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OsKASI-2 对于调控水稻膜脂不饱和水平和耐冷性是必需的。

OsKASI-2 is required for the regulation of unsaturation levels of membrane lipids and chilling tolerance in rice.

机构信息

Hunan Province Key Laboratory of Crop Sterile Germplasm Resource Innovation and Application, College of Life Sciences, Hunan Normal University, Changsha, China.

College of Agronomy, Henan Agricultural University, Zhengzhou, China.

出版信息

Plant Biotechnol J. 2024 Aug;22(8):2157-2172. doi: 10.1111/pbi.14336. Epub 2024 Mar 20.

DOI:10.1111/pbi.14336
PMID:38506090
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11258988/
Abstract

Chilling stress has seriously limited the global production and geographical distribution of rice. However, the molecular mechanisms associated with plant responses to chilling stress are less known. In this study, we revealed a member of β-ketoacyl-ACP synthase I family (KASI), OsKASI-2 which confers chilling tolerance in rice. OsKASI-2 encodes a chloroplast-localized KASI enzyme mainly expressed in the leaves and anthers of rice and strongly induced by chilling stress. Disruption of OsKASI-2 led to decreased KAS enzymatic activity and the levels of unsaturated fatty acids, which impairs degree of unsaturation of membrane lipids, thus increased sensitivity to chilling stress in rice. However, the overexpression of OsKASI-2 significantly improved the chilling tolerance ability in rice. In addition, OsKASI-2 may regulate ROS metabolism in response to chilling stress. Natural variation of OsKASI-2 might result in difference in chilling tolerance between indica and japonica accessions, and Hap1 of OsKASI-2 confers chilling tolerance in rice. Taken together, we suggest OsKASI-2 is critical for regulating degree of unsaturation of membrane lipids and ROS accumulation for maintenance of membrane structural homeostasis under chilling stress, and provide a potential target gene for improving chilling tolerance of rice.

摘要

冷胁迫严重限制了水稻的全球产量和地理分布。然而，与植物对冷胁迫反应相关的分子机制知之甚少。在本研究中，我们揭示了一个β-酮酰基-ACP 合酶 I 家族（KASI）成员 OsKASI-2，它赋予水稻耐冷性。OsKASI-2 编码一种定位于叶绿体的 KASI 酶，主要在水稻的叶片和花药中表达，并强烈受到冷胁迫的诱导。OsKASI-2 的破坏导致 KAS 酶活性和不饱和脂肪酸水平降低，这会损害膜脂的不饱和程度，从而增加水稻对冷胁迫的敏感性。然而，OsKASI-2 的过表达显著提高了水稻的耐冷能力。此外，OsKASI-2 可能通过调节 ROS 代谢来响应冷胁迫。OsKASI-2 的自然变异可能导致籼稻和粳稻品种之间耐冷性的差异，并且 OsKASI-2 的 Hap1 赋予水稻耐冷性。总之，我们认为 OsKASI-2 对于调节膜脂的不饱和程度和 ROS 积累以维持冷胁迫下的膜结构稳态至关重要，并且为提高水稻的耐冷性提供了一个潜在的靶基因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/75def39ecbf3/PBI-22-2157-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/6ee8ab9d39b0/PBI-22-2157-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/a916788fdd48/PBI-22-2157-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/837ecd324f26/PBI-22-2157-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/3336be87c5a5/PBI-22-2157-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/129eca9b4d4e/PBI-22-2157-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/4468dea0f786/PBI-22-2157-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/98adaa2e9acb/PBI-22-2157-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/75def39ecbf3/PBI-22-2157-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/6ee8ab9d39b0/PBI-22-2157-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/a916788fdd48/PBI-22-2157-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/837ecd324f26/PBI-22-2157-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/3336be87c5a5/PBI-22-2157-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/129eca9b4d4e/PBI-22-2157-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/4468dea0f786/PBI-22-2157-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/98adaa2e9acb/PBI-22-2157-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d58a/11373948/75def39ecbf3/PBI-22-2157-g002.jpg

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