013.6610551.

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Wan, Leo Q., Sylvia M. Kang, George Eng, X. Lux Lu, B. Bob Huo, Jeffrey Gimble, X. Edward Guo, Van C. Mow, and Gordana Vunjak-Novakovic. "Geometric Control of Mechanical Forces and Stem Cell Differentiation." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192680.

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How can genetic information be translated to give specific and different spatial patterns of cellular differentiation? This is an important question in developmental biology. The spatial pattern of cellular behavior is generally considered solely dependent on the gradient of morphogens, which are usually soluble and diffusible chemicals. However, cellular function, e.g., proliferation, is found to be quite different even when cells are a few microns apart. Therefore, it has been proposed that tissue form arises as a result of feedback mechanism through mechanical forces, i.e., the tissue form will affect cellular function via mechanical force.
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Hou, Yuemin, and Ji Linhong. "Gene Transcription and Translation in Design." In ASME 2015 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/detc2015-46128.

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An organism grows from very small to the whole body, while an engineering product is assembled from elements. An organism is formed autonomously and adaptable to his/her/its environment, while an engineering product can only execute very limited actions. The formation of a product determines its functionality. Nature is the best teacher for learning how structures are formed for specific functionality. This paper compares the design process with the developmental process of embryo and proposes a qualitative development framework that simulates the gene transcription and translation in biology. The key step in design is transforming behaviors to structures. This is a process from information to the form and it bears some similarity with the process from DNA to the protein in embryogenesis. Three basic steps are required from DNA to the protein: gene transcription, transport and protein synthesis, which is named as gene expression. Key mechanisms contributing to this transformation process are investigated and a qualitative development framework are constructed for a growth design process. Simple examples are presented for illustration of proposed methods.
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Slater, John H., Jordan S. Miller, Shann S. Yu, and Jennifer L. West. "Multifaceted Nano- and Micropatterned Surfaces for Cell Adhesion Manipulation." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13177.

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Surfaces displaying nano- and micropatterned cell adhesive ligands have led to numerous discoveries in cell biology. Soft lithography techniques such as microcontact printing are well suited for creating surfaces displaying micropatterns of one ligand type in a single arrangement but are difficult to implement for the creation of multifaceted surfaces that present multiple ligand types with each ligand confined to their own pattern. To better understand the influence of extracellular matrix (ECM) composition on adhesion site formation and gross cell behavior (motility, proliferation, differentiation, etc.) it would be advantageous to posses the ability to create surfaces displaying multiple patterned ligands with length scales ranging from < 0.25 μm2, the typical size of a focal complex to > 1 μm2, the size of focal adhesions. Higher spatial resolution than what is easily achieved with microcontact printing is also desired. Such surfaces would allow for the simultaneous investigations of adhesion site maturation and composition and how changes in these properties can be implemented to engineer cell behavior via cell-surface interactions.
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Reports on the topic "Developmental biology/pattern formation"

1

Agresar, Grenmarie, and Michael A. Savageau. Final Report, December, 1999. Sloan - US Department of Energy joint postdoctoral fellowship in computational molecular biology [Canonical nonlinear methods for modeling and analyzing gene circuits and spatial variations during pattern formation in embryonic development]. Office of Scientific and Technical Information (OSTI), December 1999. http://dx.doi.org/10.2172/811376.

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2

Ohad, Nir, and Robert Fischer. Regulation of Fertilization-Independent Endosperm Development by Polycomb Proteins. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695869.bard.

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Arabidopsis mutants that we have isolated, encode for fertilization-independent endosperm (fie), fertilization-independent seed2 (fis2) and medea (mea) genes, act in the female gametophyte and allow endosperm to develop without fertilization when mutated. We cloned the FIE and MEA genes and showed that they encode WD and SET domain polycomb (Pc G) proteins, respectively. Homologous proteins of FIE and MEA in other organisms are known to regulate gene transcription by modulating chromatin structure. Based on our results, we proposed a model whereby both FIE and MEA interact to suppress transcription of regulatory genes. These genes are transcribed only at proper developmental stages, as in the central cell of the female gametophyte after fertilization, thus activating endosperm development. To test our model, the following questions were addressed: What is the Composition and Function of the Polycomb Complex? Molecular, biochemical, genetic and genomic approaches were offered to identify members of the complex, analyze their interactions, and understand their function. What is the Temporal and Spatial Pattern of Polycomb Proteins Accumulation? The use of transgenic plants expressing tagged FIE and MEA polypeptides as well as specific antibodies were proposed to localize the endogenous polycomb complex. How is Polycomb Protein Activity Controlled? To understand the molecular mechanism controlling the accumulation of FIE protein, transgenic plants as well as molecular approaches were proposed to determine whether FIE is regulated at the translational or posttranslational levels. The objectives of our research program have been accomplished and the results obtained exceeded our expectation. Our results reveal that fie and mea mutations cause parent-of-origin effects on seed development by distinct mechanisms (Publication 1). Moreover our data show that FIE has additional functions besides controlling the development of the female gametophyte. Using transgenic lines in which FIE was not expressed or the protein level was reduced during different developmental stages enabled us for the first time to explore FIE function during sporophyte development (Publication 2 and 3). Our results are consistent with the hypothesis that FIE, a single copy gene in the Arabidopsis genome, represses multiple developmental pathways (i.e., endosperm, embryogenesis, shot formation and flowering). Furthermore, we identified FIE target genes, including key transcription factors known to promote flowering (AG and LFY) as well as shoot and leaf formation (KNAT1) (Publication 2 and 3), thus demonstrating that in plants, as in mammals and insects, PcG proteins control expression of homeobox genes. Using the Yeast two hybrid system and pull-down assays we demonstrated that FIE protein interact with MEA via the N-terminal region (Publication 1). Moreover, CURLY LEAF protein, an additional member of the SET domain family interacts with FIE as well. The overlapping expression patterns of FIE, with ether MEA or CLF and their common mutant phenotypes, demonstrate the versatility of FIE function. FIE association with different SET domain polycomb proteins, results in differential regulation of gene expression throughout the plant life cycle (Publication 3). In vitro interaction assays we have recently performed demonstrated that FIE interacts with the cell cycle regulatory component Retinobalsoma protein (pRb) (Publication 4). These results illuminate the potential mechanism by which FIE may restrain embryo sac central cell division, at least partly, through interaction with, and suppression of pRb-regulated genes. The results of this program generated new information about the initiation of reproductive development and expanded our understanding of how PcG proteins regulate developmental programs along the plant life cycle. The tools and information obtained in this program will lead to novel strategies which will allow to mange crop plants and to increase crop production.
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3

