TDM1 Regulation Determines the Number of Meiotic Divisions

Investor logo

Warning

This publication doesn't include Faculty of Medicine. It includes Central European Institute of Technology. Official publication website can be found on muni.cz.
Authors

CIFUENTES Marta JOLIVET Sylvie CROMER Laurence HARASHIMA Hirofumi BULANKOVA Petra RENNE Charlotte CRISMANI Wayne NOMURA Yuko NAKAGAMI Hirofumi SUGIMOTO Keiko SCHNITTGER Arp ŘÍHA Karel MERCIER Raphael

Year of publication 2016
Type Article in Periodical
Magazine / Source PLOS GENETICS
MU Faculty or unit

Central European Institute of Technology

Citation
Web http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1005856
Doi http://dx.doi.org/10.1371/journal.pgen.1005856
Field Genetics and molecular biology
Keywords ANAPHASE-PROMOTING COMPLEX/CYCLOSOME; MEIOSIS-II TRANSITION; FISSION YEAST; ARABIDOPSIS; CYCLIN; PROTEINS; APC/C; PROGRESSION; EXPRESSION; INTERKINESIS
Description Cell cycle control must be modified at meiosis to allow two divisions to follow a single round of DNA replication, resulting in ploidy reduction. The mechanisms that ensure meiosis termination at the end of the second and not at the end of first division are poorly understood. We show here that Arabidopsis thaliana TDM1, which has been previously shown to be essential for meiotic termination, interacts directly with the Anaphase-Promoting Complex. Further, mutations in TDM1 in a conserved putative Cyclin-Dependant Kinase (CDK) phosphorylation site (T16-P17) dominantly provoked premature meiosis termination after the first division, and the production of diploid spores and gametes. The CDKA; 1-CYCA1.2/TAM complex, which is required to prevent premature meiotic exit, phosphorylated TDM1 at T16 in vitro. Finally, while CYCA1;2/TAM was previously shown to be expressed only at meiosis I, TDM1 is present throughout meiosis. These data, together with epistasis analysis, lead us to propose that TDM1 is an APC/C component whose function is to ensure meiosis termination at the end of meiosis II, and whose activity is inhibited at meiosis I by CDKA; 1-TAM-mediated phosphorylation to prevent premature meiotic exit. This provides a molecular mechanism for the differential decision of performing an additional round of division, or not, at the end of meiosis I and II, respectively.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.

More info