[Krause MW] cdk-4 is a cyclin dependent kinase related to cdk-4 and cdk-6 from other organims. Homozygous cdk-4(gv3) animals usually arrest in L2 due to no, or limited, proliferation of the post-embryonic blast cells. About 3% of animals make it to a late stage of development.
cdk-4 encodes two isoforms of a cyclin-dependent serine/threonine protein kinase orthologous to human CDK4 and CDK6 (OMIM:123829 and OMIM:603368, mutated in cutanous malignant melanoma) which complex with D-type cyclins to regulate progression through the G1 phase of the cell cycle; CDK-4 activity is essential for G1 progression in postembryonic blast cells and as a result, cdk-4 mutant animals generally arrest during larval stages; the lethality generated by cdk mutations, also seen in animals doubly mutant for cdk-4 and cyd-1, a C. elegans D-type cyclin, can be suppressed by mutations in lin-35/Rb suggesting that, as in other organisms, LIN-35/Rb may be a major target of CDK-4/CYD-1 kinase activity; CDK-4 expression is first detected in neuronal and hypodermal lineages during mid-to-late embryogenesis, with postembryonic expression detected in hypodermal seam cells, cells of the P lineage which will give rise to ventral cord neurons, and cells of the somatic gonad, the vulva, and the intestine.
Enables protein serine/threonine kinase activity. Involved in nematode larval development; positive regulation of cell cycle process; and reproductive process. Predicted to be located in cytoplasm and nucleus. Predicted to be part of cyclin-dependent protein kinase holoenzyme complex. Expressed in gonad; intestine; neurons; and vulva. Used to study cancer. Human ortholog(s) of this gene implicated in several diseases, including carcinoma (multiple); central nervous system cancer (multiple); and urinary system cancer (multiple). Is an ortholog of human CDK4 (cyclin dependent kinase 4) and CDK6 (cyclin dependent kinase 6).
The deletion allele was isolated in a PCR-based screen following the method of Barstead and Moulder. The deletion break points have been identified by sequence. We have rescued the cdk-4(gv3) mutant using a wild type copy of the cdk-4 cDNA expressed under the control of cdk-4 ~3 kb of 5' flanking sequences.
Map position created from combination of previous interpolated map position (based on known location of sequence) and allele information. Therefore this is not a genetic map position based on recombination frequencies or genetic experiments. This was done on advice of the CGC.