Dickman, Martin B., and Oded Yarden. Genetic and chemical intervention in ROS signaling pathways affecting development and pathogenicity of Sclerotinia sclerotiorum. United States Department of Agriculture, July 2015. http://dx.doi.org/10.32747/2015.7699866.bard.

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Abstract: The long-term goals of our research are to understand the regulation of sclerotial development and pathogenicity in S. sclerotior11111. The focus in this project was on the elucidation of the signaling events and environmental cues involved in the regulation of these processes, utilizing and continuously developing tools our research groups have established and/or adapted for analysis of S. sclerotiorum, Our stated objectives: To take advantage of the recent conceptual (ROS/PPs signaling) and technical (amenability of S. sclerotiorumto manipulations coupled with chemical genomics and next generation sequencing) developments to address and extend our fundamental and potentially applicable knowledge of the following questions concerning the involvement of REDOX signaling and protein dephosphorylation in the regulation of hyphal/sclerotial development and pathogenicity of S. sclerotiorum: (i) How do defects in genes involved in ROS signaling affect S. sclerotiorumdevelopment and pathogenicity? (ii) In what manner do phosphotyrosinephosphatases affect S. sclerotiorumdevelopment and pathogenicity and how are they linked with ROS and other signaling pathways? And (iii) What is the nature of activity of newly identified compounds that affect S. sclerotiori,111 growth? What are the fungal targets and do they interfere with ROS signaling? We have met a significant portion of the specific goals set in our research project. Much of our work has been published. Briefly. we can summarize that: (a) Silencing of SsNox1(NADPHoxidase) expression indicated a central role for this enzyme in both virulence and pathogenic development, while inactivation of the SsNox2 gene resulted in limited sclerotial development, but the organism remained fully pathogenic. (b) A catalase gene (Scatl), whose expression was highly induced during host infection is involved in hyphal growth, branching, sclerotia formation and infection. (c) Protein tyrosine phosphatase l (ptpl) is required for sclerotial development and is involved in fungal infection. (d) Deletion of a superoxidedismutase gene (Sssodl) significantly reduced in virulence on both tomato and tobacco plants yet pathogenicity was mostly restored following supplementation with oxalate. (e) We have participated in comparative genome sequence analysis of S. sclerotiorumand B. cinerea. (f) S. sclerotiorumexhibits a potential switch between biotrophic and necrotrophic lifestyles (g) During plant­ microbe interactions cell death can occur in both resistant and susceptible events. Non­ pathogenic fungal mutants S. sclerotior111n also cause a cell death but with opposing results. We investigated PCD in more detail and showed that, although PCD occurs in both circumstances they exhibit distinctly different features. The mutants trigger a restricted cell death phenotype in the host that unexpectedly exhibits markers associated with the plant hypersensitive (resistant) response. Using electron and fluorescence microscopy, chemical effectors and reverse genetics, we have established that this restricted cell death is autophagic. Inhibition of autophagy rescued the non-pathogenic mutant phenotype. These findings indicate that autophagy is a defense response in this interaction Thus the control of cell death, dictated by the plant (autophagy) סr the fungus (apoptosis), is decisive to the outcome of certain plant­ microbe interactions. In addition to the time and efforts invested towards reaching the specific goals mentioned, both Pls have initiated utilizing (as stated as an objective in our proposal) state of the art RNA-seq tools in order to harness this technology for the study of S. sclerotiorum. The Pls have met twice (in Israel and in the US), in order to discuss .נחd coordinate the research efforts. This included a working visit at the US Pls laboratory for performing RNA-seq experiments and data analysis as well as working on a joint publication (now published). The work we have performed expands our understanding of the fundamental biology (developmental and pathogenic) of S. sclerotioז111וז. Furthermore, based on our results we have now reached the conclusion that this fungus is not a bona fide necrotroph, but can also display a biotrophic lifestyle at the early phases of infection. The data obtained can eventually serve .נ basis of rational intervention with the disease cycle of this pathogen.
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