-
Something wrong with this record ?
TDM1 Regulation Determines the Number of Meiotic Divisions
M. Cifuentes, S. Jolivet, L. Cromer, H. Harashima, P. Bulankova, C. Renne, W. Crismani, Y. Nomura, H. Nakagami, K. Sugimoto, A. Schnittger, K. Riha, R. Mercier,
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Directory of Open Access Journals
from 2005
Free Medical Journals
from 2005
Public Library of Science (PLoS)
from 2005-07-01
PubMed Central
from 2005
Europe PubMed Central
from 2005
ProQuest Central
from 2005-07-01
Open Access Digital Library
from 2005-01-01
Open Access Digital Library
from 2005-07-01
Open Access Digital Library
from 2005-01-01
Medline Complete (EBSCOhost)
from 2005-07-01
Health & Medicine (ProQuest)
from 2005-07-01
- MeSH
- Anaphase-Promoting Complex-Cyclosome metabolism MeSH
- Arabidopsis cytology genetics MeSH
- Models, Biological MeSH
- Chromosomes, Plant genetics MeSH
- Cyclins genetics metabolism MeSH
- Genes, Dominant MeSH
- Phosphorylation MeSH
- Phosphothreonine metabolism MeSH
- Epistasis, Genetic MeSH
- Genetic Testing MeSH
- Meiosis * MeSH
- Mutation genetics MeSH
- Protein Subunits metabolism MeSH
- Arabidopsis Proteins genetics metabolism MeSH
- Tetraploidy MeSH
- Tubulin metabolism MeSH
- Protein Binding MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
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.
Gregor Mendel Institute Austrian Academy of Sciences Vienna Austria
RIKEN Center for Sustainable Resource Science Suehiro Tsurumi Yokohama Japan
University of Hamburg Biozentrum Klein Flottbek Department of Developmental Biology Hamburg Germany
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc16027673
- 003
- CZ-PrNML
- 005
- 20161031124425.0
- 007
- ta
- 008
- 161005s2016 xxu f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1371/journal.pgen.1005856 $2 doi
- 024 7_
- $a 10.1371/journal.pgen.1005856 $2 doi
- 035 __
- $a (PubMed)26871453
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xxu
- 100 1_
- $a Cifuentes, Marta $u Institut Jean-Pierre Bourgin, INRA, AgroParisTech, CNRS, Université Paris-Saclay, RD10, 78026 Versailles Cedex, France.
- 245 10
- $a TDM1 Regulation Determines the Number of Meiotic Divisions / $c M. Cifuentes, S. Jolivet, L. Cromer, H. Harashima, P. Bulankova, C. Renne, W. Crismani, Y. Nomura, H. Nakagami, K. Sugimoto, A. Schnittger, K. Riha, R. Mercier,
- 520 9_
- $a 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.
- 650 _2
- $a anafázi podporující komplex $x metabolismus $7 D064173
- 650 _2
- $a Arabidopsis $x cytologie $x genetika $7 D017360
- 650 _2
- $a proteiny huseníčku $x genetika $x metabolismus $7 D029681
- 650 _2
- $a chromozomy rostlin $x genetika $7 D032461
- 650 _2
- $a cykliny $x genetika $x metabolismus $7 D016213
- 650 _2
- $a genetická epistáze $7 D004843
- 650 _2
- $a dominantní geny $7 D005799
- 650 _2
- $a genetické testování $7 D005820
- 650 12
- $a meióza $7 D008540
- 650 _2
- $a biologické modely $7 D008954
- 650 _2
- $a mutace $x genetika $7 D009154
- 650 _2
- $a fosforylace $7 D010766
- 650 _2
- $a fosfothreonin $x metabolismus $7 D010769
- 650 _2
- $a vazba proteinů $7 D011485
- 650 _2
- $a podjednotky proteinů $x metabolismus $7 D021122
- 650 _2
- $a tetraploidie $7 D057891
- 650 _2
- $a tubulin $x metabolismus $7 D014404
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Jolivet, Sylvie $u Institut Jean-Pierre Bourgin, INRA, AgroParisTech, CNRS, Université Paris-Saclay, RD10, 78026 Versailles Cedex, France.
- 700 1_
- $a Cromer, Laurence $u Institut Jean-Pierre Bourgin, INRA, AgroParisTech, CNRS, Université Paris-Saclay, RD10, 78026 Versailles Cedex, France.
- 700 1_
- $a Harashima, Hirofumi $u RIKEN Center for Sustainable Resource Science, Suehiro, Tsurumi, Yokohama, Japan.
- 700 1_
- $a Bulankova, Petra $u Gregor Mendel Institute, Austrian Academy of Sciences, Vienna, Austria.
- 700 1_
- $a Renne, Charlotte $u Institut Jean-Pierre Bourgin, INRA, AgroParisTech, CNRS, Université Paris-Saclay, RD10, 78026 Versailles Cedex, France.
- 700 1_
- $a Crismani, Wayne $u Institut Jean-Pierre Bourgin, INRA, AgroParisTech, CNRS, Université Paris-Saclay, RD10, 78026 Versailles Cedex, France.
- 700 1_
- $a Nomura, Yuko $u RIKEN Center for Sustainable Resource Science, Suehiro, Tsurumi, Yokohama, Japan.
- 700 1_
- $a Nakagami, Hirofumi $u RIKEN Center for Sustainable Resource Science, Suehiro, Tsurumi, Yokohama, Japan.
- 700 1_
- $a Sugimoto, Keiko $u RIKEN Center for Sustainable Resource Science, Suehiro, Tsurumi, Yokohama, Japan.
- 700 1_
- $a Schnittger, Arp $u University of Hamburg, Biozentrum Klein Flottbek, Department of Developmental Biology, Hamburg, Germany.
- 700 1_
- $a Riha, Karel $u Gregor Mendel Institute, Austrian Academy of Sciences, Vienna, Austria. Central European Institute of Technology (CEITEC), Masaryk University, Kamenice, Brno, Czech Republic.
- 700 1_
- $a Mercier, Raphael $u Institut Jean-Pierre Bourgin, INRA, AgroParisTech, CNRS, Université Paris-Saclay, RD10, 78026 Versailles Cedex, France.
- 773 0_
- $w MED00008920 $t PLoS genetics $x 1553-7404 $g Roč. 12, č. 2 (2016), s. e1005856
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/26871453 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y a $z 0
- 990 __
- $a 20161005 $b ABA008
- 991 __
- $a 20161031124349 $b ABA008
- 999 __
- $a ok $b bmc $g 1165987 $s 952303
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2016 $b 12 $c 2 $d e1005856 $e 20160212 $i 1553-7404 $m PLoS genetics $n PLoS Genet $x MED00008920
- LZP __
- $a Pubmed-20161005