T. Fukushige et al., THE GATA-FACTOR ELT-2 IS ESSENTIAL FOR FORMATION OF THE CAENORHABDITIS-ELEGANS INTESTINE, Developmental biology (Print), 198(2), 1998, pp. 286-302
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.