Recherche - Observatoire océanologique de Banyuls sur mer
Laboratoire Arago

 Ming-Ji FANN ( departement of Life Sciences and Institute of Genome Sciences National Yang-Ming University, Taipei, Taiwan) présentera un séminaire le 11 Février 2011 (Amphithéâtre A. Guille - Bât B 1er étage) ayant pour thème :

Toward the physiological function of the two novel members of the Cyclin dependent kinase family: CDK12 and CDK13 regulate neurite formation

CDK12 and CDK13 are cyclin-dependent kinases that contain an arginine serine-rich (RS) domain, a characteristic of the SR family, and are involved in alternative splicing regulation through interaction with cyclins L1 and L2. Expression of CDK12 and CDK13 mRNA is detected in the developing mouse embryos beginning from embryonic day 6.5 (E6.5) by in situ hybridization with higher levels of expression in the developing nervous system, suggesting that it might play a role in the neural development. Using differentiation of P19 embryonal carcinoma cells as an assay, we explored roles of CDK12 and CDK13 in neurite outgrowth. When CDK12 and CDK13 are knocked down, numbers of neurons with long neurites are decreased, although overexpression of CDK12 and CDK13 does not have effects on neurite outgrowth. We further interrogated how CDK12 and CDK13 affect the neurite outgrowth. To achieve the goal, we performed microarray analysis, semi-quantitative PCR assay and Western blotting analysis to search genes whose expression is affected by CDK12 and CDK13. Our analysis showed that CDK5 are down-regulated after knockdown of CDK12 and CDK13. CDK5 is known to be essential for neurite growth. Furthermore, overexpression of CDK5 partially rescues the neurite outgrowth defects observed when CDK12 or CDK13 is depleted.

Taken together, CDK12 and CDK13 may modulate the neurite outgrowth in P19 cells, in part, due to their effects on CDK5 expression. (This project was supported by National Science Council (NSC97-2320-B-010-026-MY2) and Ministry of Education, ROC.)