THE GATA-FACTOR ELT-2 IS ESSENTIAL FOR FORMATION OF THE CAENORHABDITIS-ELEGANS INTESTINE

The Caenorhabditis elegans elt-2 gene encodes a single-finger GATA fac tor, previously cloned by virtue of its binding to a tandem pair of GA TA sites that control the gut-specific ges-l esterase gene. In the pre sent paper, we show that elt-2 expression is completely gut specific, beginning when the embryonic gut has only two cells (one cell cycle pr ior to ges-l expression) and continuing in every cell of the gut throu ghout the life of the worm. When elt-2 is expressed ectopically using a transgenic heat-shock construct, the endogenous ges-l gene is now ex pressed in most if not all cells of the embryo; several other gut mark ers (including a transgenic elt-2-promoter::lacZ reporter construct de signed to test for elt-2 autoregulation) are also expressed ectopicall y in the same experiment. These effects are specific in that two other C. elegans GATA factors (elt-1 and elt-3) do not cause ectopic gut ge ne expression. An imprecise transposon excision was identified that re moves the entire elt-2 coding region. Homozygous elt-2 null mutants di e at the L1 larval stage with an apparent malformation or degeneration of gut cells. Although the loss of elt-2 function has major consequen ces for later gut morphogenesis and function, mutant embryos still exp ress ges-1. We suggest that elt-2 is part of a redundant network of ge nes that controls embryonic gut development; other factors may be able to compensate for elt-2 loss in the earlier stages of gut development but not in later stages. We discuss whether elements of this regulato ry network may be conserved in all metazoa. (C) 1998 Academic Press.