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Genetic screen for small body size mutants in C. elegans reveals many TGFβ pathway components
Author(s) -
SavageDunn Cathy,
Maduzia Lisa L.,
Zimmerman Cole M.,
Roberts Andrew F.,
Cohen Stephen,
Tokarz Rafal,
Padgett Richard W.
Publication year - 2003
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/gene.10184
Subject(s) - biology , caenorhabditis elegans , sma* , genetic screen , genetics , phenotype , gene , mutant , microbiology and biotechnology , signal transduction , morphogenesis , activin receptor , complementation , mathematics , combinatorics
Abstract In the nematode Caenorhabditis elegans , a TGFβ‐related signaling pathway regulates body size and male tail morphogenesis. We sought to identify genes encoding components or modifiers of this pathway in a large‐scale genetic screen. Remarkably, this screen was able to identify essentially all core components of the TGFβ signaling pathway. Among 34 Small mutants, many mutations disrupt genes encoding recognizable components of the TGFβ pathway: DBL‐1 ligand, DAF‐4 type II receptor, SMA‐6 type I receptor, and SMA‐2, SMA‐3, and SMA‐4 Smads. Moreover, we find that at least 11 additional complementation groups can mutate to the Small phenotype. Four of these 11 genes, sma ‐9, sma ‐14, sma ‐16, and sma ‐20 affect male tail morphogenesis as well as body size. Two genes, sma ‐11 and sma ‐20, also influence regulation of the developmentally arrested dauer larval stage, suggesting a role in a second characterized TGFβ pathway in C. elegans . Other genes may represent tissue‐specific factors or parallel pathways for body size control. Because of the conservation of TGFβ signaling pathways, homologs of these genes may be involved in tissue specificity and/or crosstalk of TGFβ pathways in other animals. genesis 35:239–247, 2003. © 2003 Wiley‐Liss, Inc.