Academic literature on the topic 'Elegans embryos'

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Journal articles on the topic "Elegans embryos"

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Hajeri, Vinita A., Brent A. Little, Mary L. Ladage, and Pamela A. Padilla. "NPP-16/Nup50 Function and CDK-1 Inactivation Are Associated with Anoxia-induced Prophase Arrest in Caenorhabditis elegans." Molecular Biology of the Cell 21, no. 5 (March 2010): 712–24. http://dx.doi.org/10.1091/mbc.e09-09-0787.

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Oxygen, an essential nutrient, is sensed by a multiple of cellular pathways that facilitate the responses to and survival of oxygen deprivation. The Caenorhabditis elegans embryo exposed to severe oxygen deprivation (anoxia) enters a state of suspended animation in which cell cycle progression reversibly arrests at specific stages. The mechanisms regulating interphase, prophase, or metaphase arrest in response to anoxia are not completely understood. Characteristics of arrested prophase blastomeres and oocytes are the alignment of condensed chromosomes at the nuclear periphery and an arrest of nuclear envelope breakdown. Notably, anoxia-induced prophase arrest is suppressed in mutant embryos lacking nucleoporin NPP-16/NUP50 function, indicating that this nucleoporin plays an important role in prophase arrest in wild-type embryos. Although the inactive form of cyclin-dependent kinase (CDK-1) is detected in wild-type–arrested prophase blastomeres, the inactive state is not detected in the anoxia exposed npp-16 mutant. Furthermore, we found that CDK-1 localizes near chromosomes in anoxia-exposed embryos. These data support the notion that NPP-16 and CDK-1 function to arrest prophase blastomeres in C. elegans embryos. The anoxia-induced shift of cells from an actively dividing state to an arrested state reveals a previously uncharacterized prophase checkpoint in the C. elegans embryo.
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Watts, J. L., D. G. Morton, J. Bestman, and K. J. Kemphues. "The C. elegans par-4 gene encodes a putative serine-threonine kinase required for establishing embryonic asymmetry." Development 127, no. 7 (April 1, 2000): 1467–75. http://dx.doi.org/10.1242/dev.127.7.1467.

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During the first cell cycle of Caenorhabditis elegans embryogenesis, asymmetries are established that are essential for determining the subsequent developmental fates of the daughter cells. The maternally expressed par genes are required for establishing this polarity. The products of several of the par genes have been found to be themselves asymmetrically distributed in the first cell cycle. We have identified the par-4 gene of C. elegans, and find that it encodes a putative serine-threonine kinase with similarity to a human kinase associated with Peutz-Jeghers Syndrome, LKB1 (STK11), and a Xenopus egg and embryo kinase, XEEK1. Several strong par-4 mutant alleles are missense mutations that alter conserved residues within the kinase domain, suggesting that kinase activity is essential for PAR-4 function. We find that the PAR-4 protein is present in the gonads, oocytes and early embryos of C. elegans, and is both cytoplasmically and cortically distributed. The cortical distribution begins at the late 1-cell stage, is more pronounced at the 2- and 4-cell stages and is reduced at late stages of embryonic development. We find no asymmetry in the distribution of PAR-4 protein in C. elegans embryos. The distribution of PAR-4 protein in early embryos is unaffected by mutations in the other par genes.
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Keating, H. H., and J. G. White. "Centrosome dynamics in early embryos of Caenorhabditis elegans." Journal of Cell Science 111, no. 20 (October 15, 1998): 3027–33. http://dx.doi.org/10.1242/jcs.111.20.3027.

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The early Caenorhabditis elegans embryo divides with a stereotyped pattern of cleavages to produce cells that vary in developmental potential. Differences in cleavage plane orientation arise between the anterior and posterior cells of the 2-cell embryo as a result of asymmetries in centrosome positioning. Mechanisms that position centrosomes are thought to involve interactions between microtubules and the cortex, however, these mechanisms remain poorly defined. Interestingly, in the early embryo the shape of the centrosome predicts its subsequent movement. We have used rhodamine-tubulin and live imaging techniques to study the development of asymmetries in centrosome morphology and positioning. In contrast to studies using fixed embryos, our images provide a detailed characterization of the dynamics of centrosome flattening. In addition, our observations of centrosome behavior in vivo challenge previous assumptions regarding centrosome separation by illustrating that centrosome flattening and daughter centrosome separation are distinct processes, and by revealing that nascent daughter centrosomes may become separated from the nucleus. Finally, we provide evidence that the midbody specifies a region of the cortex that directs rotational alignment of the centrosome-nucleus complex and that the process is likely to involve multiple interactions between microtubules and the cortex; the process of alignment involves oscillations and overshoots, suggesting a multiplicity of cortical sites that interact with microtubules.
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Browning, H., and S. Strome. "A sperm-supplied factor required for embryogenesis in C. elegans." Development 122, no. 1 (January 1, 1996): 391–404. http://dx.doi.org/10.1242/dev.122.1.391.

