SMA-3 Smad has specific and critical functions in DBL-1/SMA-6 TGFβ- related signaling

Cathy Savage-Dunn, Rafal Tokarz, Huang Wang, Stephen Cohen, Christina Giannikas, Richard W. Padgett

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

A TGFβ signal transduction cascade controls body size and male tail morphogenesis in the nematode Caenorhabditis elegans. We have analyzed the function of the sma-3 Smad gene, one of three Smad genes that function in this pathway. Null mutations in sma-3 are at least as severe as null mutations in the ligand and type I receptor genes, dbl-1 and sma-6, indicating that the other Smads do not function in the absence of SMA-3. Furthermore, null mutations in sma-3 do not cause defects in egg laying or in regulation of the developmentally arrested dauer larva stage, indicating no overlapping function with another C. elegans TGFβ signaling pathway. The sma-3 gene is widely expressed at all developmental stages in hermaphrodites and males. The molecular lesions associated with eight sma-3 alleles of varying severity have been determined. The missense mutations cluster in two previously identified regions important for Smad function. (C) 2000 Academic Press.

Original languageEnglish (US)
Pages (from-to)70-76
Number of pages7
JournalDevelopmental Biology
Volume223
Issue number1
DOIs
StatePublished - Jul 1 2000

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

Keywords

  • BMP
  • Caenorhabditis elegans
  • Cell size
  • Pattern formation
  • Smad
  • TGFβ

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