期刊
GENES & DEVELOPMENT
卷 16, 期 2, 页码 257-269出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.923102
关键词
muscle; myogenesis; T-box; asymmetric cell division; Twist; C. elegans
资金
- NIGMS NIH HHS [R01 GM 37706, T32 GM007231, R01 GM037706, T32 GM 07231] Funding Source: Medline
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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