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The paternal-effect embryonic-lethal gene, spe-11, is required for normal development of early C. elegans embryos. Spe-11 embryos fail to complete meiosis, form a weak eggshell, fail to orient properly the first mitotic spindle, and fail to undergo cytokinesis. Here we report cloning and sequencing of the spe-11 gene, which encodes a novel protein. As predicted by the paternal-effect mutant phenotype, the gene is expressed during spermatogenesis but is not detectable in females undergoing oogenesis, and the protein is present in mature sperm. To investigate whether SPE-11's essential function is during spermatogenesis or whether sperm-delivered SPE-11 functions in the newly fertilized embryo, we engineered animals to supply SPE-11 to the embryo through the oocyte rather than through the sperm. We found that maternal expression is sufficient for embryonic viability. This result demonstrates that SPE-11 is not required during spermatogenesis, and suggests that SPE-11 is a sperm-supplied factor that participates directly in development of the early embryo. In contrast to the many known maternal factors required for embryogenesis, SPE-11 is the first paternally contributed factor to be genetically identified and molecularly characterized.
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Edgar, L. G., N. Wolf, and W. B. Wood. "Early transcription in Caenorhabditis elegans embryos." Development 120, no. 2 (February 1, 1994): 443–51. http://dx.doi.org/10.1242/dev.120.2.443.

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We have analysed early transcription in devitellinized, cultured embryos of the nematode Caenorhabditis elegans by two methods: measurement of [32P]UTP uptake into TCA-precipitable material and autoradiographic detection of [3H]UTP labelling both in the presence and absence of alpha-amanitin. RNA synthesis was first detected at the 8- to 12-cell stage, and alpha-amanitin sensitivity also appeared at this time, during the cleavages establishing the major founder cell lineages. The requirements for maternally supplied versus embryonically produced gene products in early embryogenesis were examined in the same culture system by observing the effects of alpha-amanitin on cell division and the early stereotyped lineage patterns. In the presence of high levels of alpha-amanitin added at varying times from two cells onward, cell division continued until approximately the 100-cell stage and then stopped during a single round of cell division. The characteristic unequal early cleavages, orientation of cleavage planes and lineage-specific timing of early divisions were unaffected by alpha-amanitin in embryos up to 87 cells. These results indicate that embryonic transcription starts well before gastrulation in C. elegans embryos, but that although embryonic transcripts may have important early functions, maternal products can support at least the mechanics of the first 6 to 7 cell cycles.
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Zhang, Haining, Jayne M. Squirrell, and John G. White. "RAB-11 Permissively Regulates Spindle Alignment by Modulating Metaphase Microtubule Dynamics in Caenorhabditis elegans Early Embryos." Molecular Biology of the Cell 19, no. 6 (June 2008): 2553–65. http://dx.doi.org/10.1091/mbc.e07-09-0862.

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Alignment of the mitotic spindle along a preformed axis of polarity is crucial for generating cell diversity in many organisms, yet little is known about the role of the endomembrane system in this process. RAB-11 is a small GTPase enriched in recycling endosomes. When we depleted RAB-11 by RNAi in Caenorhabditis elegans, the spindle of the one-cell embryo failed to align along the axis of polarity in metaphase and underwent violent movements in anaphase. The distance between astral microtubules ends and the anterior cortex was significantly increased in rab-11(RNAi) embryos specifically during metaphase, possibly accounting for the observed spindle alignment defects. Additionally, we found that normal ER morphology requires functional RAB-11, particularly during metaphase. We hypothesize that RAB-11, in conjunction with the ER, acts to regulate cell cycle–specific changes in astral microtubule length to ensure proper spindle alignment in Caenorhabditis elegans early embryos.
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Lee, Kenneth K., Yosef Gruenbaum, Perah Spann, Jun Liu, and Katherine L. Wilson. "C. elegans Nuclear Envelope Proteins Emerin, MAN1, Lamin, and Nucleoporins Reveal Unique Timing of Nuclear Envelope Breakdown during Mitosis." Molecular Biology of the Cell 11, no. 9 (September 2000): 3089–99. http://dx.doi.org/10.1091/mbc.11.9.3089.

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Emerin, MAN1, and LAP2 are integral membrane proteins of the vertebrate nuclear envelope. They share a 43-residue N-terminal motif termed the LEM domain. We found three putative LEM domain genes inCaenorhabditis elegans, designated emr-1,lem-2, and lem-3. We analyzedemr-l, which encodes Ce-emerin, andlem-2, which encodes Ce-MAN1. Ce-emerin and Ce-MAN1 migrate on SDS-PAGE as 17- and 52-kDa proteins, respectively. Based on their biochemical extraction properties and immunolocalization, both Ce-emerin and Ce-MAN1 are integral membrane proteins localized at the nuclear envelope. We used antibodies against Ce-MAN1, Ce-emerin, nucleoporins, and Ce-lamin to determine the timing of nuclear envelope breakdown during mitosis in C. elegans. The C. elegans nuclear envelope disassembles very late compared with vertebrates and Drosophila. The nuclear membranes remained intact everywhere except near spindle poles during metaphase and early anaphase, fully disassembling only during mid-late anaphase. Disassembly of pore complexes, and to a lesser extent the lamina, depended on embryo age: pore complexes were absent during metaphase in >30-cell embryos but existed until anaphase in 2- to 24-cell embryos. Intranuclear mRNA splicing factors disassembled after prophase. The timing of nuclear disassembly in C. elegans is novel and may reflect its evolutionary position between unicellular and more complex eukaryotes.
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Basham, Stephen E., and Lesilee S. Rose. "The Caenorhabditis elegans polarity gene ooc-5 encodes a Torsin-related protein of the AAA ATPase superfamily." Development 128, no. 22 (November 15, 2001): 4645–56. http://dx.doi.org/10.1242/dev.128.22.4645.

