Cell polarity and gastrulation inC. elegans

Development ◽  
2002 ◽  
Vol 129 (2) ◽  
pp. 387-397 ◽  
Author(s):  
Jeremy Nance ◽  
James R. Priess
Keyword(s):  
Cell Fate ◽  
Cell Polarity ◽  
Normal Development ◽  
Control Cell ◽  
Embryonic Cells ◽  
Par Proteins ◽  
Cell Contacts ◽  
C Elegans ◽  
Muscle Myosin

Gastrulation in C. elegans embryos involves formation of a blastocoel and the ingression of surface cells into the blastocoel. Mutations in the par-3 gene cause abnormal separations between embryonic cells, suggesting that the PAR-3 protein has a role in blastocoel formation. In normal development, PAR proteins localize to either the apical or basal surfaces of cells prior to blastocoel formation; we demonstrate that this localization is determined by cell contacts. Cells that ingress into the blastocoel undergo an apical flattening associated with an apical concentration of non-muscle myosin. We provide evidence that ingression times are determined by genes that control cell fate, though interactions with neighboring cells can prevent ingression.

TLP-1 is an asymmetric cell fate determinant that responds to Wnt signals and controls male tail tip morphogenesis in C. elegans

Development ◽  
2002 ◽  
Vol 129 (6) ◽  
pp. 1497-1508 ◽  
Author(s):  
Xiaojun Zhao ◽  
Ying Yang ◽  
David H. A. Fitch ◽  
Michael A. Herman
Keyword(s):  
T Cell ◽  
Cell Fate ◽  
Cell Polarity ◽  
Zinc Finger Protein ◽  
Control Cell ◽  
Nematode Species ◽  
Cell Fates ◽  
Male Tail ◽  
C Elegans ◽  
Tail Tip

We have isolated mutations defining a new gene, tlp-1, that affect asymmetric cell fates and morphogenesis during the development of the C. elegans tail. tlp-1 mutations cause defects in the specification of asymmetric cell fates in the descendants of the T blast cell, whose polarity is controlled by Wnt signaling and cause abnormal male tail development leading to the formation of a posterior protrusion reminiscent of ‘leptoderan’, or pointy tailed, nematode species. In wild-type C. elegans males, which have a ‘peloderan’ or rounded tail, retraction of the tail tip hypodermis involves a temporally ordered set of cell fusions and changes in cell shape that appear to be heterochronically delayed in tlp-1 males, suggesting that subtle changes in these events can bring about evolutionary changes in morphology. tlp-1 encodes a C2H2 zinc-finger protein that is a member of the Sp family of transcription factors. A TLP-1::GFP fusion protein is expressed in the nuclei of many cells during early embryogenesis and then becomes restricted primarily to posterior cells. At hatching, it is expressed in several head neurons, the posterior intestine cells, tail hypodermal cells, the T cells and specific T-cell descendents in a pattern that suggests TLP-1 may be asymmetrically expressed during the divisions of the T cell lineage. Furthermore, the asymmetry of TLP-1 expression and function appears to be controlled by Wnt signals that control T cell polarity. These results suggest that tlp-1 encodes a transcription factor required for cellular asymmetry that functions downstream of Wnt signals that control cell polarity, as well as in cell fusion and patterning in the C. elegans tail.

scholarly journals Classical cadherins control nucleus and centrosome position and cell polarity

2009 ◽  
Vol 185 (5) ◽  
pp. 779-786 ◽  
Author(s):  
Isabelle Dupin ◽  
Emeline Camand ◽  
Sandrine Etienne-Manneville
Keyword(s):  
Cell Polarity ◽  
Control Cell ◽  
Cell Types ◽  
Free Cell ◽  
Cell Polarization ◽  
Cell Interactions ◽  
Spatial Cues ◽  
Cell Contacts ◽  
Classical Cadherins ◽  
Cell Cell

