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糖基转移酶样蛋白 ABI8/ELD1/KOB1 通过调节纤维素生物合成促进拟南芥下胚轴伸长。

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

机构信息

Key Laboratory of Photobiology, Institute of Botany, Chinese Academy of Sciences, Beijing, 100093, China; University of the Chinese Academy of Sciences, Beijing, 100049, China.

出版信息

Plant Cell Environ. 2015 Mar;38(3):411-22. doi: 10.1111/pce.12395. Epub 2014 Aug 5.

Abstract

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.

摘要

幼苗去黄化(光形态建成)是植物中一个重要的光调控发育过程。在这里,我们表明,破坏编码糖基转移酶样蛋白的基因 ABA 不敏感 8(ABI8)/伸长有效 1(ELD1)/KOBITO1(KOB1),导致在所有检查的光照条件下甚至在黑暗中短下胚轴伸长。我们发现 ABI8 转录本水平在光下以光质 A 依赖的方式下调。此外,光通过 26S 蛋白酶体降解途径使 ABI8 蛋白不稳定。我们表明 ABI8 促进了参与细胞伸长和纤维素合成的基因的表达。一致地,abi8 突变体中的纤维素含量减少,并且应用 2,6-二氯苯腈(纤维素生物合成的抑制剂)模拟了 abi8 突变体表型。此外,我们发现光敏色素和隐花色素光受体负调控,而组成型光形态建成 1 正调控纤维素合成。我们还表明,伸长下胚轴 5 直接结合到 ABI8 和几个纤维素合成基因的启动子上,并在光照条件下抑制它们的表达。总之,我们的研究表明,ABI8 通过调节纤维素生物合成作为光抑制下胚轴伸长的负因子发挥作用。

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