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The PAR proteins are required for polarity and asymmetric localization of cell fate determinants in C. elegans embryos. In addition, several of the PAR proteins are conserved and localized asymmetrically in polarized cells in Drosophila, Xenopus and mammals. We have previously shown that ooc-5 and ooc-3 mutations result in defects in spindle orientation and polarity in early C. elegans embryos. In particular, mutations in these genes affect the re-establishment of PAR protein asymmetry in the P1 cell of two-cell embryos. We now report that ooc-5 encodes a putative ATPase of the Clp/Hsp100 and AAA superfamilies of proteins, with highest sequence similarity to Torsin proteins; the gene for human Torsin A is mutated in individuals with early-onset torsion dystonia, a neuromuscular disease. Although Clp/Hsp100 and AAA family proteins have roles in diverse cellular activities, many are involved in the assembly or disassembly of proteins or protein complexes; thus, OOC-5 may function as a chaperone. OOC-5 protein co-localizes with a marker of the endoplasmic reticulum in all blastomeres of the early C. elegans embryo, in a pattern indistinguishable from that of OOC-3 protein. Furthermore, OOC-5 localization depends on the normal function of the ooc-3 gene. These results suggest that OOC-3 and OOC-5 function in the secretion of proteins required for the localization of PAR proteins in the P1 cell, and may have implications for the study of torsion dystonia.
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Zilberman, Yuliya, Joshua Abrams, Dorian C. Anderson, and Jeremy Nance. "Cdc42 regulates junctional actin but not cell polarization in the Caenorhabditis elegans epidermis." Journal of Cell Biology 216, no. 11 (September 13, 2017): 3729–44. http://dx.doi.org/10.1083/jcb.201611061.

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During morphogenesis, adherens junctions (AJs) remodel to allow changes in cell shape and position while preserving adhesion. Here, we examine the function of Rho guanosine triphosphatase CDC-42 in AJ formation and regulation during Caenorhabditis elegans embryo elongation, a process driven by asymmetric epidermal cell shape changes. cdc-42 mutant embryos arrest during elongation with epidermal ruptures. Unexpectedly, we find using time-lapse fluorescence imaging that cdc-42 is not required for epidermal cell polarization or junction assembly, but rather is needed for proper junctional actin regulation during elongation. We show that the RhoGAP PAC-1/ARHGAP21 inhibits CDC-42 activity at AJs, and loss of PAC-1 or the interacting linker protein PICC-1/CCDC85A-C blocks elongation in embryos with compromised AJ function. pac-1 embryos exhibit dynamic accumulations of junctional F-actin and an increase in AJ protein levels. Our findings identify a previously unrecognized molecular mechanism for inhibiting junctional CDC-42 to control actin organization and AJ protein levels during epithelial morphogenesis.
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Rose, L. S., and K. Kemphues. "The let-99 gene is required for proper spindle orientation during cleavage of the C. elegans embryo." Development 125, no. 7 (April 1, 1998): 1337–46. http://dx.doi.org/10.1242/dev.125.7.1337.

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The orientation of cell division is a critical aspect of development. In 2-cell C. elegans embryos, the spindle in the posterior cell is aligned along the long axis of the embryo and contributes to the unequal partitioning of cytoplasm, while the spindle in the anterior cell is oriented transverse to the long axis. Differing spindle alignments arise from blastomere-specific rotations of the nuclear-centrosome complex at prophase. We have found that mutations in the maternally expressed gene let-99 affect spindle orientation in all cells during the first three cleavages. During these divisions, the nuclear-centrosome complex appears unstable in position. In addition, in almost half of the mutant embryos, there are reversals of the normal pattern of spindle orientations at second cleavage: the spindle of the anterior cell is aligned with the long axis of the embryo and nuclear rotation fails in the posterior cell causing the spindle to form transverse to the long axis. In most of the remaining embryos, spindles in both cells are transverse at second cleavage. The distributions of several asymmetrically localized proteins, including P granules and PAR-3, are normal in early let-99 embryos, but are perturbed by the abnormal cell division orientations at second cleavage. The accumulation of actin and actin capping protein, which marks the site involved in nuclear rotation in 2-cell wild-type embryos, is abnormal but is not reversed in let-99 mutant embryos. Based on these data, we conclude that let-99(+) is required for the proper orientation of spindles after the establishment of polarity, and we postulate that let-99(+) plays a role in interactions between the astral microtubules and the cortical cytoskeleton.
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Dissertations / Theses on the topic "Elegans embryos"

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Bringmann, Henrik Philipp. "Experiments concerning the mechanism of cytokinesis in Caenorhabditis elegans embryos." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2007. http://nbn-resolving.de/urn:nbn:de:swb:14-1170257008922-66010.

