HAG3, a Histone Acetyltransferase, Affects UV-B Responses by Negatively Regulating the Expression of DNA Repair Enzymes and Sunscreen Content in Arabidopsis thaliana

被引:27
|
作者
Fina, Julieta P. [1 ]
Casati, Paula [1 ]
机构
[1] Univ Nacl Rosario, Ctr Estudios Fotosintet & Bioquim CEFOBI, RA-2000 Rosario, Argentina
关键词
DNA damage; GNAT familiy; Histone acetyltransferases; UV-B damage; CHROMATIN-REMODELING PROTEINS; GENOME-WIDE IDENTIFICATION; POLYMERASE-II HOLOENZYME; ELONGATOR COMPLEX; CELL-PROLIFERATION; TRANSCRIPTIONAL ADAPTER; MERISTEM ACTIVITY; GENE-EXPRESSION; DAMAGE RESPONSE; HOLO-ELONGATOR;
D O I
10.1093/pcp/pcv054
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Histone acetylation is regulated by histone acetyltransferases and deacetylases. In Arabidopsis, there are 12 histone acetyltransferases and 18 deacetylases. Histone acetyltransferases are organized in four families: the GNAT/HAG, the MYST, the p300/CBP and the TAFII250 families. Previously, we demonstrated that Arabidopsis mutants in the two members of the MYST acetyltransferase family show increased DNA damage after UV-B irradiation. To investigate further the role of other histone acetyltransferases in UV-B responses, a putative role for enzymes of the GNAT family, HAG1, HAG2 and HAG3, was analyzed. HAG transcripts are not UV-B regulated; however, hag3 RNA interference (RNAi) transgenic plants show a lower inhibition of leaf and root growth by UV-B, higher levels of UV-B-absorbing compounds and less UV-B-induced DNA damage than Wassilewskija (Ws) plants, while hag1 RNAi transgenic plants and hag2 mutants do not show significant differences from wild-type plants. Transcripts for UV-B-regulated genes are highly expressed under control conditions in the absence of UV-B in hag3 RNAi transgenic plants, suggesting that the higher UV-B tolerance may be due to increased levels of proteins that participate in UV-B responses. Together, our data provide evidence that HAG3, directly or indirectly, participates in UV-B-induced DNA damage repair and signaling.
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页码:1388 / 1400
页数:13
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