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Distinct roles of the Src family kinases, SRC‐1 and KIN‐22, that are negatively regulated by CSK‐1 in C. elegans
Author(s) -
Hirose Takashi,
Koga Makoto,
Ohshima Yasumi,
Okada Masato
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)03819-x
Subject(s) - proto oncogene tyrosine protein kinase src , caenorhabditis elegans , biology , kinase , gene , phenotype , tyrosine protein kinase csk , microbiology and biotechnology , rna interference , sh3 domain , src family kinase , genetics , rna
To elucidate the primitive roles of the Src family kinases (SFKs), here we characterized Caenorhabditis elegans orthologues of SFKs ( src‐1 and kin‐22 ) and their regulator kinase Csk ( csk‐1 ). SRC‐1 and KIN‐22 possess the C‐terminal regulatory tyrosines characteristic of SFKs, and their activities are negatively regulated by CSK‐1 in a yeast expression system. The src‐1 and csk‐1 genes are co‐expressed in some head neurons, the anchor cell and the tail region, while kin‐22 and csk‐1 genes are co‐expressed in pharyngeal muscles and tail region. Expression of KIN‐22 induced morphological defects in the pharynx, whereas expression of SRC‐1 did not show any overt phenotype in adult. RNA interference of src‐1 , but not that of kin‐22 , caused a developmental arrest in early development. These results suggest that SRC‐1 and KIN‐22 play distinct roles under the control of CSK‐1.