So far, over 50 spontaneous male sterile mutants of tomato have been described and most of them are categorized as genetic male sterility. To date, the mechanism of tomato genetic male sterility remained unclear. In this study, differential proteomic analysis is performed between genetic male sterile line (2-517), which carries the male sterility (ms1035 ) gene, and its wild-type (VF-11) using isobaric tags for relative and absolute quantification-based strategy. A total of 8272 proteins are quantified in the 2-517 and VF-11 lines at the floral bud and florescence stages. These proteins are involved in different cellular and metabolic processes, which express obvious functional tendencies toward the hydroxylation of the ω-carbon in fatty acids, the tricarboxylic acid cycle, the glycolytic, and pentose phosphate pathways. Based on the results, a protein network explaining the mechanisms of tomato genetic male sterility is proposed, finding the compromising fat acid metabolism may cause the male sterility. These results are confirmed by parallel reaction monitoring, quantitative Real-time PCR (qRT-PCR), and physiological assays. Taken together, these results provide new insights into the metabolic pathway of anther abortion induced by ms1035 and offer useful clues to identify the crucial proteins involved in genetic male sterility in tomato.

中文翻译：

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基于iTRAQ的蛋白质组学揭示了西红柿ms1035基因通过损害脂肪酸代谢导致男性不育。

迄今为止，已经描述了超过50个番茄的自发雄性不育突变体，其中大多数被归类为遗传雄性不育。迄今为止，番茄遗传雄性不育的机理仍不清楚。在这项研究中，使用基于相对定量和绝对定量的等压标记，在携带雄性不育（ms1035）基因的雄性不育遗传系（2-517）与野生型（VF-11）之间进行差异蛋白质组分析。战略。在花蕾和花期，在2-517和VF-11品系中共定量了8272种蛋白质。这些蛋白质参与不同的细胞和代谢过程，这些过程表现出明显的功能趋向，即脂肪酸中ω-碳的羟基化，三羧酸循环，糖酵解和戊糖磷酸途径。根据结果​​，提出了一个蛋白质网络来解释番茄遗传雄性不育的机理，发现破坏脂肪酸代谢可能导致雄性不育。这些结果通过平行反应监测，定量实时PCR（qRT-PCR）和生理测定得到证实。综上所述，这些结果为ms1035诱导的花药流产的代谢途径提供了新的见识，并提供了有用的线索来鉴定参与番茄遗传雄性不育的关键蛋白质。