研究报告

PHOT2介导拟南芥下胚轴向光弯曲调节子的筛选与鉴定

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  • 棉花生物学国家重点实验室/植物逆境生物学重点实验室/河南大学生命科学学院, 开封 475004

收稿日期: 2013-03-29

  修回日期: 2013-09-02

  网络出版日期: 2014-06-03

基金资助

P2SA介导PHOT2调节拟南芥下胚轴向光弯曲机制分析;NOA1调控水杨酸诱导的拟南芥根波动生长机制分析

Isolation and Characterization of Regulators Involved in PHOT2-mediated Phototropism of Hypocotyls in Arabidopsis

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  • State Key Laboratory of Cotton Biology, Key Laboratory of Plant Stress Biology, College of Life Sciences, Henan University, Kaifeng 475004, China

Received date: 2013-03-29

  Revised date: 2013-09-02

  Online published: 2014-06-03

摘要

向光素(PHOT1和PHOT2)功能冗余调节单侧强蓝光诱导的拟南芥(Arabidopsis thaliana)黄化苗下胚轴向光弯曲表现功能冗余, 限制了人们对PHOT2信号转导机制的深入研究。通过化学诱变剂甲基磺酸乙酯(EMS)诱变拟南芥phot1突变体, 避开PHOT1基因的干扰, 寻找PHOT2下游信号分子。研究结果表明, 已成功筛选到1株遗传稳定的下胚轴向蓝光不弯曲突变体。遗传分析结果显示, 该突变体可能是PHOT2下游信号分子突变, 将其命名为p2sa1(phototropin2 signaling associated1)。用100 μmol·m–2·s–1强蓝光单侧照射, phot1p2sa1下胚轴向光弯曲缺失, 呈现phot1phot2双突变的表型, 然而phot1p2sa1在强蓝光下叶绿体避光正常, 明显不同于phot1phot2。实验证实P2SA1可能位于PHOT2的下游, 参与调节PHOT2介导的拟南芥下胚轴向光弯曲反应。

本文引用格式

赵翔, 王琳丹, 李园园, 赵青平, 张骁 . PHOT2介导拟南芥下胚轴向光弯曲调节子的筛选与鉴定[J]. 植物学报, 2014 , 49(3) : 254 -261 . DOI: 10.3724/SP.J.1259.2014.00254

Abstract

Previous research suggested that phototropins (PHOT1 and PHOT2) contribute redundantly to high-intensity blue light (HBL)-induced phototropic curvature of hypocotyls in Arabidopsis thaliana, which restricts our understanding of the mechanism of PHOT2 signal transduction. We used the phot1 mutant of A. thaliana with an ethylmethane sulphonate mutation to screen HBL-insensitive mutants, avoiding the disruption of PHOT1 activity, and successfully isolated the mutant p2sa1 (phototropin2 signaling associated1). Genetic analysis revealed that the mutant is controlled by a single recessive nuclear gene. Compared with phot1, the phot1p2sa1 mutant lost phototropism on irradiation with 100 μmol·m–2·s–1 unilateral blue light, which was consistent with phot1phot2. However, phot1p2sa1 showed chloroplast avoidance of HBL, which was not consistent with phot1phot2. P2SA1 may be located downstream of PHOT2 and involved in the regulation of the hypocotyl bending response to HBL.

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