Tan Qian, Zhang Xu, Luo Qian, Xu Yi-Chun, Zhang Jie, Liang Wan-Qi
Joint International Research Laboratory of Metabolic and Developmental Sciences, State Key Laboratory of Hybrid Rice, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.
Rice (N Y). 2024 Jan 5;17(1):3. doi: 10.1186/s12284-023-00681-w.
HEI10 is a conserved E3 ubiquitin ligase involved in crossover formation during meiosis, and is thus essential for both male and female gamete development. Here, we have discovered a novel allele of HEI10 in rice that produces a truncated HEI10 protein missing its N-terminal RING domain, namely sh1 (shorter hei10 1). Unlike previously reported hei10 null alleles that are completely sterile, sh1 exhibits complete male sterility but retains partial female fertility. The causative sh1 mutation is a 76 kb inversion between OsFYVE4 and HEI10, which breaks the integrity of both genes. Allelic tests and complementation assays revealed that the gamete developmental defects of sh1 were caused by disruption of HEI10. Further studies demonstrated that short HEI10 can correctly localise to the nucleus, where it could interact with other proteins that direct meiosis; expressing short HEI10 in hei10 null lines partially restores female fertility. Our data reveal an intriguing mutant allele of HEI10 with differential effects on male and female fertility, providing a new tool to explore similarities and differences between male and female meiosis.
HEI10是一种保守的E3泛素连接酶,参与减数分裂过程中的交叉形成,因此对雄配子和雌配子的发育都至关重要。在这里,我们在水稻中发现了一个新的HEI10等位基因,它产生一种缺失其N端RING结构域的截短型HEI10蛋白,即sh1(较短的hei10 1)。与先前报道的完全不育的hei10无效等位基因不同,sh1表现出完全雄性不育,但保留部分雌性育性。导致sh1突变的原因是OsFYVE4和HEI10之间发生了76 kb的倒位,这破坏了两个基因的完整性。等位基因测试和互补试验表明,sh1的配子发育缺陷是由HEI10的破坏引起的。进一步的研究表明,短HEI10可以正确定位于细胞核,在那里它可以与其他指导减数分裂的蛋白质相互作用;在hei10无效系中表达短HEI10可部分恢复雌性育性。我们的数据揭示了一个有趣的HEI10突变等位基因,对雄性和雌性育性有不同影响,为探索雄性和雌性减数分裂之间的异同提供了一个新工具。