cdk-2;skn-1

Cyclin-Dependent Kinase family;Cyclin-dependent kinase 2

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Locus: CELE_K03E5.3

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Wormbase description: cdk-2 encodes the C. elegans ortholog of cyclin-dependent kinase 2; along with CYE-1 (cyclin E), CDK-2 is required for the G1/S transition in somatic cells, centrosome assembly and polarity establishment in the embryo, proliferation of germ cells, and suppression of terminal differentiation in quiescent cells after asymmetric division; CYE-1 and CDK-2 also regulate the germline mitosis/meiosis decision through post-translational regulation of GLD-1, likely direct phosphorylation.

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Protein skinhead-1;SKiNhead

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Locus: CELE_T19E7.2

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Wormbase description: skn-1 encodes a bZip transcription factor orthologous to the mammalian Nrf (Nuclear factor-erythroid-related factor) transcription factors; during early embryogenesis, maternally provided SKN-1 is required for specification of the EMS blastomere, a mesendodermal precursor that gives rise to pharyngeal, muscle, and intestinal cells; later, during postembryonic development, SKN-1 functions in the p38 MAPK pathway to regulate the oxidative stress response and in parallel to DAF-16/FOXO in the DAF-2-mediated insulin/IGF-1-like signaling pathway to regulate adult lifespan; in vitro assays indicate that SKN-1 can be directly phosphorylated by the AKT-1, AKT-2, and SGK-1 kinases that lie downstream of DAF-2 in the insulin signaling pathway and in vivo experiments suggest that this phosphorylation is essential for regulation of SKN-1 nuclear accumulation and hence, transcriptional regulator activity; in the early embryo, SKN-1 is detected at highest levels in nuclei of the P1 blastomere and its descendants through the 8-cell stage of embryogenesis; later in embryogenesis, SKN-1 is observed in all hypodermal and intestinal nuclei, with reporter constructs indicating that intestinal expression begins as early as the 50-100-cell stage; in larvae and young adults, SKN-1::GFP reporters are expressed in the intestine and ASI neurons, with expression in intestinal nuclei enhanced under conditions of stress or reduced DAF-2 signaling.

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