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In C. elegans, the Sma/Mab TGF
This article has been cited by other articles:
Development ePress online publication date 21 Jun 2006
doi: 10.1242/dev.02476
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133/15/2887
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Research article
An antagonistic role for the C. elegans Schnurri homolog SMA-9 in modulating TGF
signaling during mesodermal patterning
* Author for correspondence (e-mail: jl53{at}cornell.edu)
signaling pathway regulates body size and male tail patterning. SMA-9, the C. elegans homolog of Schnurri, has been shown to function as a downstream component to mediate the Sma/Mab TGF
signaling pathway in these processes. We have discovered a new role for SMA-9 in dorsoventral patterning of the C. elegans post-embryonic mesoderm, the M lineage. In addition to a small body size, sma-9 mutant animals exhibit a dorsal-to-ventral fate transformation within the M lineage. This M lineage defect of sma-9 mutants is unique in that animals carrying mutations in all other known components of the TGF
pathway exhibit no M lineage defects. Surprisingly, mutations in the core components of the Sma/Mab TGF
signaling pathway suppressed the M lineage defects of sma-9 mutants without suppressing their body size defects. We show that this suppression specifically happens within the M lineage. Our studies have uncovered an unexpected role of SMA-9 in antagonizing the TGF
signaling pathway during mesodermal patterning, suggesting a novel mode of function for the SMA-9/Schnurri family of proteins.
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N. M. Amin, K. Hu, D. Pruyne, D. Terzic, A. Bretscher, and J. Liu
A Zn-finger/FH2-domain containing protein, FOZI-1, acts redundantly with CeMyoD to specify striated body wall muscle fates in the Caenorhabditis elegans postembryonic mesoderm
Development,
January 1, 2007;
134(1):
19 - 29.
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© The Company of Biologists Ltd 2006