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In my thesis I aimed to contribute to the understanding of the mechanism of cytokinesis in C. elegans embryos. I wanted to analyze the relative contributions of different spindle parts – microtubule asters and the midzone - to cytokinesis furrow positioning. I developed a UV laser-based severing assay that allows the spatial separation of the region midway between the asters and the spindle midzone. The spindle is severed asymmetrically between one aster and the midzone. I found that the spindle provides two consecutive signals that can each position a cytokinesis furrow: microtubule asters provide a first signal, and the spindle midzone provides a second signal. The use of mutants that do not form a midzone suggested that the aster-positioned furrow is able to divide the cell alone without a spindle midzone. Analysis of cytokinesis in hypercontracile mutants suggests that the aster-positioned cytokinesis furrow and the midzone positioned furrow inhibit each other by competing for cortical contractile elements. I then wanted to identify the molecular pathway responsible for cytokinesis furrow positioning in response to the microtubule asters. To this end, I performed an RNAi screen, which identified a role for LET-99 in cytokinesis: LET-99 appeared to be required for aster-positioned cytokinesis but not midzone-positioned cytokinesis. LET-99 localizes as a cortical band that overlaps with the cytokinesis furrow. Mechanical displacement of the spindle demonstrated that the spindle positions cortical LET-99 at the site of furrow formation. The furrow localization of LET-99 depended on G proteins, and consistent with this finding, G proteins are also required for aster-positioned cytokinesis. (Anlage: Quick time movies, 466, 67 MB)
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Bringmann, Henrik Philipp. "Experiments concerning the mechanism of cytokinesis in Caenorhabditis elegans embryos." Doctoral thesis, Technische Universität Dresden, 2006. https://tud.qucosa.de/id/qucosa%3A25039.

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In my thesis I aimed to contribute to the understanding of the mechanism of cytokinesis in C. elegans embryos. I wanted to analyze the relative contributions of different spindle parts – microtubule asters and the midzone - to cytokinesis furrow positioning. I developed a UV laser-based severing assay that allows the spatial separation of the region midway between the asters and the spindle midzone. The spindle is severed asymmetrically between one aster and the midzone. I found that the spindle provides two consecutive signals that can each position a cytokinesis furrow: microtubule asters provide a first signal, and the spindle midzone provides a second signal. The use of mutants that do not form a midzone suggested that the aster-positioned furrow is able to divide the cell alone without a spindle midzone. Analysis of cytokinesis in hypercontracile mutants suggests that the aster-positioned cytokinesis furrow and the midzone positioned furrow inhibit each other by competing for cortical contractile elements. I then wanted to identify the molecular pathway responsible for cytokinesis furrow positioning in response to the microtubule asters. To this end, I performed an RNAi screen, which identified a role for LET-99 in cytokinesis: LET-99 appeared to be required for aster-positioned cytokinesis but not midzone-positioned cytokinesis. LET-99 localizes as a cortical band that overlaps with the cytokinesis furrow. Mechanical displacement of the spindle demonstrated that the spindle positions cortical LET-99 at the site of furrow formation. The furrow localization of LET-99 depended on G proteins, and consistent with this finding, G proteins are also required for aster-positioned cytokinesis. (Anlage: Quick time movies, 466, 67 MB)
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Schlaitz, Anne-Lore. "Regulation of Mitotic Spindle Assembly in Caenorhabditis elegans Embryos." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2007. http://nbn-resolving.de/urn:nbn:de:swb:14-1181247079528-57268.

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The mitotic spindle is a bipolar microtubule-based structure that mediates proper cell division by segregating the genetic material and by positioning the cytokinesis cleavage plane. Spindle assembly is a complex process, involving the modulation of microtubule dynamics, microtubule focusing at spindle poles and the formation of stable microtubule attachments to chromosomes. The cellular events leading to spindle formation are highly regulated, and mitotic kinases have been implicated in many aspects of this process. However, little is known about their counteracting phosphatases. A screen for genes required for early embryonic cell divisions in C. elegans identified rsa-1 (for regulator of spindle assembly 1), a putative Protein Phosphatase 2A (PP2A) regulatory subunit whose silencing causes defects in spindle formation. Upon rsa-1(RNAi), spindle poles collapse onto each other and microtubule amounts are strongly reduced. My thesis work demonstrates that RSA-1 indeed functions as a PP2A regulatory subunit. RSA-1 associates with the PP2A enzyme and recruits it to centrosomes. The centrosome binding of PP2A furthermore requires the new protein RSA-2 as well as the core centrosomal protein SPD-5 and is based on a hierarchical protein-protein interaction pathway. When PP2A is lacking at centrosomes after rsa-1(RNAi), the centrosomal amounts of two critical mitotic effectors, the microtubule destabilizer KLP-7 and the kinetochore microtubule stabilizer TPXL-1, are altered. KLP-7 is increased, which may account for the reduction of microtubule outgrowth from centrosomes in rsa-1(RNAi) embryos. TPXL-1 is lost from centrosomes, which may explain why spindle poles collapse in the absence of RSA-1. TPXL-1 physically associates with RSA-1 and RSA-2, suggesting that it is a direct target of PP2A. In summary, this work defines the role of a novel PP2A complex in mitotic spindle assembly and suggests a model for how different microtubule re-organization steps might be coordinated during spindle formation.
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Schonegg, Stephanie. "Rho GTPase family members in establishment of polarity in C. elegans embryos." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1139490285625-55732.

