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Non‐receptor tyrosine kinase CSK‐1 controls pharyngeal muscle organization in Caenorhabditis elegans
Author(s) -
Takata Nozomu,
Itoh Bunsho,
Misaki Kazuyo,
Hirose Takashi,
Yonemura Shigenobu,
Okada Masato
Publication year - 2009
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2008.01275.x
Subject(s) - biology , caenorhabditis elegans , receptor tyrosine kinase , tyrosine kinase , ror1 , microbiology and biotechnology , receptor , kinase , genetics , signal transduction , gene , platelet derived growth factor receptor , growth factor
C‐terminal Src kinase (Csk) is a non‐receptor type of tyrosine kinase, and serves as an essential negative regulator of Src family tyrosine kinases (SFKs) in vertebrates. However, analyses of Csk and SFKs from primitive animals suggest that the Csk‐mediated mechanisms regulating SFK activity might diverge between evolutional branches, different tissues or SFK family members. We examined in vivo roles of CSK‐1, a Caenorhabditis elegans orthologue of Csk, by generating animals lacking csk‐1 function. Although some csk‐1 mutants died during embryogenesis, the majority of mutants died during the first stage of larval development. In csk‐1 mutants, the function of pharyngeal muscles, the major site of CSK‐1 expression, was severely damaged. The pumping of pharyngeal grinder cells became arrhythmic, causing disabled feeding. Electron microscopy showed that pharyngeal muscle filaments were disorientated in the csk‐1 mutants. These indicate that CSK‐1 is crucial for proper organization of pharyngeal muscles. However, the growth arrest phenotype in csk‐1 mutants could not be suppressed by src‐1 and/or src‐2 mutation, and SRC‐1 was not significantly activated in the csk‐1 mutants. These results suggest that CSK‐1 has an essential function in organization of pharyngeal muscle filaments that does not require C. elegans SFKs.