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The T-box factor MLS-1 acts as a molecular switch during specification of nonstriated muscle in C. elegans
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...
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Published in: | Genes & development 2002-01, Vol.16 (2), p.257-269 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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. |
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ISSN: | 0890-9369 1549-5477 |
DOI: | 10.1101/gad.923102 |