Reproductive failure in cotton caused by drought has been reported to be closely associated with alterations in pistil fertility; however, the mechanism of the effect of drought on pistil fertility in cotton is less studied. We hypothesized that drought would inhibit the ovule formation to alter pistil potential fertility. To address this hypothesis, we conducted a water deficit induction experiment with a cotton cultivar, Dexiamian 1. Results showed that drought damaged the cytological structure of the developing ovules. This resulted in a lower ovule number, finally leading to lower cottonseed number and boll weight. And the decreased ovule number was closely related to the reactive oxygen species (ROS) accumulation in pistil during ovule development. Further analysis of antioxidant metabolism found that in the enzymatic antioxidant system, drought decreased the activities of superoxide dismutase (SOD) and catalase (CAT), resulting in the accumulation of superoxide anion () and hydrogen peroxide (H2O2). Regarding the non‐enzymatic antioxidant system, the elevated glutathione reductase gene (GhGR) expression under drought promoted the glutathione (GSH) accumulation; however, the decreased dehydroascorbate reductase gene (GhDHAR2) expression under drought inhibited the conversion of GSH to ascorbic acid (AsA). Although the increased monodehydroascorbate reductase gene (GhMDHAR) expression under drought promoted AsA accumulation, drought‐induced reduced ascorbate peroxidase gene (GhAPX) expression inhibited the reduction of H2O2 by AsA, which ultimately led to higher AsA content and H2O2 content. We conclude that drought impedes the ovule formation by disturbing pistil's antioxidant metabolic homeostasis to destruct the cytological structure of the developing ovules.

中文翻译：

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棉花胚珠发育过程中土壤干旱破坏了棉花雌蕊的抗氧化平衡，阻碍了胚珠的形成

据报道，干旱引起的棉花繁殖障碍与雌蕊生育力的改变密切相关。然而，干旱对棉花雌蕊育性影响的机制研究较少。我们假设干旱会抑制胚珠形成，从而改变雌蕊的潜在育性。为了解决这一假设，我们对棉花品种德夏棉1号进行了水分亏缺诱导实验。结果表明，干旱损害了发育中胚珠的细胞学结构。这导致胚珠数量减少，最终导致棉籽数量和棉铃重量降低。胚珠数量的减少与胚珠发育过程中雌蕊中活性氧（ROS）的积累密切相关。进一步分析抗氧化代谢发现，在酶促抗氧化系统中，干旱降低了超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性，导致超氧阴离子（）和过氧化氢（H）的积累。2氧2）。关于非酶抗氧化系统，升高的谷胱甘肽还原酶基因（生长激素受体) 干旱下的表达促进了谷胱甘肽（GSH）的积累；然而，脱氢抗坏血酸还原酶基因减少（GHDAR2)在干旱条件下的表达抑制了GSH向抗坏血酸(AsA)的转化。虽然增加的单脱氢抗坏血酸还原酶基因（甘德哈尔）干旱下的表达促进AsA积累，干旱诱导的抗坏血酸过氧化物酶基因减少（GhAPX)表达抑制H的减少2氧2AsA，最终导致更高的 AsA 含量和 H2氧2内容。我们得出的结论是，干旱通过扰乱雌蕊的抗氧化代谢稳态来破坏发育中胚珠的细胞学结构，从而阻碍胚珠形成。