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雄性不育基因的丧失功能导致玉米花药中严重的氧化应激和代谢紊乱。

The Loss-Function of the Male Sterile Gene / Results in Severely Oxidative Stress and Metabolic Disorder in Maize Anthers.

机构信息

Shunde Graduate School, Zhongzhi International Institute of Agricultural Biosciences, Research Center of Biology and Agriculture, University of Science and Technology Beijing, Beijing 100024, China.

Beijing Engineering Laboratory of Main Crop Bio-Tech Breeding, Beijing International Science and Technology Cooperation Base of Bio-Tech Breeding, Beijing Solidwill Sci-Tech Co., Ltd., Beijing 100192, China.

出版信息

Cells. 2022 Jul 27;11(15):2318. doi: 10.3390/cells11152318.

DOI:10.3390/cells11152318
PMID:35954161
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9367433/
Abstract

In plants, oxidative stress and metabolic reprogramming frequently induce male sterility, however our knowledge of the underlying molecular mechanism is far from complete. Here, a maize genic male-sterility (GMS) mutant () with a loss-of-function of the gene encoding glycerol-3-phosphate acyltransferase 6 (GPAT6) displayed severe deficiencies in the development of a four-layer anther wall and microspores and excessive reactive oxygen species (ROS) content in anthers. In anthers, transcriptome analysis identified thousands of differentially expressed genes that were functionally enriched in stress response and primary metabolism pathways. Further investigation revealed that 64 genes involved in ROS production, scavenging, and signaling were specifically changed in expression levels in anthers compared to the other five investigated GMS lines. The severe oxidative stress triggered premature tapetal autophagy and metabolic reprogramming mediated mainly by the activated SnRK1-bZIP pathway, as well as the TOR and PP2AC pathways, proven by transcriptome analysis. Furthermore, 20 reported maize GMS genes were altered in expression levels in anthers. The excessive oxidative stress and the metabolic reprogramming resulted in severe phenotypic deficiencies in anthers. These findings enrich our understanding of the molecular mechanisms by which ROS and metabolic homeostasis impair anther and pollen development in plants.

摘要

在植物中,氧化应激和代谢重编程常导致雄性不育,但我们对其潜在分子机制的了解还远远不够。在这里,一个玉米基因雄性不育(GMS)突变体(),其甘油-3-磷酸酰基转移酶 6(GPAT6)基因失活,表现出四层花药壁和小孢子发育严重缺陷,花药中活性氧(ROS)含量过高。在 突变体的花药中,转录组分析鉴定了数千个差异表达基因,这些基因在应激反应和初级代谢途径中具有功能富集。进一步的研究表明,与其他五种研究的 GMS 系相比,在 突变体的花药中,有 64 个与 ROS 产生、清除和信号转导相关的基因在表达水平上发生了特异性变化。严重的氧化应激触发了过早的绒毡层自噬和代谢重编程,主要由激活的 SnRK1-bZIP 途径以及 TOR 和 PP2AC 途径介导,这一点通过转录组分析得到了证明。此外,在 突变体的花药中,有 20 个报道的玉米 GMS 基因的表达水平发生了改变。过多的氧化应激和代谢重编程导致 突变体的花药严重表型缺陷。这些发现丰富了我们对 ROS 和代谢平衡如何损害植物花药和花粉发育的分子机制的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/4353c53d9178/cells-11-02318-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/5f9705840e60/cells-11-02318-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/a25ef078d556/cells-11-02318-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/66a6ee7be51b/cells-11-02318-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/678ea8b490ca/cells-11-02318-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/420193207f9f/cells-11-02318-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/706a8360323a/cells-11-02318-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/ba4b54a4952e/cells-11-02318-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/32a7c0d9936a/cells-11-02318-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/4353c53d9178/cells-11-02318-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/5f9705840e60/cells-11-02318-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/a25ef078d556/cells-11-02318-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/66a6ee7be51b/cells-11-02318-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/678ea8b490ca/cells-11-02318-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/420193207f9f/cells-11-02318-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/706a8360323a/cells-11-02318-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/ba4b54a4952e/cells-11-02318-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/32a7c0d9936a/cells-11-02318-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca2e/9367433/4353c53d9178/cells-11-02318-g009.jpg

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