A novel DAG-dependent mechanism links PKCɑ and Cyclin B1 regulating cell cycle progression
PDF | HTML | Supplementary Files | How to cite
Metrics: PDF 2516 views | HTML 2623 views | ?
Alessandro Poli1, Giulia Ramazzotti1, Alessandro Matteucci2, Lucia Manzoli1, Annalisa Lonetti1, Pann-Ghill Suh3, James A. McCubrey4, Lucio Cocco1
1Cell Signaling Laboratory, Department of Biomedical Sciences, University of Bologna, Bologna, Italy
2CNR-National Research Council of Italy, Institute of Molecular Genetics, Bologna, Italy
3School of Nano-Biotechnology and Chemical Engineering, Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea
4Department of Microbiology and Immunology, Brody School of Medicine, East Carolina University, Greenville, NC, USA
Lucio Cocco, e-mail: [email protected].
Keywords: PKC, Cyclin, Cell Cycle, PLC, DAG, nuclei
Received: September 02, 2014 Accepted: October 06, 2014 Published: October 24, 2014
Through the years, different studies showed the involvement of Protein Kinase C (PKC) in cell cycle control, in particular during G1/S transition. Little is known about their role at G2/M checkpoint. In this study, using K562 human erythroleukemia cell line, we found a novel and specific mechanism through which the conventional isoform PKCα positively affects Cyclin B1 modulating G2/M progression of cell cycle. Since the kinase activity of this PKC isoform was not necessary in this process, we demonstrated that PKCα, physically interacting with Cyclin B1, avoided its degradation and stimulated its nuclear import at mitosis. Moreover, the process resulted to be strictly connected with the increase in nuclear diacylglycerol levels (DAG) at G2/M checkpoint, due to the activity of nuclear Phospholipase C β1 (PLCβ1), the only PLC isoform mainly localized in the nucleus of K562 cells. Taken together, our findings indicated a novel DAG dependent mechanism able to regulate the G2/M progression of the cell cycle.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.