Key Message

Pollen abortion could be mainly attributed to abnormal meiosis in the mutant. Multiomics analysis uncovered significant epigenetic variations between the mutant and its wild type during the pollen abortion process.

Abstract

Male sterility caused by aborted pollen can result in seedless fruit. A seedless Ponkan mandarin mutant (bud sport) was used to compare the transcriptome, methylome, and metabolome with its progenitor to understand the mechanism of citrus pollen abortion. Cytological observations showed that the anther of the mutant could form microspore mother cells, although the microspores failed to develop fertile pollen at the anther dehiscence stage. Based on pollen phenotypic analysis, pollen abortion could be mainly attributed to abnormal meiosis in the mutant. A transcriptome analysis uncovered the molecular mechanisms underlying pollen abortion between the mutant and its wild type. A total of 5421 differentially expressed genes were identified, and some of these genes were involved in the meiosis, hormone biosynthesis and signaling, carbohydrate, and flavonoid pathways. A total of 50,845 differentially methylated regions corresponding to 15,426 differentially methylated genes in the genic region were found between the mutant and its wild type by the methylome analysis. The expression level of these genes was negatively correlated with their methylation level, especially in the promoter regions. In addition, 197 differential metabolites were identified between the mutant and its wild type based on the metabolome analysis. The transcription and metabolome analysis further indicated that the expression of genes in the flavonoid, carbohydrate, and hormone metabolic pathways was significantly modulated in the pollen of the mutant. These results indicated that demethylation may alleviate the silencing of carbohydrate genes in the mutant, resulting in excessive starch and sugar hydrolysis and thereby causing pollen abortion in the mutant.

中文翻译：

---

无核柑橘突变体花粉流产过程中转录组、甲基化组和代谢组的比较分析。

关键信息

花粉流产主要归因于突变体中的异常减数分裂。多组学分析揭示了花粉流产过程中突变体与其野生型之间的显着表观遗传变异。

抽象的

由花粉败育引起的雄性不育可导致无核果实。使用无籽 Ponkan mandarin 突变体 (bud sport) 比较转录组、甲基化组和代谢组及其祖细胞，以了解柑橘花粉流产的机制。细胞学观察表明，突变体的花药可以形成小孢子母细胞，但小孢子在花药开裂阶段未能发育出可育花粉。基于花粉表型分析，花粉流产可能主要归因于突变体中的异常减数分裂。转录组分析揭示了突变体与其野生型之间花粉流产的分子机制。共鉴定出5421个差异表达基因，其中一些基因参与减数分裂、激素生物合成和信号转导、碳水化合物、和类黄酮途径。通过甲基化组分析，在突变体与其野生型之间共发现了50845个差异甲基化区域，对应于基因区域中的15426个差异甲基化基因。这些基因的表达水平与其甲基化水平呈负相关，尤其是在启动子区域。此外，基于代谢组分析，在突变体与其野生型之间鉴定出 197 种差异代谢物。转录和代谢组分析进一步表明，黄酮类化合物、碳水化合物和激素代谢途径中基因的表达在突变体的花粉中受到显着调节。这些结果表明去甲基化可以减轻突变体中碳水化合物基因的沉默，