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Vol. 16, No. 2, pp. 257-269, January 15, 2002
1 Department of Embryology, Carnegie Institution of
Washington, Baltimore, Maryland 21210, USA; 2 Graduate
Program in Biology, The Johns Hopkins University,
Baltimore, Maryland 21218, USA
We have isolated mutations in a gene mls-1 that is required
for proper specification of nonstriated muscle fates in
Caenorhabditis elegans. Loss of MLS-1 activity causes uterine
muscle precursors to forego their normal fates, instead differentiating
as vulval muscles. We have cloned mls-1 and shown that the
product is a member of the T-box family of transcriptional regulators.
MLS-1 acts as a cell fate determinant in that ectopic expression can transform other cell types to uterine muscle precursors. Uterine muscle
patterning is executed by regulation of MLS-1 at several different
levels. The mls-1 promoter is activated by the C. elegans orthologs of Twist and Daughterless, but is only active in
a subset of the lineage where these two transcription factors are
present. mls-1 activity also appears to be regulated by
posttranscriptional processes, as expression occurs in both uterine and
vulval muscle precursors.
[Key Words: Muscle; myogenesis; T-box; asymmetric cell division; Twist; C. elegans]
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