Disruption of a Upf1-like helicase-encoding gene OsPLS2 triggers light-dependent premature leaf senescence in rice
Disruption of a Upf1-like helicase-encoding gene OsPLS2 triggers light-dependent premature leaf senescence in rice
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类Upf1解旋酶编码基因OsPLS2的破坏引发水稻光依赖性叶片早衰
DOI：
10.1007/s11103-019-00848-4
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发表时间：
2019-05-01
影响因子：
5.1
通讯作者：
Pan, Gang
中科院分区：
文献类型：
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作者：
Gong, Pan;Luo, Yanmin;Pan, Gang
OsPLS2基因座编码一个类似upf1的解旋酶。在水稻突变体OsPLS2中，破坏OsPLS2加速了光依赖性叶片衰老。叶片衰老是一个复杂的生理过程，受遗传和环境因素共同控制，但其潜在的分子机制尚不明确。在这项研究中，我们报道了一个新的Oryza sativa叶片早衰突变体（ospls2）。通过图谱克隆，在编码upf1样解旋酶的OsPLS2基因的第13个内含子的第1个核苷酸上确定了G-to-A替换。该突变导致OsPLS2信使的剪接异常，并导致其全长蛋白翻译中断，表明OsPLS2在调节叶片衰老中起负作用。野生型水稻随着叶片衰老，OsPSL2蛋白水平逐渐下降。遮荫和光过滤研究表明，ospls2表型是光刺激的结果，具有光氧化应激和活性氧积累的特征。当持续暴露于远红光、外源H2O2和/或脱落酸（ABA）时，ospls2突变体持续了超敏性叶片衰老。与此一致的是，光敏色素基因下调，光敏色素相互作用因子（phytochrome - interacting FACTORS, PIFs）和WRKY基因上调，激活了ospls2的光和ROS信号通路，都促进了叶片衰老。综上所述，这些数据表明，OsPLS2在水稻叶片衰老中发挥了重要作用，其破坏引发了水稻叶片的光依赖性衰老。
The OsPLS2 locus was isolated and cloned by map-based cloning that encodes a Upf1-like helicase. Disruption of OsPLS2 accelerated light-dependent leaf senescence in the rice mutant of ospls2. Leaf senescence is a very complex physiological process controlled by both genetic and environmental factors, however its underlying molecular mechanisms remain elusive. In this study, we report a novel Oryza sativa premature leaf senescence mutant (ospls2). Through map-based cloning, a G-to-A substitution was determined at the 1st nucleotide of the 13th intron in the OsPLS2 gene that encodes a Upf1-like helicase. This mutation prompts aberrant splicing of OsPLS2 messenger and consequent disruption of its full-length protein translation, suggesting a negative role of OsPLS2 in regulating leaf senescence. Wild-type rice accordingly displayed a progressive drop of OsPSL2 protein levels with age-dependent leaf senescence. Shading and light filtration studies showed that the ospls2 phenotype, which was characteristic of photo-oxidative stress and reactive oxygen species (ROS) accumulation, was an effect of irritation by light. When continuously exposed to far-red light, exogenous H2O2 and/or abscisic acid (ABA), the ospls2 mutant sustained hypersensitive leaf senescence. In consistence, light and ROS signal pathways in ospls2 were activated by down-regulation of phytochrome genes, and up-regulation of PHYTOCHROME-INTERACTING FACTORS (PIFs) and WRKY genes, all promoting leaf senescence. Together, these data indicated that OsPLS2 played an essential role in leaf senescence and its disruption triggered light-dependent leaf senescence in rice.