The T-box factor MLS-1 acts as a molecular switch during specification of nonstriated muscle in C. elegans (original) (raw)

  1. Stephen A. Kostas1,2 and
  2. Andrew Fire1,3
  3. 1Department of Embryology, Carnegie Institution of Washington, Baltimore, Maryland 21210, USA; 2Graduate Program in Biology, The Johns Hopkins University, Baltimore, Maryland 21218, USA

Abstract

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.

Footnotes