TheC. elegansHand gene controls embryogenesis and early gonadogenesis

Abstract

The C. elegans genome encodes a single Hand bHLH transcription factor. Either hnd-1(RNAi) or a hnd-1 deletion causes partially penetrant defects in viability and gonadogenesis. Dead embryos and young larvae are often misshapen at the posterior end. Our primary focus has been the role of hnd-1 in gonadogenesis. Wild-type C. elegans has two somatic gonadal precursors and two primordial germ cells in stereotyped positions within its four-celled gonadal primordium. The hnd-1 gene affects the presence and position of both the somatic gonadal precursors and primordial germ cells within the primordium, but does not appear to have any role in later gonadogenesis. hnd-1 probably acts within the somatic gonadal precursors or their mesodermal predecessors; defects in primordial germ cells and germ line appear to be secondary. In hnd-1 mutants, somatic gonadal precursors are generated normally, but are not maintained properly and sometimes die. A similar role in controlling the maintenance of precursor fates has been described for other genes governing early organogenesis, including the zebrafish Hand gene hands off. We also report the discovery of two genes, ehn-1 and ehn-3, that have overlapping functions with hnd-1 in embryogenesis and gonadogenesis.

Defining the transcriptional redundancy of early bodywall muscle development in C. elegans: evidence for a unified theory of animal muscle development

“…Interestingly, a synthetic lethal analysis using RNA interference (RNAi) and available mutants identified unc-120 interactions with both hlh-1 and hnd-1, suggesting these three factors might define a "muscle module" (Baugh et al 2005b). However, bodywall muscle development was not assayed in this study, and genetic studies failed to find interactions between hlh-1 and hnd-1 mutants affecting bodywall myogenesis (Mathies et al 2003). This suggested that the synthetic lethality observed between hlh-1 and hnd-1 in the RNAi screen may be due, in part or in whole, to defects in nonmuscle lineages.…”

“…Previous studies of hnd-1 have described its expression and mutant phenotypes (Mathies et al 2003). Reporter gene studies showed a very dynamic pattern of hnd-1 expression in early embryos, including transient expression in most, if not all, bodywall muscle lineages.…”

“…For hnd-1, a deletion null allele had been previously characterized (Mathies et al 2003). Genetically defined nulls (all point mutants) have also been previously characterized for hlh-1 (Chen et al 1992.…”

“…In vertebrates, the HAND factors are best known for their role in cardiac ventricle development Srivastava et al 1995), although studies also demonstrate more widespread functions in embryonic and extraembryonic tissue development (for review, see Firulli 2003). In C. elegans, the hnd-1 gene was first identified as a regulator of somatic gonad precursor (SGP) cell development (Mathies et al 2003). Interestingly, reporter gene studies suggested that hnd-1 was also expressed in early embryonic blastomeres, including those that exclusively give rise to bodywall muscle cells.…”

A “FLP-Out” System for Controlled Gene Expression in Caenorhabditis elegans

“…Using KpnI and XbaI, the FLP recombinase cDNA fragment was excised from pGC92 and ligated to KpnI/NheI-digested pPD118.26 or pPD118.28 (A. Fire, S. Xu, J. Fleenor, J. Ahnn and G. Seydoux, personal communication; http lag-2-promoter driven FLP recombinase plasmid pGC158 [P lag-2 T FLPTlet-858(39)]: We created a lag-2-driven FLP, pGC158, by replacing GFPTunc-54(39) from pJK590 (Blelloch et al 1999;Mathies et al 2003) between XmaI and ApaI with the FLPTlet-858(39) fragment cut from pGC94 with the same restriction enzymes.…”