DEPDC1B coordinates de-adhesion events and cell-cycle progression at mitosis
Stefano Marchesi1, Francesca Montani2, Gianluca Deflorian3
1Istituto Europeo di Oncologia (IEO), 20141 Milan, Italy; Fondazione IFOM-Istituto FIRC di Oncologia Molecolare, 20139 Milan, Italy; Center for Genomic Science of IIT@SEMM, Istituto Italiano di Tecnologia (IIT), 20139 Milan, Italy.
DEPDC1B protein coordinates cell rounding and division commitment by dismantling focal adhesions. This adhesion signaling mechanism is crucial for mitotic progression and development in zebrafish.
Area of Science:
- Cell Biology
- Molecular Biology
- Developmental Biology
Background:
- Cell rounding, detachment, and increased rigidity are hallmarks of mitosis.
- Dismantling of focal adhesions (FAs) is critical for these mitotic events.
- The link between mitotic reshaping and commitment to divide remains unclear.
Purpose of the Study:
- To investigate the role of DEPDC1B in coordinating cell adhesion and cell-cycle progression during mitosis.
- To elucidate the molecular mechanism by which DEPDC1B regulates focal adhesion dynamics.
- To examine the in vivo relevance of the DEPDC1B signaling pathway in developmental processes.
Main Methods:
- Protein interaction studies to define the DEPDC1B/RhoA/PTPRF complex.
- Cell-based assays to observe focal adhesion dynamics and cell morphology.
- Zebrafish developmental studies to assess mitotic dynamics in vivo.
Main Results:
- DEPDC1B accumulates in G2 and inhibits a RhoA-signaling complex involving PTPRF at focal adhesions.
- DEPDC1B competes with RhoA for PTPRF interaction, promoting FA dismantling.
- The DEPDC1B/RhoA/PTPRF axis controls mitotic dynamics during zebrafish development.
Conclusions:
- DEPDC1B is a key regulator coordinating focal adhesion disassembly with cell-cycle progression.
- This adhesion-dependent signaling pathway is essential for proper mitotic reshaping and development.
- The findings reveal a novel mechanism linking cell adhesion to cell division control.
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