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减数分裂I向减数分裂II的异常转变导致了柑橘无核人工杂种的雄性不育。

Abnormal transition from meiosis I to meiosis II induces male sterility in a seedless artificial hybrid of citrus.

作者信息

Rao Zhixiong, Sun Ruotian, Liu Shengjun, Ai Wanqi, Song Lizhi, Wang Xia, Xu Qiang

机构信息

National Key Laboratory for Germplasm Innovation & Utilization of Horticultural Crops, College of Horticulture and Forestry Sciences, Huazhong Agricultural University, Wuhan, 430070 Hubei Province China.

出版信息

Mol Breed. 2024 Dec 16;45(1):1. doi: 10.1007/s11032-024-01521-5. eCollection 2025 Jan.

Abstract

UNLABELLED

Male sterility is an important trait for breeding and for the seedless fruit production in citrus. We identified one seedling which exhibiting male sterility and seedlessness (named hereafter), from a cross between two fertile parents, with sour orange () as seed parent and Ponkan mandarin () as pollen parent. Analysis using pollen viability staining, scanning electron microscopy (SEM), and transmission electron microscopy (TEM) revealed that the mature pollen of the was aborted, displaying collapse and deformity. Further cytological analysis identified the abnormal formation of monad, dyad, and tetrad instead of the normal tetrad formation, leading to meiotic failure in the seedless hybrid. By comparative transcript profiling of meiotic anther of fertile and sterile hybrids, we observed significant downregulation of () and genes in the hybrid, which known to control the transition from meiosis I to meiosis II in plants. These results indicated abnormal meiosis led to the male sterility of the seedless hybrid and that the decreased activities of kinases and cyclins may associated with the failure of the transition of meiosis I to meiosis II during anthers development.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s11032-024-01521-5.

摘要

未标注

雄性不育是柑橘育种和无籽果实生产中的一个重要性状。我们从两个可育亲本的杂交后代中鉴定出一株表现出雄性不育和无籽的幼苗(以下简称该幼苗),以酸橙()为母本,椪柑()为父本。通过花粉活力染色、扫描电子显微镜(SEM)和透射电子显微镜(TEM)分析发现,该幼苗的成熟花粉败育,表现为塌陷和畸形。进一步的细胞学分析发现,该无籽杂种中形成的是异常的单核、二分体和四分体,而不是正常的四分体,导致减数分裂失败。通过对可育和不育杂种减数分裂期花药的转录组比较分析,我们观察到该杂种中已知控制植物减数分裂I向减数分裂II转变的()和基因显著下调。这些结果表明,异常减数分裂导致了无籽杂种的雄性不育,激酶和细胞周期蛋白活性的降低可能与花药发育过程中减数分裂I向减数分裂II转变的失败有关。

补充信息

在线版本包含可在10.1007/s11032-024-01521-5获取的补充材料。

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本文引用的文献

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Nat Plants. 2020 Feb;6(2):131-142. doi: 10.1038/s41477-020-0597-3. Epub 2020 Feb 13.

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