Control of cell polarity is crucial during tissue morphogenesis and renewal, and depends on spatial cues provided by the extracellular environment. Using micropatterned substrates to impose reproducible cell–cell interactions, we show that in the absence of other polarizing cues, cell–cell contacts are the main regulator of nucleus and centrosome positioning, and intracellular polarized organization. In a variety of cell types, including astrocytes, epithelial cells, and endothelial cells, calcium-dependent cadherin-mediated cell–cell interactions induce nucleus and centrosome off-centering toward cell–cell contacts, and promote orientation of the nucleus–centrosome axis toward free cell edges. Nucleus and centrosome off-centering is controlled by N-cadherin through the regulation of cell interactions with the extracellular matrix, whereas the orientation of the nucleus–centrosome axis is determined by the geometry of N-cadherin–mediated contacts. Our results demonstrate that in addition to the specific function of E-cadherin in regulating baso-apical epithelial polarity, classical cadherins control cell polarization in otherwise nonpolarized cells.

scholarly journals RhoGAP RGA-8 supports morphogenesis in C. elegans by polarizing epithelia through CDC-42

2019 ◽  
Author(s):  
Hamidah Raduwan ◽  
Shashikala Sasidharan ◽  
Luigy Cordova Burgos ◽  
Andre G. Wallace ◽  
Martha C. Soto
Keyword(s):  
Cell Shape ◽  
Control Cell ◽  
Molecular Data ◽  
Regulatory Motifs ◽  
C Elegans ◽  
Cell Embryo ◽  
Embryonic Morphogenesis ◽  
The One ◽  
Muscle Myosin ◽  
Shape Changes

AbstractCDC-42 regulation of non-muscle myosin/NMY-2 is required for polarity maintenance in the one-cell embryo of C. elegans. CDC-42 and NMY-2 regulate polarity throughout embryogenesis, but their contribution to later events of morphogenesis are less understood. We have shown that epidermal enclosure requires the GTPase CED-10/Rac1 and WAVE/Scar complex, its effector, to promote protrusions that drive enclosure through the branch actin regulator Arp2/3. Our analysis here of RGA-8, a homolog of SH3BP1/Rich1/ARHGAP17/Nadrin, with BAR and RhoGAP motifs, suggests it regulates CDC-42, so that NMY-2 promotes two events of epidermal morphogenesis: ventral enclosure and elongation. Genetic and molecular data suggest RGA-8 regulates CDC-42, and the CDC-42 effectors WSP-1 and MRCK-1, in parallel to F-BAR proteins TOCA-1 and TOCA-2. The RGA-8-CDC-42-WSP-1 pathway enriches myosin in migrating epidermal cells during ventral enclosure. We propose TOCA proteins and RGA-8 use BAR domains to localize and regenerate CDC-42 activity, thus regulating F-actin levels, through the branched actin regulator WSP-1, and myosin polarity through the myosin kinase MRCK-1. Regulated CDC-42 thus polarizes epithelia, to control cell migrations and cell shape changes of embryonic morphogenesis.SummaryRGA-8, a protein with membrane binding and actin regulatory motifs, promotes embryonic morphogenesis by localizing active CDC-42 in developing epithelia, thus controlling actin and actin motors during cell movements.

scholarly journals Biology of the Caenorhabditis elegans Germline Stem Cell System

Genetics ◽  
2019 ◽  
Vol 213 (4) ◽  
pp. 1145-1188 ◽  
Author(s):  
E. Jane Albert Hubbard ◽  
Tim Schedl
Keyword(s):  
Stem Cell ◽  
Caenorhabditis Elegans ◽  
Cell Fate ◽  
Control Cell ◽  
Cell System ◽  
Germline Stem Cell ◽  
Cell Systems ◽  
Stem Cell Fate ◽  
C Elegans ◽  
Stem Cell System