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Cell polarity is required for asymmetric division, a mechanism to generate cell diversity by distributing fate determinants unequally to daughter cells. The establishment of polarity requires the evolutionarily conserved partitioning-defective (PAR) proteins as well as the actin cytoskeleton. In Caenorhabditis elegans one-cell embryos, the PAR proteins are segregated into an anterior (PAR-3, PAR-6) and a posterior (PAR-1, PAR-2) corticaldomain. The formation of PAR polarity correlates with anterior-posterior differences in the contractile activity of the cortex, known as "contractile polarity". It is thought that regulation of contractile polarity controls the establishment of PAR polarity, but detailed evidence to support this idea is lacking. To investigate how modulation of the actomyosin cytoskeleton affects polarity establishment, the acto-myosin cytoskeleton was perturbed by RNA-mediated interference (RNAi) of two Rho GTPases, CDC-42 and RHO-1. To examine how Rho GTPases are implemented in actin remodeling, it is important to analyze how their activity is controlled and how different activities affect polarity formation. The role of two putative Rho GTPase regulators, the Rho GTPase exchange factor (GEF) ECT-2 and the Rho GTPase activating protein (GAP) K09H11.3 were analyzed with respect to polarity formation. The formation of polarity was analyzed by using GFP-labeled proteins, and several different tracking methods were used to investigate the establishment of contractile and PAR polarity in more detail.This study demonstrates that both RHO-1 and CDC-42 are involved in polarity establishment in C. elegans embryos. But importantly, both act by different mechanisms. RHO-1 organizes the acto-myosin cytoskeleton into a contractile network, and therefore is essential for the formation of contractile polarity. The organization of the acto-myosin cytoskeleton is critical to ensure proper PAR protein distribution. Furthermore, a balance of RHO-1 activity by the GEF ECT-2 and the GAP K09H11.3 appears to be important for cortical contractility, for PAR protein domain size and for mutual exclusion of the PAR proteins. Although CDC-42 was shown to be a universal regulator of the actin cytoskeleton, CDC-42 acts downstream of contractile polarity. CDC-42 is required for linking PAR-6 to the cortex. In the absence of RHO-1 and ECT-2, PAR-6 and CDC-42 are not localized to the anterior cortex. This suggests that RHO-1, by organizing the actomyosin cytoskeleton into a contractile network, regulates the segregation of CDC-42 to the anterior cortex, and concomitantly PAR-6 localization. This study shows that the distribution of PAR is related to cortical activity and supports the model that the actin cytoskeleton plays an important role in polarity establishment.
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Schonegg, Stephanie. "Rho GTPase family members in establishment of polarity in C. elegans embryos." Doctoral thesis, Technische Universität Dresden, 2005. https://tud.qucosa.de/id/qucosa%3A24640.

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Cell polarity is required for asymmetric division, a mechanism to generate cell diversity by distributing fate determinants unequally to daughter cells. The establishment of polarity requires the evolutionarily conserved partitioning-defective (PAR) proteins as well as the actin cytoskeleton. In Caenorhabditis elegans one-cell embryos, the PAR proteins are segregated into an anterior (PAR-3, PAR-6) and a posterior (PAR-1, PAR-2) corticaldomain. The formation of PAR polarity correlates with anterior-posterior differences in the contractile activity of the cortex, known as "contractile polarity". It is thought that regulation of contractile polarity controls the establishment of PAR polarity, but detailed evidence to support this idea is lacking. To investigate how modulation of the actomyosin cytoskeleton affects polarity establishment, the acto-myosin cytoskeleton was perturbed by RNA-mediated interference (RNAi) of two Rho GTPases, CDC-42 and RHO-1. To examine how Rho GTPases are implemented in actin remodeling, it is important to analyze how their activity is controlled and how different activities affect polarity formation. The role of two putative Rho GTPase regulators, the Rho GTPase exchange factor (GEF) ECT-2 and the Rho GTPase activating protein (GAP) K09H11.3 were analyzed with respect to polarity formation. The formation of polarity was analyzed by using GFP-labeled proteins, and several different tracking methods were used to investigate the establishment of contractile and PAR polarity in more detail.This study demonstrates that both RHO-1 and CDC-42 are involved in polarity establishment in C. elegans embryos. But importantly, both act by different mechanisms. RHO-1 organizes the acto-myosin cytoskeleton into a contractile network, and therefore is essential for the formation of contractile polarity. The organization of the acto-myosin cytoskeleton is critical to ensure proper PAR protein distribution. Furthermore, a balance of RHO-1 activity by the GEF ECT-2 and the GAP K09H11.3 appears to be important for cortical contractility, for PAR protein domain size and for mutual exclusion of the PAR proteins. Although CDC-42 was shown to be a universal regulator of the actin cytoskeleton, CDC-42 acts downstream of contractile polarity. CDC-42 is required for linking PAR-6 to the cortex. In the absence of RHO-1 and ECT-2, PAR-6 and CDC-42 are not localized to the anterior cortex. This suggests that RHO-1, by organizing the actomyosin cytoskeleton into a contractile network, regulates the segregation of CDC-42 to the anterior cortex, and concomitantly PAR-6 localization. This study shows that the distribution of PAR is related to cortical activity and supports the model that the actin cytoskeleton plays an important role in polarity establishment.
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Tenlen, Jennifer R. "Linking PAR polarity proteins to cell fate regulation : analysis of MEX-5 localization in Caenorhabditis elegans embryos /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/5009.

