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Two cell‐cycle regulated SET‐domain proteins interact with proliferating cell nuclear antigen (PCNA) in Arabidopsis
Author(s) -
Raynaud Cécile,
Sozzani Rosangela,
Glab Nathalie,
Domenichini Séverine,
Perennes Claudette,
Cella Rino,
Kondorosi Eva,
Bergounioux Catherine
Publication year - 2006
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2006.02799.x
Subject(s) - proliferating cell nuclear antigen , microbiology and biotechnology , biology , dna replication , cell cycle , subcellular localization , arabidopsis , dna repair , replication factor c , dna polymerase delta , nuclear localization sequence , nuclear protein , control of chromosome duplication , eukaryotic dna replication , transcription factor , cell , dna , genetics , cytoplasm , gene , rna , reverse transcriptase , mutant
Summary The proliferating cell nuclear antigen (PCNA) functions as a sliding clamp for DNA polymerase, and is thus a key actor in DNA replication. It is also involved in DNA repair, maintenance of heterochromatic regions throughout replication, cell cycle regulation and programmed cell death. Identification of PCNA partners is therefore necessary for understanding these processes. Here we identify two Arabidopsis SET‐domain proteins that interact with PCNA: ATXR5 and ATXR6. A truncated ATXR5Δex2, incapable of interacting with PCNA, also occurs in planta . ATXR6 , upregulated during the S phase, is upregulated by AtE2F transcription factors, suggesting that it is required for S‐phase progression. The two proteins differ in their subcellular localization: ATXR5 has a dual localization in plastids and in the nucleus, whereas ATXR6 is solely nuclear. This indicates that the two proteins may play different roles in plant cells. However, overexpression of either ATXR5 or ATXR6 causes male sterility because of the degeneration of defined cell types. Taken together, our results suggest that both proteins may play a role in the cell cycle or DNA replication, and that the activity of ATXR5 may be regulated via its subcellular localization.