DNA replication factor C1 mediates genomic stability and transcriptional gene silencing in Arabidopsis
KAUST DepartmentDesert Agriculture Initiative
Biological and Environmental Sciences and Engineering (BESE) Division
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AbstractGenetic screening identified a suppressor of ros1-1, a mutant of REPRESSOR OF SILENCING1 (ROS1; encoding a DNA demethylation protein). The suppressor is a mutation in the gene encoding the largest subunit of replication factor C (RFC1). This mutation of RFC1 reactivates the unlinked 35S-NPTII transgene, which is silenced in ros1 and also increases expression of the pericentromeric Athila retrotransposons named transcriptional silent information in a DNA methylationindependent manner. rfc1 is more sensitive than the wild type to the DNA-damaging agent methylmethane sulphonate and to the DNA inter- and intra- cross-linking agent cisplatin. The rfc1 mutant constitutively expresses the G2/M-specific cyclin CycB1;1 and other DNA repair-related genes. Treatment with DNA-damaging agents mimics the rfc1 mutation in releasing the silenced 35S-NPTII, suggesting that spontaneously induced genomic instability caused by the rfc1 mutation might partially contribute to the released transcriptional gene silencing (TGS). The frequency of somatic homologous recombination is significantly increased in the rfc1 mutant. Interestingly, ros1 mutants show increased telomere length, but rfc1 mutants show decreased telomere length and reduced expression of telomerase. Our results suggest that RFC1 helps mediate genomic stability and TGS in Arabidopsis thaliana. © 2010 American Society of Plant Biologists.
SponsorsThis work was supported by the National Nature Science Foundation of China (30630004 and 30721062), the National Transgenic Research Project (2008ZX08009-002), and the Program of Introducing Talents of Discipline to Universities (B06003) and Chinese Universities Scientific Fund to Z.G. We thank Yuelin Zhang for sharing the T-DNA lines provided by the ABRC (Columbus, OH).
JournalTHE PLANT CELL ONLINE
PubMed Central IDPMC2929113
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