High impact information on elt-2

• Moreover, we show that pha-4 expression in the C. elegans gut is regulated by elt-2, a C. elegans gut-specific GATA-factor and possible homolog of the Drosophila gene serpent, which influences fork head expression in the fly gut [1].
• Likewise, mtl-2 is not expressed in nematodes in which elt-2 has been disrupted [2].
• However, there is as yet no direct evidence that elt-2 does or does not control ges-1 [3].
• The longest open reading frame in the elt-2 cDNA codes for a protein of M(r) 47,000 with a single zinc finger domain, similar (approximately 75% amino acid identity) to the C-terminal fingers of all other two-fingered GATA factors isolated to date [3].
• The elt-2 gene is expressed as an SL1 trans-spliced message, which can be detected at all stages of development except oocytes; however, elt-2 message levels are 5-10-fold higher in embryos than in other stages [3].

Biological context of elt-2

• Although the loss of elt-2 function has major consequences for later gut morphogenesis and function, mutant embryos still express ges-1 [4].
• In the present paper, we show that elt-2 expression is completely gut specific, beginning when the embryonic gut has only two cells (one cell cycle prior to ges-1 expression) and continuing in every cell of the gut throughout the life of the worm [4].
• When elt-2 is expressed ectopically using a transgenic heat-shock construct, the endogenous ges-1 gene is now expressed in most if not all cells of the embryo; several other gut markers (including a transgenic elt-2-promoter::lacZ reporter construct designed to test for elt-2 autoregulation) are also expressed ectopically in the same experiment [4].

Anatomical context of elt-2

• We have identified and characterised a homologue of the C. elegans GATA transcription factor elt-2, a central regulator of endoderm development, from the parasitic nematode Haemonchus contortus [5].

Regulatory relationships of elt-2

• Ectopic expression of elt-4 cDNA within the embryo does not cause detectable ectopic expression of biochemical markers of gut differentiation; furthermore, ectopic elt-4 expression neither inhibits nor enhances the ectopic marker expression caused by ectopic elt-2 expression [6].

Other interactions of elt-2

• We found no evidence that elt-4 provided backup functions for elt-2 [6].

Analytical, diagnostic and therapeutic context of elt-2

• Electrophoretic mobility shift assays show that the C. elegans GATA transcription factor ELT-2 specifically binds to these elements [2].

References