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Wu, Edlyn. "MicroRNA-mediated deadenylation of natural UTRs in C. elegans embryos is prevalent and requires miRISC collaboration." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86859.

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MicroRNAs (miRNAs) are small RNAs that play a pivotal role in post-transcriptional gene regulation. These regulatory RNAs associate with the Argonaute proteins to form the miRNA-induced silencing complexes (miRISCs). In metazoans, miRISCs typically target mRNAs by imperfectly binding to complementary sites in 3' untranslated regions (3'UTRs), thereby affecting the translation of the targets, and/or reducing their stability. Despite the significant roles miRNAs play in various biological processes, the mechanistic details of how they regulate gene expression remain unclear. Using a C. elegans embryonic in vitro system, we focus on the mechanism for miRNA mode of action, and the significance of the poly(A) tail in miRNA-mediated silencing during development. We show that our miRNA luciferase reporters underwent deadenylation starting at 20 minutes of incubation of the RNA with C. elegans extract, and this process is dependent on the Argonautes involved in the miRNA pathway, ALG-1 and ALG-2. We also detect the presence of an RNA decay intermediate within two hours of target RNA-extract incubation. The appearance of this intermediate is independent of the m7GTP cap, indicating a 3'->5' decay pathway occurring in coordination or independently of miRNA-mediated deadenylation. Furthermore, we present here our screen for endogenous targets of the maternal miR-35-42 family, a miRNA family abundantly expressed in the embryo and essential for embryogenesis, via deadenylation assays. From our screen, we identified the tolloid/BMP-1 family member, toh-1, as a deadenylated target of miR-35-42. The pro-apoptotic egl-1 was also identified as a target of miR-35-42, as well as the zygotically expressed miR-58. Our findings demonstrate that more than half of the predicted natural UTRs were deadenylated in a miRNA-dependent manner. We also show that a minimum spacing is required for miRISCs to efficiently silence their targets, and we illustrate that at least two separate miRISC-bin
Les microARNs (miARNs) sont des petits ARNs qui jouent un rôle important dans la régulation post-transcriptionnelle des gènes. Ces ARNs régulateurs s'associent à des protéines, nommées les Argonautes, afin de former un complexe de répression induit par les miARNs (miRISCs). Chez les métazoaires, les miRISCs ciblent l'expression des gènes par une hybridation imparfaite avec la région non-codante en 3' (3'UTR) de l'ARN messager (ARNm) ciblé, ce qui a pour effet d'affecter la traduction des ARNm, et/ou de réduire leur stabilité. Malgré le fait que les miARNs jouent plusieurs rôles significatifs dans divers processus biologiques, leur mécanisme de contrôle de régulation génique demeure incompris. En utilisant un système in vitro chez les embryons de C. elegans, on se concentre sur le mécanisme d'action des miARNs et sur l'importance de la queue de poly(A) dans la répression des ARNm par le biais de miARNs pendant le développement. Nos résultats démontrent que suite à l'incubation de l'ARN avec l'extrait de C. elegans, nos gènes rapporteurs de luciférase-miARN ont commencé à être déadénylés après 20 minutes. Ce procédé est dépendant des Argonautes ALG-1 et ALG-2. On a aussi détecté la présence d'un deuxième ARN intermédiaire plus court après deux heures d'incubation de l'ARNm ciblé avec l'extrait. L'apparition de cet intermédiaire est indépendante du cap m7GTP, indiquant une voie de dégradation 3'->5'. On présente également un essai de déadénylation pour examiner les ARNm endogènes ciblés par la famille des miARNs maternelles, miR-35-42. Cette famille de miARNs est exprimée abondamment dans l'embryon et est essentielle pour l'embryogenèse. On a identifié un membre de la famille tolloid/BMP-1, toh-1, comme un ARNm ciblé et déadénylé. Le pro-apoptotique egl-1 a aussi été identifié comme un ARNm ciblé de la famille miR-35-42 ainsi que de miR-58, un miARN exprimé zygotiquement. Nos résultats démontrent$
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Redemann, Stefanie, Jacques Pecreaux, Nathan W. Goehring, Khaled Khairy, Ernst H. K. Stelzer, Anthony A. Hyman, and Jonathon Howard. "Membrane Invaginations Reveal Cortical Sites that Pull on Mitotic Spindles in One-Cell C. elegans Embryos." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-185631.

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Asymmetric positioning of the mitotic spindle in C. elegans embryos is mediated by force-generating complexes that are anchored at the plasma membrane and that pull on microtubules growing out from the spindle poles. Although asymmetric distribution of the force generators is thought to underlie asymmetric positioning of the spindle, the number and location of the force generators has not been well defined. In particular, it has not been possible to visualize individual force generating events at the cortex. We discovered that perturbation of the acto-myosin cortex leads to the formation of long membrane invaginations that are pulled from the plasma membrane toward the spindle poles. Several lines of evidence show that the invaginations, which also occur in unperturbed embryos though at lower frequency, are pulled by the same force generators responsible for spindle positioning. Thus, the invaginations serve as a tool to localize the sites of force generation at the cortex and allow us to estimate a lower limit on the number of cortical force generators within the cell.
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Redemann, Stefanie, Jacques Pecreaux, Nathan W. Goehring, Khaled Khairy, Ernst H. K. Stelzer, Anthony A. Hyman, and Jonathon Howard. "Membrane Invaginations Reveal Cortical Sites that Pull on Mitotic Spindles in One-Cell C. elegans Embryos." PloS, 2010. https://tud.qucosa.de/id/qucosa%3A29013.

