An antagonistic role for the C-elegans Schnurri homolog SMA-9 in modulating TGFβ signaling during mesodermal patterning

被引:39
作者
Foehr, Marisa L.
Lindy, Amanda S.
Fairbank, Rachel C.
Amin, Nirav M.
Xu, Ming
Yanowitz, Judith
Fire, Andrew Z.
Liu, Jun [1 ]
机构
[1] Cornell Univ, Dept Mol Biol & Genet, Ithaca, NY 14853 USA
[2] Carnegie Inst Sci, Dept Embryol, Baltimore, MD 21218 USA
[3] Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA
[4] Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA
来源
DEVELOPMENT | 2006年 / 133卷 / 15期
关键词
mesoderm; dorsoventral patterning; M lineage; TGF beta; SMA-9; Schnurri; Sma/Mab; dbl-1; sma-2; sma-3; sma-4; sma-6; daf-4; C; elegans;
D O I
10.1242/dev.02476
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
In C. elegans, the Sma/Mab TGF beta 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 beta 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 beta pathway exhibit no M lineage defects. Surprisingly, mutations in the core components of the Sma/Mab TGF beta 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 beta signaling pathway during mesodermal patterning, suggesting a novel mode of function for the SMA-9/Schnurri family of proteins.
引用
收藏
页码:2887 / 2896
页数:10
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