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一种保守的MYB转录因子,参与维管植物和单细胞藻类中的磷饥饿信号传导。

A conserved MYB transcription factor involved in phosphate starvation signaling both in vascular plants and in unicellular algae.

作者信息

Rubio V, Linhares F, Solano R, Martín A C, Iglesias J, Leyva A, Paz-Ares J

机构信息

Centro Nacional de Biotecnología, Campus de Cantoblanco, 28049 Madrid, Spain.

出版信息

Genes Dev. 2001 Aug 15;15(16):2122-33. doi: 10.1101/gad.204401.

Abstract

Plants have evolved a number of adaptive responses to cope with growth in conditions of limited phosphate (Pi) supply involving biochemical, metabolic, and developmental changes. We prepared an EMS-mutagenized M(2) population of an Arabidopsis thaliana transgenic line harboring a reporter gene specifically responsive to Pi starvation (AtIPS1::GUS), and screened for mutants altered in Pi starvation regulation. One of the mutants, phr1 (phosphate starvation response 1), displayed reduced response of AtIPS1::GUS to Pi starvation, and also had a broad range of Pi starvation responses impaired, including the responsiveness of various other Pi starvation-induced genes and metabolic responses, such as the increase in anthocyanin accumulation. PHR1 was positionally cloned and shown be related to the PHOSPHORUS STARVATION RESPONSE 1 (PSR1) gene from Chlamydomonas reinhardtii. A GFP::PHR1 protein fusion was localized in the nucleus independently of Pi status, as is the case for PSR1. PHR1 is expressed in Pi sufficient conditions and, in contrast to PSR1, is only weakly responsive to Pi starvation. PHR1, PSR1, and other members of the protein family share a MYB domain and a predicted coiled-coil (CC) domain, defining a subtype within the MYB superfamily, the MYB-CC family. Therefore, PHR1 was found to bind as a dimer to an imperfect palindromic sequence. PHR1-binding sequences are present in the promoter of Pi starvation-responsive structural genes, indicating that this protein acts downstream in the Pi starvation signaling pathway.

摘要

植物已经进化出多种适应性反应,以应对在磷酸盐(Pi)供应有限条件下的生长,这涉及生化、代谢和发育变化。我们制备了一个拟南芥转基因系的EMS诱变M(2)群体,该转基因系携带一个对Pi饥饿有特异性反应的报告基因(AtIPS1::GUS),并筛选了在Pi饥饿调节方面发生改变的突变体。其中一个突变体phr1(磷酸盐饥饿反应1)对Pi饥饿时AtIPS1::GUS的反应减弱,并且还广泛损害了一系列Pi饥饿反应,包括各种其他Pi饥饿诱导基因的反应性和代谢反应,如花色苷积累的增加。PHR1通过定位克隆被证明与莱茵衣藻的磷饥饿反应1(PSR1)基因相关。与PSR1一样,GFP::PHR1蛋白融合物在细胞核中的定位与Pi状态无关。PHR1在Pi充足的条件下表达,并且与PSR1不同,它对Pi饥饿的反应较弱。PHR1、PSR1和该蛋白家族的其他成员共享一个MYB结构域和一个预测的卷曲螺旋(CC)结构域,定义了MYB超家族中的一个亚型,即MYB-CC家族。因此,发现PHR1以二聚体形式结合到一个不完全回文序列上。Pi饥饿反应性结构基因的启动子中存在PHR1结合序列,表明该蛋白在Pi饥饿信号通路中起下游作用。

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