Gregor Mendel Instituten Academy of science
Gregor Mendel Instituten Academy of science
Cifuentes M.,French National Institute for Agricultural Research |
Jolivet S.,French National Institute for Agricultural Research |
Cromer L.,French National Institute for Agricultural Research |
Harashima H.,RIKEN |
And 10 more authors.
PLoS Genetics | Year: 2016
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. © 2016 Cifuentes et al.
Derboven E.,Gregor Mendel Instituten Academy of science |
Ekker H.,Campus Science Support Facilities |
Kusenda B.,Gregor Mendel Instituten Academy of science |
Bulankova P.,Gregor Mendel Instituten Academy of science |
And 2 more authors.
PLoS Genetics | Year: 2014
The CST (Cdc13/CTC1-STN1-TEN1) complex was proposed to have evolved kingdom specific roles in telomere capping and replication. To shed light on its evolutionary conserved function, we examined the effect of STN1 dysfunction on telomere structure in plants. STN1 inactivation in Arabidopsis leads to a progressive loss of telomeric DNA and the onset of telomeric defects depends on the initial telomere size. While EXO1 aggravates defects associated with STN1 dysfunction, it does not contribute to the formation of long G-overhangs. Instead, these G-overhangs arise, at least partially, from telomerase-mediated telomere extension indicating a deficiency in C-strand fill-in synthesis. Analysis of hypomorphic DNA polymerase α mutants revealed that the impaired function of a general replication factor mimics the telomeric defects associated with CST dysfunction. Furthermore, we show that STN1-deficiency hinders re-replication of heterochromatic regions to a similar extent as polymerase α mutations. This comparative analysis of stn1 and pol α mutants suggests that STN1 plays a genome-wide role in DNA replication and that chromosome-end deprotection in stn1 mutants may represent a manifestation of aberrant replication through telomeres. © 2014 Derboven et al.
Sasaki E.,Gregor Mendel Instituten Academy of science |
Zhang P.,Gregor Mendel Instituten Academy of science |
Zhang P.,University of Southern California |
Atwell S.,University of Southern California |
And 3 more authors.
PLoS Genetics | Year: 2015
Understanding how genetic variation interacts with the environment is essential for understanding adaptation. In particular, the life cycle of plants is tightly coordinated with local environmental signals through complex interactions with the genetic variation (G x E). The mechanistic basis for G x E is almost completely unknown. We collected flowering time data for 173 natural inbred lines of Arabidopsis thaliana from Sweden under two growth temperatures (10°C and 16°C), and observed massive G x E variation. To identify the genetic polymorphisms underlying this variation, we conducted genome-wide scans using both SNPs and local variance components. The SNP-based scan identified several variants that had common effects in both environments, but found no trace of G x E effects, whereas the scan using local variance components found both. Furthermore, the G x E effects appears to be concentrated in a small fraction of the genome (0.5%). Our conclusion is that G x E effects in this study are mostly due to large numbers of allele or haplotypes at a small number of loci, many of which correspond to previously identified flowering time genes. © 2015 Sasaki et al.