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Asymmetric positioning of the mitotic spindle in C. elegans embryos is mediated by force-generating complexes that are anchored at the plasma membrane and that pull on microtubules growing out from the spindle poles. Although asymmetric distribution of the force generators is thought to underlie asymmetric positioning of the spindle, the number and location of the force generators has not been well defined. In particular, it has not been possible to visualize individual force generating events at the cortex. We discovered that perturbation of the acto-myosin cortex leads to the formation of long membrane invaginations that are pulled from the plasma membrane toward the spindle poles. Several lines of evidence show that the invaginations, which also occur in unperturbed embryos though at lower frequency, are pulled by the same force generators responsible for spindle positioning. Thus, the invaginations serve as a tool to localize the sites of force generation at the cortex and allow us to estimate a lower limit on the number of cortical force generators within the cell.
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Samandar, eweis Dureen. "Asymmetric division in single cell nematode embryos outside the Caenorhabditis genus." Electronic Thesis or Diss., Université Paris sciences et lettres, 2021. http://www.theses.fr/2021UPSLS063.

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La division cellulaire asymétrique est un processus essentiel du développement. Ce processus ainsi que sa régulation ont fait l’objet de nombreuses études chez l’embryon de Caenorhabditis elegans. La division asymétrique de l'embryon unicellulaire est un processus conservé à travers les espèces de nématodes, cependant les caractéristiques cellulaires menant à la division sont étonnamment variables. Au cours de mon doctorat, j'ai voulu étudier ces différences en utilisant deux embryons non-C. elegans : Diploscapter pachys et Pristionchus pacificus. D. pachys est le parent parthénogénétique le plus proche de C. elegans. La polarité étant induite par le sperme chez C. elegans, on ne peut expliquer ce qui brise la symétrie chez D. pachys. Mes résultats montrent que le noyau occupe le plus souvent l’hémisphère de D. pachys qui deviendra le pole postérieur. Dans les embryons où il est astreint à un pôle par centrifugation, le noyau fini par revenir à son pôle préférentiel. Même si l’embryon est polarisé, l’agitation corticale et le cytosquelette d’actine semblent identiques aux deux pôles. D’autre part, la position du fuseau méiotique est corrélée avec la future cellule postérieure. Dans certains ovocytes, on observe des structures de microtubules émanant du fuseau méiotique combiné à un faible enrichissement en actine au future pôle postérieur. Finalement, mon principal projet de thèse montre que la polarité de D. pachys est atteinte durant la méiose, au cours de laquelle le fuseau méiotique pourrait jouer un rôle par un mécanisme présent mais inhibé chez C. elegans. Chez P. pacificus, la transgénèse biolistique a été récemment utilisée avec succès. Toutefois, par manque d’un marqueur de sélection fiable, il était illusoire de poursuivre cette approche. En conclusion, les résultats de ma thèse contribuent à une meilleure compréhension de l’embryogénèse hors C. elegans. Ils soulignent l’importance de ces espèces dans l’optique d’études comparatives
Asymmetric cell division is an essential process of development. The process and its regulation have been studied extensively in the Caenorhabditis elegans embryo. Asymmetric division of the single-cell embryo is a conserved process in nematode species, however, the cellular features leading up to division are surprisingly variable. During my PhD, I aimed to study these differences by using two non-C. elegans embryos: Diploscapter pachys and Pristionchus pacificus. D. pachys is the closest parthenogenetic relative to C. elegans. Since the polarity cue in C. elegans is brought by the sperm, how polarity is triggered in D. pachys remains unknown. My results show that the nucleus inhabits principally the hemisphere of the D. pachys embryo that will become the posterior pole. Moreover, in embryos where the nucleus is forced to one pole by centrifugation, it returns to its preferred pole. Although the embryo is polarized, cortical ruffling and actin cytoskeleton at both poles appear identical. Interestingly, the location of the meiotic spindle also correlates with the future posterior cell. In some oocytes, a slight actin enrichment along with unusual microtubule structures emanating from the meiotic spindle are observed at the future posterior pole. Overall, my main PhD project shows that polarity of the D. pachys embryo is attained during meiosis wherein the meiotic spindle could potentially be playing a role by a mechanism that may be present but suppressed in C. elegans. For P. pacificus, biolistic transgenesis has been shown recently successful. However, due to a lack of a stringent selection marker, the continuation of this project was unfeasible during my PhD. Altogether, the results of my PhD add to the understanding of non-C. elegans early embryogenesis and emphasizes on the importance of using these species for comparative studies
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Book chapters on the topic "Elegans embryos"

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Tzur, Yonatan B., and Yosef Gruenbaum. "Nuclear Envelope Breakdown and Reassembly in C. elegans." In Nuclear Envelope Dynamics in Embryos and Somatic Cells, 103–10. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0129-9_8.

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Tegha-Dunghu, Justus, Eva M. Gusnowski, and Martin Srayko. "Measuring Microtubule Growth and Gliding in Caenorhabditis elegans Embryos." In Methods in Molecular Biology, 103–16. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0329-0_7.