Stem cell systems regulate tissue development and maintenance. The germline stem cell system is essential for animal reproduction, controlling both the timing and number of progeny through its influence on gamete production. In this review, we first draw general comparisons to stem cell systems in other organisms, and then present our current understanding of the germline stem cell system in Caenorhabditis elegans. In contrast to stereotypic somatic development and cell number stasis of adult somatic cells in C. elegans, the germline stem cell system has a variable division pattern, and the system differs between larval development, early adult peak reproduction and age-related decline. We discuss the cell and developmental biology of the stem cell system and the Notch regulated genetic network that controls the key decision between the stem cell fate and meiotic development, as it occurs under optimal laboratory conditions in adult and larval stages. We then discuss alterations of the stem cell system in response to environmental perturbations and aging. A recurring distinction is between processes that control stem cell fate and those that control cell cycle regulation. C. elegans is a powerful model for understanding germline stem cells and stem cell biology.

The maternal par genes and the segregation of cell fate specification activities in early Caenorhabditis elegans embryos

Development ◽  
1997 ◽  
Vol 124 (19) ◽  
pp. 3815-3826 ◽  
Author(s):  
B. Bowerman ◽  
M.K. Ingram ◽  
C.P. Hunter
Keyword(s):  
Cell Fate ◽  
Expression Patterns ◽  
Control Cell ◽  
Gene Products ◽  
Cell Fate Specification ◽  
Loss Of Function ◽  
C Elegans ◽  
Embryonic Polarity ◽  
Early Embryos ◽  
Anterior Posterior

After fertilization in C. elegans, activities encoded by the maternally expressed par genes appear to establish cellular and embryonic polarity. Loss-of-function mutations in the par genes disrupt anterior-posterior (a-p) asymmetries in early embryos and result in highly abnormal patterns of cell fate. Little is known about how the early asymmetry defects are related to the cell fate patterning defects in par mutant embryos, or about how the par gene products affect the localization and activities of developmental regulators known to specify the cell fate patterns made by individual blastomeres. Examples of such regulators of blastomere identity include the maternal proteins MEX-3 and GLP-1, expressed at high levels anteriorly, and SKN-1 and PAL-1, expressed at high levels posteriorly in early embryos. To better define par gene functions, we examined the expression patterns of MEX-3, PAL-1 and SKN-1, and we analyzed mex-3, pal-1, skn-1 and glp-1 activities in par mutant embryos. We have found that mutational inactivation of each par gene results in a unique phenotype, but in no case do we observe a complete loss of a-p asymmetry. We conclude that no one par gene is required for all a-p asymmetry and we suggest that, in some cases, the par genes act independently of each other to control cell fate patterning and polarity. Finally, we discuss the implications of our findings for understanding how the initial establishment of polarity in the zygote by the par gene products leads to the proper localization of more specifically acting regulators of blastomere identity.

scholarly journals PLK-1 Regulation of Asymmetric Cell Division in the Early C. elegans Embryo

2021 ◽  
Vol 8 ◽  
Author(s):  
Amelia J. Kim ◽  
Erik E. Griffin
Keyword(s):  
Cell Division ◽  
Cell Fate ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Asymmetric Cell Division ◽  
Critical Role ◽  
Cell Cortex ◽  
C Elegans ◽  
Mitotic Kinase ◽  
Centrosome Separation

PLK1 is a conserved mitotic kinase that is essential for the entry into and progression through mitosis. In addition to its canonical mitotic functions, recent studies have characterized a critical role for PLK-1 in regulating the polarization and asymmetric division of the one-cell C. elegans embryo. Prior to cell division, PLK-1 regulates both the polarization of the PAR proteins at the cell cortex and the segregation of cell fate determinants in the cytoplasm. Following cell division, PLK-1 is preferentially inherited to one daughter cell where it acts to regulate the timing of centrosome separation and cell division. PLK1 also regulates cell polarity in asymmetrically dividing Drosophila neuroblasts and during mammalian planar cell polarity, suggesting it may act broadly to connect cell polarity and cell cycle mechanisms.

