The Gene ANTHER DEHISCENCE REPRESSOR (ADR) Controls Male Fertility by Suppressing the ROS Accumulation and Anther Cell Wall Thickening in Arabidopsis
The Gene ANTHER DEHISCENCE REPRESSOR (ADR) Controls Male Fertility by Suppressing the ROS Accumulation and Anther Cell Wall Thickening in Arabidopsis
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DOI：
10.1038/s41598-019-41382-z
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发表时间：
2019-03-25
影响因子：
4.6
通讯作者：
Yang, Chang-Hsien
中科院分区：
文献类型：
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作者：
Dai, Shu-Yu;Hsu, Wei-Han;Yang, Chang-Hsien
植物雄性不育是由激素变化、胁迫、细胞质改变和核基因突变等多种刺激引起的。本研究对拟南芥雄性不育调控基因ADR进行了功能分析。在ADR：：GUS花中，在幼芽的花药中检测到强的GUS活性，但在成熟花中检测到低的GUS活性。ADR +GFP融合蛋白可通过N-肉豆蔻酰化修饰，靶向过氧化物酶体。ADR在转基因拟南芥中的异位表达导致花药不裂导致雄性不育。35 S：：ADR花药开裂的缺陷是由于活性氧积累减少，改变了花药药室内壁的次生增厚，抑制了NST 1和NST 2的表达，这是通过调节花药药室内壁细胞次生壁增厚来实现花药开裂所必需的。这种缺陷可以通过外用过氧化氢（H2 O2）来挽救。这些结果表明，ADR必须是N-肉豆蔻酰化的，并在花发育的早期阶段靶向过氧化物酶体，通过抑制ROS积累和NST 1/NST 2表达来负调控花药开裂。
Male sterility in plants is caused by various stimuli such as hormone changes, stress, cytoplasmic alterations and nuclear gene mutations. The gene ANTHER DEHISCENCE REPRESSOR (ADR), which is involved in regulating male sterility in Arabidopsis, was functionally analyzed in this study. In ADR::GUS flowers, strong GUS activity was detected in the anthers of young flower buds but was low in mature flowers. ADR +GFP fusion proteins, which can be modified by N-myristoylation, were targeted to peroxisomes. Ectopic expression of ADR in transgenic Arabidopsis plants resulted in male sterility due to anther indehiscence. The defect in anther dehiscence in 35S::ADR flowers is due to the reduction of ROS accumulation, alteration of the secondary thickening in the anther endothecium and suppression of the expression of NST1 and NST2, which are required for anther dehiscence through regulation of secondary wall thickening in anther endothecia I cells. This defect could be rescued by external application of hydrogen peroxide (H2O2). These results demonstrated that ADR must be N-myristoylated and targeted to the peroxisome during the early stages of flower development to negatively regulate anther dehiscence by suppressing ROS accumulation and NST1/NST2 expression.