spacer gif spacer gif spacer gif spacer gif ARCHIVE ANNOUNCEMENT! spacer gif
 QUICK SEARCH:   [advanced]


spacer gif
     Home     Help     Feedback     Subscriptions     Archive     Search    

The fully linked HTML version of this article has now been published.
Development ePress online publication date 21 Jun 2006
doi: 10.1242/dev.02476


This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
dev.02476v1
133/15/2887    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Foehr, M. L.
Right arrow Articles by Liu, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Foehr, M. L.
Right arrow Articles by Liu, J.

Research article

An antagonistic role for the C. elegans Schnurri homolog SMA-9 in modulating TGF{beta} signaling during mesodermal patterning


Marisa L. Foehr, Amanda S. Lindy, Rachel C. Fairbank, Nirav M. Amin, Ming Xu, Judith Yanowitz, Andrew Z. Fire, and Jun Liu*
* Author for correspondence (e-mail: jl53{at}cornell.edu)

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.




This article has been cited by other articles:


Home page
DevelopmentHome page
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.
[Abstract] [Full Text] [PDF]




© The Company of Biologists Ltd 2006