Endomesoderm specification in <i>Caenorhabditis elegans</i> and other nematodes

Maduro, Morris

doi:10.1002/bies.20480

Cited by 44 publications

(39 citation statements)

References 104 publications

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“…This conserved mechanism has been reported across the animal kingdom, including in ecdysozoans (Maduro, 2006;Sulston et al, 1983), lophotrochozoans (Gillis et al, 2007), echinoderms (Logan et al, 1999), urochordates (Nishida and Satoh, 1985), and vertebrates (Fukuda and Kikuchi, 2005;Kimelman and Griffin, 2000). In C. elegans, for example, the endomesoderm tissue arises at the fourcell stage and segregates into endoderm and mesoderm with the next cell division, mainly through the asymmetric activity of a Wnt/MAPK pathway (Maduro, 2006;Sulston et al, 1983).…”

Section: Introductionmentioning

confidence: 81%

Dynamics of Delta/Notch signaling on endomesoderm segregation in the sea urchin embryo

Croce

McClay

2010

Development

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SUMMARYEndomesoderm is the common progenitor of endoderm and mesoderm early in the development of many animals. In the sea urchin embryo, the Delta/Notch pathway is necessary for the diversification of this tissue, as are two early transcription factors, Gcm and FoxA, which are expressed in mesoderm and endoderm, respectively. Here, we provide a detailed lineage analysis of the cleavages leading to endomesoderm segregation, and examine the expression patterns and the regulatory relationships of three known regulators of this cell fate dichotomy in the context of the lineages. We observed that endomesoderm segregation first occurs at hatched blastula stage. Prior to this stage, Gcm and FoxA are co-expressed in the same cells, whereas at hatching these genes are detected in two distinct cell populations. Gcm remains expressed in the most vegetal endomesoderm descendant cells, while FoxA is downregulated in those cells and activated in the above neighboring cells. Initially, Delta is expressed exclusively in the micromeres, where it is necessary for the most vegetal endomesoderm cell descendants to express Gcm and become mesoderm. Our experiments show a requirement for a continuous Delta input for more than two cleavages (or about 2.5 hours) before Gcm expression continues in those cells independently of further Delta input. Thus, this study provides new insights into the timing mechanisms and the molecular dynamics of endomesoderm segregation during sea urchin embryogenesis and into the mode of action of the Delta/Notch pathway in mediating mesoderm fate.

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Section: Introductionmentioning

confidence: 81%

Dynamics of Delta/Notch signaling on endomesoderm segregation in the sea urchin embryo

Croce

McClay

2010

Development

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“…A pathway involving Wnt signaling promotes the expression of two GATA transcription factors END-1/END-3 that induce gut cell fate and gut granule formation (Maduro 2006). These transcription factors promote the expression of genes at the E 2 stage, precisely when glo-3 expression initiates (Figure 6), suggesting that glo-3 may be a direct transcriptional target of END-1/END-3.…”

Section: ) Had Similar Localizations and Morphologies Inmentioning

confidence: 99%

glo-3, a Novel Caenorhabditis elegans Gene, Is Required for Lysosome-Related Organelle Biogenesis

Rabbitts¹,

Ciotti

Miller

et al. 2008

Genetics

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Gut granules are specialized lysosome-related organelles that act as sites of fat storage in Caenorhabditis elegans intestinal cells. We identified mutations in a gene, glo-3, that functions in the formation of embryonic gut granules. Some glo-3(À) alleles displayed a complete loss of embryonic gut granules, while other glo-3(À) alleles had reduced numbers of gut granules. A subset of glo-3 alleles led to mislocalization of gut granule contents into the intestinal lumen, consistent with a defect in intracellular trafficking. glo-3(À) embryos lacking gut granules developed into adults containing gut granules, indicating that glo-3(1) function may be differentially required during development. We find that glo-3(1) acts in parallel with or downstream of the AP-3 complex and the PGP-2 ABC transporter in gut granule biogenesis. glo-3 encodes a predicted membrane-associated protein that lacks obvious sequence homologs outside of nematodes. glo-3 expression initiates in embryonic intestinal precursors and persists almost exclusively in intestinal cells through adulthood. GLO-3TGFP localizes to the gut granule membrane, suggesting it could play a direct role in the trafficking events at the gut granule. smg-1(À) suppression of glo-3(À) nonsense alleles indicates that the C-terminal half of GLO-3, predicted to be present in the cytoplasm, is not necessary for gut granule formation. Our studies identify GLO-3 as a novel player in the formation of lysosome-related organelles.

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“…Cell fate specification and gastrulation are often coordinated by the same transcription factors, which regulate both cell-identity genes and genes that control gastrulation movements. For example, the C. elegans endodermal precursor E is specified through the combined action of GATA transcription factors END-1 and END-3 (Maduro, 2006). The daughters of E (Ea and Ep) initiate gastrulation when they constrict their apical surfaces and ingress into the interior of the embryo (Nance and Priess, 2002;Lee and Goldstein, 2003).…”

Section: Introductionmentioning

confidence: 99%

An E-cadherin-mediated hitchhiking mechanism forC. elegansgerm cell internalization during gastrulation

Chihara

Nance

2012

Development

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SUMMARYGastrulation movements place endodermal precursors, mesodermal precursors and primordial germ cells (PGCs) into the interior of the embryo. Somatic cell gastrulation movements are regulated by transcription factors that also control cell fate, coupling cell identity and position. By contrast, PGCs in many species are transcriptionally quiescent, suggesting that they might use alternative gastrulation strategies. Here, we show that C. elegans PGCs internalize by attaching to internal endodermal cells, which undergo morphogenetic movements that pull the PGCs into the embryo. We show that PGCs enrich HMR-1/E-cadherin at their surfaces to stick to endoderm. HMR-1 expression in PGCs is necessary and sufficient to ensure internalization, suggesting that HMR-1 can promote PGC-endoderm adhesion through a mechanism other than homotypic trans interactions between the two cell groups. Finally, we demonstrate that the hmr-1 3Ј untranslated region promotes increased HMR-1 translation in PGCs. Our findings reveal that quiescent PGCs employ a post-transcriptionally regulated hitchhiking mechanism to internalize during gastrulation, and demonstrate a morphogenetic role for the conserved association of PGCs with the endoderm.

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Endomesoderm specification in Caenorhabditis elegans and other nematodes

Cited by 44 publications

References 104 publications

Dynamics of Delta/Notch signaling on endomesoderm segregation in the sea urchin embryo

Dynamics of Delta/Notch signaling on endomesoderm segregation in the sea urchin embryo

glo-3, a Novel Caenorhabditis elegans Gene, Is Required for Lysosome-Related Organelle Biogenesis

An E-cadherin-mediated hitchhiking mechanism forC. elegansgerm cell internalization during gastrulation

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