Mutations in a conserved replication protein suppress transcriptional gene silencing in a DNA- methylation-independent manner in Arabidopsis

Avnish Kapoor, Manu Agarwal, Andrea Andreucci, Xianwu Zheng, Zhizhong Gong, Paul M. Hasegawa, Ray A. Bressan, Jian Kang Zhu

Research output: Contribution to journalArticlepeer-review

59 Scopus citations

Abstract

Mutations in the DNA glycosylase/lyase ROS1 cause transcriptional silencing of the linked RD29A-LUC and 35S-NPTII transgenes in Arabidopsis [1]. We report here that mutations in the Arabidopsis RPA2 locus release the silencing of 35S-NPTII but not RD29A-LUC in the ros1 mutant background. The rpa2 mutation also leads to enhanced expression of some transposons. Neither DNA methylation nor siRNAs at any of the reactivated loci are blocked by rpa2. Histone H3 methylation at lysine 4 was increased and histone H3 methylation at lysine 9 was decreased at the 35S promoter in the ros1rpa2 mutant compared to the ros1 background. RPA2 encodes a nuclear protein similar to the second subunit of the replication protein A conserved from yeast to mammals. Ectopic expression of the Arabidopsis RPA2 could complement the yeast rfa2 (rpa2) mutant. These results suggest an essential role of RPA2 in the maintenance of transcriptional gene silencing at specific loci in a DNA-methylation-independent manner. In addition, we found that rpa2 mutants are hypersensitive to the genotoxic agent methyl methanesulphonate, and the RPA2 protein interacts with ROS1 in vitro and in vivo, suggesting that RPA2 also functions together with ROS1 in DNA repair.

Original languageEnglish
Pages (from-to)1912-1918
Number of pages7
JournalCurrent Biology
Volume15
Issue number21
DOIs
StatePublished - 8 Nov 2005
Externally publishedYes

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