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. Author manuscript; available in PMC: 2018 Mar 6.
Published in final edited form as: Curr Biol. 2017 Feb 23;27(5):661–672. doi: 10.1016/j.cub.2017.01.056

Figure 5. CDK-8 Functions Together with Mediator Complex Proteins and in Parallel to HLH-3 to Promote I4 Neurogenesis, Most Likely by Inhibiting CYH-1 and CDK-7.

Figure 5

(A) Disruption of cdk-8 or cic-1 in the hlh-3 null mutant n5469 enhances I4 misspecification.

(B) Expressing a wild-type (WT), but not a kinase-dead (KD), copy of cdk-8 cDNA using the dpy-22 promoter rescues I4 misspecification in cdk-8; hlh-3 double mutants.

(C) Overexpression of phosphomimetic CYH-1DD, but not non-phosphorylatable CYH-1AA, using the dpy-22 promoter suppresses I4 defects in cdk-8; hlh-3 mutants.

(D) Overexpression of kinase-dead CDK-7KD, but not phosphomimetic CDK-7EE, using the dpy-22 promoter rescues I4 defects in cdk-8; hlh-3 mutants. o.e., overexpression. Mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001 by Student’s t test. See also Figures S5 and S6.