4.7 Article

Overproduction of Chl b Retards Senescence Through Transcriptional Reprogramming in Arabidopsis

期刊

PLANT AND CELL PHYSIOLOGY
卷 53, 期 3, 页码 505-517

出版社

OXFORD UNIV PRESS
DOI: 10.1093/pcp/pcs006

关键词

Arabidopsis; Chloroplast; Chlorophyllide a oxygenase; Photosynthesis; Senescence

资金

  1. The Ministry of Education, Culture, Sports, Science and Technology, Japan [23570042, 17GS0314]
  2. Deutsche Forschungsgemeinschaft [MU 1199/14-1]
  3. Grants-in-Aid for Scientific Research [23570042, 23657026, 21370014] Funding Source: KAKEN

向作者/读者索取更多资源

Leaf senescence is a developmentally and environmentally regulated process which includes global changes in gene expression. Using Arabidopsis as a model, we modified Chl arrangement in photosystems by overexpressing the catalytic domain (the C domain) of chlorophyllide a oxygenase (CAO) fused with the linker domain (the B domain) of CAO and green fluorescent protein (GFP). In these plants (referred to as the BCG plants for the B and C domains of CAO and GFP), the Chl a/b ratio was drastically decreased and Chl b was incorporated into core antenna complexes. The BCG plants exhibited a significant delay of both developmental and dark-induced leaf senescence. The photosynthetic apparatus, CO2 fixation enzymes and the chloroplast structure were lost in wild-type plants during senescence, while BCG plants retained them longer than the wild type. Large-scale quantitative real-time PCR analyses of 1,880 transcription factor (TF) genes showed that 241 TFs are differentially expressed between BCG plants and wild-type plants at senescence, similar to 40% of which are known senescence-associated genes (SAGs). Expression profiling also revealed the down-regulation of a large number of additional non-TF SAGs. In contrast, genes involved in photosynthesis were up-regulated, while those encoding Chl degradation enzymes were down-regulated in BCG plants. These results demonstrate that alteration of pigment composition in the photosynthetic apparatus retards senescence through transcriptional reprogramming.

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