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First published online 21 June 2006
doi: 10.1242/dev.02476

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

¹ Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.
² Department of Embryology, Carnegie Institution of Washington, 3520 San Martin Drive, Baltimore, MD 21218, USA.
³ Departments of Pathology and Genetics, Stanford University School of Medicine, 300 Pasteur Drive-L235, Stanford, CA 94305, USA.

^* Author for correspondence (e-mail: jl53{at}cornell.edu)

Accepted 31 May 2006

In C. elegans, the Sma/Mab TGFß 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 TGFß 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 TGFß pathway exhibit no M lineage defects. Surprisingly, mutations in the core components of the Sma/Mab TGFß 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 TGFß signaling pathway during mesodermal patterning, suggesting a novel mode of function for the SMA-9/Schnurri family of proteins.

Key words: Mesoderm, Dorsoventral patterning, M lineage, TGFß, SMA-9, Schnurri, Sma/Mab, dbl-1, sma-2, sma-3, sma-4, sma-6, daf-4, C. elegans

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