Fig. S6.
A model depicting the possible mechanism of how CDK12 contributes to courtship learning in Drosophila. (A) Memory of courtship conditioning in Canton-S males. After a 5-h training with a mated female, the CI was determined during 10 min of testing with a tester; right after training; 1, 2, 3, or 6 h later; or 1, 2, 3, 4, 5, 6, or 8 d later. Squares and circles represent the mean CIs of trained males and age-matched shams, respectively. Error bars indicate SEM. The MI was calculated by dividing the mean of CItest by the mean of CIsham. (B) The schematics illustrating procedures used to analyze Drosophila courtship memory. The MI was calculated by dividing the CItest by the mean of the CIsham. If MI is ≥1, it indicates that there is no memory. (C and D) Courtship MIs were measured in (C) CDK12-depleted and (D) CycK-depleted flies. Significance was estimated using the Student’s t test. The CDK12 and CycK knockdowns in the MBs of adult flies were driven by OK107-GAL4. (E) A model depicting the mechanism by which the CDK12/CycK complex counteracts heterochromatin enrichment and regulates the expression of neuronal genes. In the presence of CDK12/CycK, the Ser2 of the CTD in RNAPII is phosphorylated and maintains the processes of transcriptional elongation. The RNAPII elongation complex together with other histone remodeling factors, including histone acetyltransferase, prevent the ectopic accumulations of H3K9me2/HP1 from the enriched 3′ region toward the promoter region. In the absence of CDK12/CycK, RNAPII loses the phosphorylation at Ser2, which may lead to a reduction in its elongating activity and further increases the levels of H3K9me2 and HP1. The heterochromatinization caused by the ectopic accumulations of H3K9me2 and HP1 results in the transcriptional attenuation of specific genes, such as neuronal genes, when they are required to be highly activated at specific developmental stages. n.s., Not significant. *P < 0.05; **P < 0.001; ***P < 0.0001.