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O’Toole, Eileen, and Thomas Müller-Reichert. "Electron Tomography of Microtubule End-Morphologies in C. elegans Embryos." In Methods in Molecular Biology, 135–44. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-993-2_8.

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Wood, William B. "Determination of Pattern and Fate in Early Embryos of Caenorhabditis elegans." In The Molecular Biology of Cell Determination and Cell Differentiation, 57–78. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-6817-9_2.

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O’Connell, Kevin F., and Andy Golden. "Confocal Imaging of the Microtubule Cytoskeleton in C. elegans Embryos and Germ Cells." In Confocal Microscopy, 257–72. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-60761-847-8_13.

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Mikl, Martin, and Carrie R. Cowan. "Cell Polarity in One-Cell C. elegans Embryos: Ensuring an Accurate and Precise Spatial Axis During Development." In Cell Polarity 2, 3–32. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14466-5_1.

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Farhadifar, Reza, and Daniel Needleman. "Automated Segmentation of the First Mitotic Spindle in Differential Interference Contrast Microcopy Images of C. elegans Embryos." In Methods in Molecular Biology, 41–45. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0329-0_3.

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Robertson, Scott, and Rueyling Lin. "The Oocyte-to-Embryo Transition." In Germ Cell Development in C. elegans, 351–72. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4015-4_12.

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Hardin, Jeff, Joel Serre, Ryan King, Elise Walck-Shannon, and David Reiner. "Imaging Epidermal Cell Rearrangement in the C. elegans Embryo." In Methods in Molecular Biology, 345–76. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2035-9_22.

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Fielmich, Lars-Eric, and Sander van den Heuvel. "Polarity Control of Spindle Positioning in the C. elegans Embryo." In Cell Polarity 2, 119–41. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14466-5_5.

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Conference papers on the topic "Elegans embryos"

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Oibayashi, Takumi, Takaya Ueda, Yuki Kimura, Yukako Tohsato, and Ikuko Nishikawa. "Phenotype Anomaly Detection in Early C. elegans Embryos by Variational Auto-Encoder." In 2021 IEEE 9th International Conference on Bioinformatics and Computational Biology (ICBCB). IEEE, 2021. http://dx.doi.org/10.1109/icbcb52223.2021.9459228.

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Kolotuev, Irina. "Virtual correlative light microscopy-EM Time Series of C. elegans: Automated Single Cell Identification in embryos during development." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.328.

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Aviles-Espinosa, Rodrigo, Susana I. C. O. Santos, Andreas Brodschelm, Wilhelm G. Kaenders, Cesar Alonso-Ortega, David Artigas, and Pablo Loza-Alvarez. "In-vivo third-harmonic generation microscopy at 1550nm three-dimensional long-term time-lapse studies in living C. elegans embryos." In SPIE BiOS, edited by Jose-Angel Conchello, Carol J. Cogswell, Tony Wilson, and Thomas G. Brown. SPIE, 2011. http://dx.doi.org/10.1117/12.874931.

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Dong, Li, Jingwei Zhang, Thomas Lehnert, and Martin A. M. Gijs. "8-Channel single embryo pipette for accurate C. elegans bioassays." In 2018 IEEE Micro Electro Mechanical Systems (MEMS). IEEE, 2018. http://dx.doi.org/10.1109/memsys.2018.8346755.

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Datta, Rupsa, Kelsey Tweed, and Melissa Skala. "Label-free metabolic imaging of early C. elegans embryo development." In Optical Molecular Probes, Imaging and Drug Delivery. Washington, D.C.: OSA, 2021. http://dx.doi.org/10.1364/omp.2021.oth1e.4.

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Wang, Yijie, Jun Chen, Yuan Zhang, and Kee-Hong Kim. "Measurements of Morphology and Locomotion of Caenorhabditis Elegans With Digital Holographic Microscopy." In ASME 2020 Fluids Engineering Division Summer Meeting collocated with the ASME 2020 Heat Transfer Summer Conference and the ASME 2020 18th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/fedsm2020-20177.

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Abstract Digital holographic microscopy (DHM) enables 3D volumetric measurements of small objects with high magnification. DHM has been applied to measure a variety of experimental studies, including turbulent boundary layer, spray droplets, individual cells, development of zebrafish embryo, etc. In this study, a DHM system is applied to measure the morphology and locomotion of two groups of Caenorhabditis Elegans (C. Elegans) with different development conditions (ATGL-1 group and n2 group) in an 8-day time period from their hatching to the adult stage, whose body lengths range from hundreds of micrometers to one millimeter. The length and volume are determined to describe the morphology of the C. Elegans at different development stages. The locomotion of the C. Elegans is divided into linear motion and curl motion. The kinetic energy derived from the two types of motion describes the extent of how active the C. Elegans is. The statistics of morphology and locomotion of the two groups of C. Elegans are compared at different development stages to illustrate the influence of the applied development conditions.
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Petrášek, Zdeněk, Carsten Hoege, Anthony A. Hyman, and Petra Schwille. "Two-photon fluorescence imaging and correlation analysis applied to protein dynamics in C. elegans embryo." In Biomedical Optics (BiOS) 2008, edited by Ammasi Periasamy and Peter T. C. So. SPIE, 2008. http://dx.doi.org/10.1117/12.761722.

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