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PMID:16251208
| Citation |
Itoh, B, Hirose, T, Takata, N, Nishiwaki, K, Koga, M, Ohshima, Y and Okada, M (2005) SRC-1, a non-receptor type of protein tyrosine kinase, controls the direction of cell and growth cone migration in C. elegans. Development 132:5161-72 |
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| Abstract |
Src family tyrosine kinase (SFK) has been implicated in the regulation of cell adhesion and migration during animal development. We show that SRC-1, an ortholog of SFK, plays an essential role in directing cell migration in Caenorhabditis elegans. The mutation in the src-1 gene results in defective distal tip cell (DTC)-directed gonad morphogenesis in an activity-dependent and DTC cell-autonomous manners. In the src-1 mutants, DTCs fail to turn and continue their centrifugal migration along the ventral muscles. The effect of the src-1 mutation is suppressed by mutations in genes that function in the CED/Rac pathway, suggesting that SRC-1 in DTCs is an upstream regulator of a Rac pathway that controls cytoskeletal remodeling. In the src-1 mutant, the expression of unc-5/netrin receptor is normally regulated, and neither the precocious expression of UNC-5 nor the mutation in the unc-5 gene significantly affects the DTC migration defect. These data suggest that SRC-1 acts in the netrin signaling in DTCs. The src-1 mutant also exhibits cell-autonomous defects in the migration and growth cone path-finding of Q neuroblast descendants AVM and PVM. However, these roles of SRC-1 do not appear to involve the CED/Rac pathway. These findings show that SRC-1 functions in responding to various extracellular guidance cues that direct the cell migration via disparate signaling pathways in different cell types. |
| Links |
PubMed Online version:10.1242/dev.02103 |
| Keywords |
Animals; Body Patterning; Caenorhabditis elegans/growth & development; Caenorhabditis elegans Proteins/physiology; Cell Movement/physiology; Gonads/growth & development; Growth Cones/physiology; Histone Acetyltransferases; Mutation; Nuclear Receptor Coactivator 1; Protein-Tyrosine Kinases/physiology; Receptors, Cell Surface/physiology; Signal Transduction; Transcription Factors/genetics; Transcription Factors/physiology |
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