Glycosyltransferase-like protein ABI8/ELD1/KOB1 promotes Arabidopsis hypocotyl elongation through regulating cellulose biosynthesis

作  者:Wang X, Jing YJ, Zhang BC, Zhou YH, Lin RC*
影响因子:5.906
刊物名称:Plant Cell and Environment
出版年份:2015
卷:38  期:3  页码:411-422

论文摘要:

  Seedling de-etiolation (photomorphogenesis) is an important light-regulated developmental process in plants. Here, we showed that disruption of the gene encoding a glycosyltransferase-like protein, ABA INSENSITIVE 8 (ABI8)/ELONGATION EFFECTIVE 1 (ELD1)/KOBITO1 (KOB1), caused short-hypocotyl elongation under all light conditions examined and even in darkness. We found that the ABI8 transcript level was down-regulated by light in a phytochrome A-dependent manner. Furthermore, light destabilized ABI8 protein via the 26S proteasome degradation pathway. We showed that ABI8 promoted the expression of genes involved in cell elongation and cellulose synthesis. Consistently, the cellulose content was reduced in the abi8 mutants and application of 2, 6-dichlorobenzonitrile (an inhibitor of cellulose biosynthesis) mimicked the abi8 mutant phenotype. Moreover, we found that phytochrome and cryptochrome photoreceptors negatively, whereas CONSTITUTIVE PHOTOMORPHOGENIC 1 positively, regulated cellulose synthesis. We also showed that ELONGATED HYPOCOTYL 5 directly bound to the promoters of ABI8 and several cellulose synthesis genes and repressed their expression in light conditions. Taken together, our study reveals that ABI8 functions as a negative factor in light inhibition of hypocotyl elongation through modulating cellulose biosynthesis. This study elucidates a molecular mechanism on how light regulates cellulose synthesis and hypocotyl elongation during plant photomorphogenic growth. The authors demonstrate that ABI8 is a negative regulator of light-inhibition of hypocotyl growth and that HY5 transcription factor directly represses ABI8 expression. ABI8 are down-regulated by light both at the transcription and post-translational levels.

全文链接:http://onlinelibrary.wiley.com/doi/10.1111/pce.12395/abstract