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PWL1,一种 G 型凝集素受体样激酶,正向调控叶片衰老和耐热性,但负向调控水稻对黄单胞菌的抗性。

PWL1, a G-type lectin receptor-like kinase, positively regulates leaf senescence and heat tolerance but negatively regulates resistance to Xanthomonas oryzae in rice.

机构信息

National Key Facility for Crop Gene Resources and Genetic Improvement, Institute of Crop Sciences, Chinese Academy of Agricultural Sciences, Beijing, China.

Institute of Rice Research, Guangdong Academy of Agricultural Sciences, Guangzhou, China.

出版信息

Plant Biotechnol J. 2023 Dec;21(12):2525-2545. doi: 10.1111/pbi.14150. Epub 2023 Aug 14.

DOI:10.1111/pbi.14150
PMID:37578160
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10651159/
Abstract

Plant leaf senescence, caused by multiple internal and environmental factors, has an important impact on agricultural production. The lectin receptor-like kinase (LecRLK) family members participate in plant development and responses to biotic and abiotic stresses, but their roles in regulating leaf senescence remain elusive. Here, we identify and characterize a rice premature withered leaf 1 (pwl1) mutant, which exhibits premature leaf senescence throughout the plant life cycle. The pwl1 mutant displayed withered and whitish leaf tips, decreased chlorophyll content, and accelerated chloroplast degradation. Map-based cloning revealed an amino acid substitution (Gly412Arg) in LOC_Os03g62180 (PWL1) was responsible for the phenotypes of pwl1. The expression of PWL1 was detected in all tissues, but predominantly in tillering and mature leaves. PWL1 encodes a G-type LecRLK with active kinase and autophosphorylation activities. PWL1 is localized to the plasma membrane and can self-associate, mainly mediated by the plasminogen-apple-nematode (PAN) domain. Substitution of the PAN domain significantly diminished the self-interaction of PWL1. Moreover, the pwl1 mutant showed enhanced reactive oxygen species (ROS) accumulation, cell death, and severe DNA fragmentation. RNA sequencing analysis revealed that PWL1 was involved in the regulation of multiple biological processes, like carbon metabolism, ribosome, and peroxisome pathways. Meanwhile, interfering of biological processes induced by the PWL1 mutation also enhanced heat sensitivity and resistance to bacterial blight and bacterial leaf streak with excessive accumulation of ROS and impaired chloroplast development in rice. Natural variation analysis indicated more variations in indica varieties, and the vast majority of japonica varieties harbour the PWL1 allele. Together, our results suggest that PWL1, a member of LecRLKs, exerts multiple roles in regulating plant growth and development, heat-tolerance, and resistance to bacterial pathogens.

摘要

植物叶片衰老受多种内部和环境因素的影响,对农业生产有重要影响。凝集素受体样激酶(LecRLK)家族成员参与植物发育以及对生物和非生物胁迫的响应,但它们在调节叶片衰老中的作用尚不清楚。在这里,我们鉴定并表征了一个水稻早衰叶片 1(pwl1)突变体,该突变体在整个植物生命周期中表现出叶片早衰。pwl1 突变体表现为叶片尖端枯萎变白,叶绿素含量降低,叶绿体降解加速。基于图谱的克隆揭示 LOC_Os03g62180(PWL1)中的一个氨基酸替换(Gly412Arg)是导致 pwl1 表型的原因。PWL1 的表达在所有组织中均有检测到,但在分蘖和成熟叶片中表达量更高。PWL1 编码一种具有活性激酶和自身磷酸化活性的 G 型 LecRLK。PWL1 定位于质膜上,可以自组装,主要由纤溶酶原-苹果-线虫(PAN)结构域介导。PAN 结构域的替换显著削弱了 PWL1 的自相互作用。此外,pwl1 突变体表现出增强的活性氧(ROS)积累、细胞死亡和严重的 DNA 片段化。RNA 测序分析表明,PWL1 参与了多个生物过程的调节,如碳代谢、核糖体和过氧化物酶体途径。同时,PWL1 突变引起的生物过程干扰也增强了水稻的耐热性和对细菌性条斑病和细菌性疫病的抗性,导致 ROS 过度积累和叶绿体发育受损。自然变异分析表明,籼稻品种中存在更多的变异,而绝大多数粳稻品种则含有 PWL1 等位基因。综上所述,我们的研究结果表明,PWL1 作为 LecRLKs 的一员,在调节植物生长发育、耐热性和抗细菌病原体方面发挥着多种作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/2a9b255466e3/PBI-21-2525-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/4d3bd07735f9/PBI-21-2525-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/31d4ff29e956/PBI-21-2525-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/403fb9449b33/PBI-21-2525-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/66b3954442be/PBI-21-2525-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/f2ed9a7f96fe/PBI-21-2525-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/adb517ad80ec/PBI-21-2525-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/89d2625ebef9/PBI-21-2525-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/3dac50bff99b/PBI-21-2525-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/2a9b255466e3/PBI-21-2525-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/4d3bd07735f9/PBI-21-2525-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/31d4ff29e956/PBI-21-2525-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/403fb9449b33/PBI-21-2525-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/66b3954442be/PBI-21-2525-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/f2ed9a7f96fe/PBI-21-2525-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/adb517ad80ec/PBI-21-2525-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/89d2625ebef9/PBI-21-2525-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/3dac50bff99b/PBI-21-2525-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d581/11376742/2a9b255466e3/PBI-21-2525-g007.jpg

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