Cr. Egan et al., A GUT-TO-PHARYNX TAIL SWITCH IN EMBRYONIC EXPRESSION OF THE CAENORHABDITIS-ELEGANS GES-1 GENE CENTERS ON 2 GATA SEQUENCES, Developmental biology, 170(2), 1995, pp. 397-419
The Caenorhabditis elegans ges-1 gene (gut esterase No. 1) is expresse
d only in the intestinal lineage, beginning when the developing gut ha
s only four to eight cells. We analyze the sequence requirements for t
his tissue-specific gene regulation by injecting deleted/mutated const
ructs of the ges-l gene into a viable ges-l (null) strain of worms and
assaying heritably transformed embryos by esterase histochemistry. Ma
ny deletion constructs accurately reconstitute the wildtype gut-specif
ic ges-l expression. However, deletions in the neighborhood of 1100 bp
upstream of the ges-l ATG abolish ges-l expression in the developing
gut, while at the same time activating ges-l expression in cells of th
e pharynx/tail that appear to belong to the sister lineage of the gut.
Deletions of a 36-bp DNA region containing two tandem WGATAR sequence
s are sufficient to cause this gut-to-pharynx/tail switch in expressio
n pattern. Deletion of either one of the WGATAR sites or deletion of a
n adjoining downstream region directs ges-l expression only in a restr
icted set of cells of the anterior gut. The ges-1 GATA region acts lik
e a gut-specific enhancer in that: (i) it restores ges-l gut expressio
n when reinserted elsewhere into the GATA-deleted ges-1 gene; and (ii)
multiple copies direct gut expression of an hsp16-lacZ reporter gene.
The ges-l GATA-region also acts as the site of the pharynx/tail repre
ssion in that reinsertion elsewhere into the GATA-deleted ges-1 constr
uct causes repression of ges-1 in the pharynx/tail. However, multiple
copies of the GATA region are not able to repress the heat-induced exp
ression of an hsp16-lacZ reporter gene, suggesting that the pharynx/ta
il repression mechanism is specific to the ges-l environment. Finally,
mutation rather than deletion of the individual GATA sequences sugges
ts that gut activation and pharynx/tail repression may be due to separ
ate factors. We present a molecular model that summarizes these result
s. The ges-l control circuitry appears surprisingly complex for what m
ight have been expected to be the simplest possible example of a nones
sential gene expressed early in a clonal embryonic lineage. (C) 1995 A
cademic Press, Inc.