Dwarf and short grain 1, encoding a putative U-box protein regulates cell division and elongation in rice

被引:38
作者
Wang, Nan [1 ]
Xing, Yadi [1 ]
Lou, Qijin [1 ]
Feng, Ping [1 ]
Liu, Song [1 ]
Zhu, Meidan [1 ]
Yin, Wuzhong [1 ]
Fang, Shunran [1 ]
Lin, Yan [1 ]
Zhang, Tianquan [1 ]
Sang, Xianchun [1 ]
He, Guanghua [1 ]
机构
[1] Southwest Univ, Lab Applicat & Safety Control Genetically Modifie, Rice Res Inst, Chongqing 400716, Peoples R China
基金
中国国家自然科学基金;
关键词
Brassinosteroid; Multiple hormone pathways; Cell division; Cell elongation; HETEROTRIMERIC G-PROTEIN; BRASSINOSTEROID SIGNAL-TRANSDUCTION; ALPHA-SUBUNIT; NEGATIVE REGULATOR; DOWNSTREAM TARGET; PROTEASOME SYSTEM; RECEPTOR KINASES; PLANT HORMONES; ABSCISIC-ACID; MUTANT;
D O I
10.1016/j.jplph.2016.11.012
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Plant hormones coordinate a plant's responses to environmental stimuli and the endogenous developmental programs for cell division and elongation. Brassinosteroids are among the most important of these hormones in plant development. Recently, the ubiquitin-26S-proteasome system was identified to play a key role in hormone biology. In this study, we analyzed the function of a rice (Oryza sativa) gene, DSG1, which encodes a U-box E3 ubiquitin ligase. In the dsg1 mutant (an allelic mutant of tud1), the lengths of the roots, internodes, panicles, and seeds were shorter than that in the wild-type, which was due to defects in cell division and elongation. In addition, the leaves of the dsg1 mutant were wider and curled. The DSG1 protein is nuclear- and cytoplasm-localized and does not show tissue specificity in terms of its expression, which occurs in roots, culms, leaves, sheaths, and spikelets. The dsg1 mutant is less sensitive to brassinosteroid treatment than the wild-type, and DSGI expression is negatively regulated by brassi-nosteroids, ethylene, auxin, and salicylic acid. These results demonstrate that DSGI positively regulates cell division and elongation and may be involved in multiple hormone pathways. (C) 2016 Elsevier GmbH. All rights reserved.
引用
收藏
页码:84 / 94
页数:11
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