<i>end-1</i> encodes an apparent GATA factor that specifies the endoderm precursor in <i>Caenorhabditis elegans</i> embryos

Zhu, Jiangwen; Hill, Russell J.; Heid, Paul J.; Fukuyama, Masamitsu; Sugimoto, Akihiro; Priess, James R; Rothman, Joel H.

doi:10.1101/gad.11.21.2883

Cited by 207 publications

(211 citation statements)

References 65 publications

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“…Related GATA-binding proteins may also influence endoderm differentiation, based on studies in mouse 19 and lower organisms such as Drosophila and C. elegans. 21 It is tempting to speculate that GATA-binding proteins may have a role in the maintenance of the malignant phenotype in YSTs. It is of interest that recent data have linked GATAbinding proteins with antiapoptotic processes, which often operate in malignant cells.…”

Section: Discussionmentioning

confidence: 99%

Transcription Factor GATA-4 Is Expressed in Pediatric Yolk Sac Tumors

Siltanen

Anttonen

Heikkilä

et al. 1999

The American Journal of Pathology

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Pediatric yolk sac tumors (YSTs) are rare, highly malignant tumors occurring in the gonads of children and young adults, and at extragonadal sites in young children. 1 These tumors are also termed endodermal sinus tumors because of their resemblance to the endoderm sinus of the rodent placenta. 2 Indeed the morphological appearance of these neoplasms recapitulates the structure of the mammalian yolk sac. Pure YSTs exhibit a labyrinthine histology with papillary processes and endoderm-lined cavities, termed Schiller-Duval bodies, supported by a loose stroma.

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Section: Discussionmentioning

confidence: 99%

Transcription Factor GATA-4 Is Expressed in Pediatric Yolk Sac Tumors

Siltanen

Anttonen

Heikkilä

et al. 1999

The American Journal of Pathology

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“…[53][54][55][56][57][58][59][60] In mammals, genetic evidence that definitively demonstrates a requirement for FoxA and GATA factors in controlling competency of the endoderm to adopt a hepatic fate has been difficult to produce. This is due either to functional redundancy between individual FoxA and GATA factor proteins or an essential role for some of these factors prior to the onset of hepatic development.…”

Section: From Where Do Hepatic Cells Arise?mentioning

confidence: 99%

Embryonic development of the liver†

2005

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“…The med genes are proposed to specify both the C. elegans endoderm and that portion of the C. elegans mesoderm deriving from the MS blastomere ( Figure 1). To specify the endoderm, the MED-1 and MED-2 factors are proposed to directly activate the zygotic expression of a redundant pair of genes called end-1 and end-3, which also encode GATAtype factors (Zhu et al 1997(Zhu et al , 1998Maduro et al 2001;Maduro and Rothman 2002;Broitman-Maduro et al 2005). This endoderm specification step takes place in the E cell, the clonal progenitor of the intestine, within a permissive environment associated with lowered nuclear levels of the HMG protein POP-1 (Lin et al 1995(Lin et al , 1998Rocheleau et al 1997;Thorpe et al 1997;Lo et al 2004).…”

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confidence: 99%

Reevaluation of the Role of the med-1 and med-2 Genes in Specifying the Caenorhabditis elegans Endoderm

Goszczynski

McGhee

2005

Genetics

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The med-1 and med-2 genes encode a pair of essentially identical GATA factor-related transcription factors that have been proposed to be necessary for specification of the C. elegans endoderm (intestine or E lineage) as well as part of the C. elegans mesoderm. med-1 and med-2 are proposed to be the direct downstream targets and the principal effectors of the maternally provided SKN-1 transcription factor; med-1 and med-2 would thus occupy the pivotal interface between maternal and zygotic control of gene expression. The conclusion that med-1 and med-2 are necessary for C. elegans endoderm specification was based on a partially penetrant (50%) loss of endoderm markers produced by RNA-mediated interference (RNAi). To determine whether this partial penetrance reflects: (i) inefficient RNAi against early zygotic transcripts, (ii) experimental uncertainty in the expected level of endoderm loss in skn-1 nulls, or (iii) additional redundancy in the pathway of endoderm specification, we constructed worm strains that segregate embryos lacking both the med-1 gene (because of a gene-specific deletion) and the med-2 gene (using either of two chromosomal deficiencies). Contrary to expectations, we observe that only 3-20% of med-2(ÿ); med-1(ÿ) embryos do not express markers of endoderm differentiation. Furthermore, we found no evidence for a maternal contribution of the med genes to endoderm specification. We conclude that the major pathway(s) for endoderm specification in C. elegans must be independent of the med-1 and med-2 genes. T HE Caenorhabditis elegans endoderm (intestine or E lineage) is clonally derived from a single cell, the E cell, in the eight-cell embryo (Sulston et al. 1983). The early endoderm is one of the few C. elegans lineages for which a plausible specification pathway has been proposed in molecular detail, beginning with maternally provided transcription factors, progressing through several waves of zygotically produced transcription factors, and ending with gene products that function in the terminally differentiated intestine (see review by Maduro and Rothman 2002; see also Baugh et al. 2003Baugh et al. , 2005Robertson et al. 2004). Figure 1 summarizes the regulatory cascade proposed for specification of the C. elegans endoderm. The maternally provided b-ZIP-like transcription factor SKN-1 is essential for correct specification of the fate of the EMS blastomere of the four-cell embryo (Bowerman et al. 1992(Bowerman et al. , 1993. Within the EMS cell, SKN-1 is proposed to directly activate the zygotic expression of two genes called med-1 and med-2, which encode zinc-finger proteins related to GATA-type transcription factors but with atypical binding sites (Maduro et al. 2001;Maduro and Rothman 2002;Broitman-Maduro et al. 2005).These two small intronless genes are 98% identical and, for convenience, are often referred to simply as the med genes (mesendoderm-determining); they are the principal subjects of this article. The med genes are proposed to specify both the C. elegans endoderm and that p...

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end-1 encodes an apparent GATA factor that specifies the endoderm precursor in Caenorhabditis elegans embryos

Cited by 207 publications

References 65 publications

Transcription Factor GATA-4 Is Expressed in Pediatric Yolk Sac Tumors

Transcription Factor GATA-4 Is Expressed in Pediatric Yolk Sac Tumors

Embryonic development of the liver†

Reevaluation of the Role of the med-1 and med-2 Genes in Specifying the Caenorhabditis elegans Endoderm

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