The expression of the C. elegans labial-like Hox gene ceh-13 during early embryogenesis relies on cell fate and on anteroposterior cell polarity

Development ◽  
1997 ◽  
Vol 124 (21) ◽  
pp. 4193-4200 ◽  
Author(s):  
C. Wittmann ◽  
O. Bossinger ◽  
B. Goldstein ◽  
M. Fleischmann ◽  
R. Kohler ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cell Polarity ◽  
Hox Genes ◽  
Positional Information ◽  
Precursor Cell ◽  
Body Parts ◽  
Hox Gene ◽  
C Elegans ◽  
Fate Determinants ◽  
Cell Fate Determinants

Clusters of homeobox-containing HOM-C/hox genes determine the morphology of animal body plans and body parts and are thought to mediate positional information. Here, we describe the onset of embryonic expression of ceh-13, the Caenorhabditis elegans orthologue of the Drosophila labial gene, which is the earliest gene of the C. elegans Hox gene cluster to be activated in C. elegans development. At the beginning of gastrulation, ceh-13 is asymmetrically expressed in posterior daughters of anteroposterior divisions, first in the posterior daughter of the intestinal precursor cell E and then in all posterior daughters of the AB descendants ABxxx. In this paper, we present evidence that supports position-independent activation of ceh-13 during early C. elegans embryogenesis, which integrates cell fate determinants and cell polarity cues. Our findings imply that mechanisms other than cell-extrinsic anteroposterior positional signals play an important role in the activation and regulation of the C. elegans Hox gene ceh-13.

The Caenorhabditis elegans polarity gene ooc-5 encodes a Torsin-related protein of the AAA ATPase superfamily

Development ◽  
2001 ◽  
Vol 128 (22) ◽  
pp. 4645-4656 ◽  
Author(s):  
Stephen E. Basham ◽  
Lesilee S. Rose
Keyword(s):  
Cell Fate ◽  
Protein Complexes ◽  
Sequence Similarity ◽  
Normal Function ◽  
Par Proteins ◽  
Torsion Dystonia ◽  
Aaa Atpase ◽  
C Elegans ◽  
Fate Determinants ◽  
Cell Fate Determinants

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.

scholarly journals A C. elegans patched gene, ptc-1, functions in germ-line cytokinesis

2000 ◽  
Vol 14 (15) ◽  
pp. 1933-1944
Author(s):  
Patricia E. Kuwabara ◽  
Min-Ho Lee ◽  
Tim Schedl ◽  
Gregory S.X.E. Jefferis
Keyword(s):  
Membrane Proteins ◽  
Cell Fate ◽  
Germ Line ◽  
Essential Gene ◽  
Control Cell ◽  
Large Family ◽  
Detectable Effect ◽  
C Elegans ◽  
Downstream Effectors ◽  
Body Patterning

Patched (Ptc), initially identified in Drosophila, defines a class of multipass membrane proteins that control cell fate and cell proliferation. Biochemical studies in vertebrates indicate that the membrane proteins Ptc and Smoothened (Smo) form a receptor complex that binds Hedgehog (Hh) morphogens. Smo transduces the Hh signal to downstream effectors. The Caenorhabditis elegans genome encodes two Ptc homologs and one related pseudogene but does not encode obvious Hh or Smo homologs. We have analyzed ptc-1 by RNAi and mutational deletion and find that it is an essential gene, although the absence of ptc-1 has no detectable effect on body patterning or proliferation. Therefore, the C. elegans ptc-1 gene is functional despite the lack of Hh and Smo homologs. We find that the activity and expression of ptc-1 is essentially confined to the germ line and its progenitors. ptc-1 null mutants are sterile with multinucleate germ cells arising from a probable cytokinesis defect. We have also identified a surprisingly large family of PTC-related proteins containing sterol-sensing domains, including homologs of Drosophila dispatched, in C. elegans and other phyla. These results suggest that the PTC superfamily has multiple functions in animal development.

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