Laboratory of Plant Breeding, Research Faculty of Agriculture, Hokkaido University, Sapporo, 060-8589, Japan.
Plant Cell Rep. 2010 Apr;29(4):359-69. doi: 10.1007/s00299-010-0827-7. Epub 2010 Feb 27.
BT-type cytoplasmic male sterility (CMS) in rice is associated with accumulation of unprocessed dicistronic RNA containing a duplicated atp6 (B-atp6) and an unusual open reading frame, orf79, encoding a cytotoxic peptide in mitochondria. The male-sterile state of BT-type CMS is stably maintained by backcrossing the plants with line Taichung 65 (T65) that has no restorer gene and is completely suppressed by the presence of the Rf1 gene through the processing of B-atp6-orf79 RNA. A variant of the T65 line, T65(T), has a weak restoration function conferred by the Ifr1 gene, which is genetically independent of the Rf1 gene. However, not much is known about the mechanism(s). In a study to examine whether the mechanism involved in fertility restoration by Ifr1 is analogous to restoration mediated by Rf1, the transcript profile of B-atp6-orf79 in male-sterile plants was compared with that in fertility restored plants obtained by crossing male-sterile plants with T65(T). The cellular level of unprocessed B-atp6-orf79 RNA was reduced in the restored plants, but no change in processing efficiency or the quantity of B-atp6-orf79 DNA was detected. These results suggest that Ifr1 restores fertility through reducing either the transcription rate of B-atp6-orf79 or the stability of its primary transcripts, a mechanism distinct from that involved in fertility restoration of BT-type CMS by Rf1.
水稻 BT 型细胞质雄性不育(CMS)与未加工的双顺反子 RNA 的积累有关,该 RNA 含有重复的 atp6(B-atp6)和一个异常的开放阅读框 orf79,该框在线粒体中编码细胞毒性肽。通过与没有恢复基因的台中 65 号(T65)系回交,BT 型 CMS 的雄性不育状态得以稳定维持,并且由于 Rf1 基因的存在,B-atp6-orf79 RNA 的加工完全抑制了雄性可育性。T65 系的一个变体 T65(T)具有由 Ifr1 基因赋予的弱恢复功能,该基因在遗传上与 Rf1 基因无关。然而,关于其机制知之甚少。在一项研究中,为了检查 Ifr1 参与育性恢复的机制是否与 Rf1 介导的恢复机制类似,比较了雄性不育植物中 B-atp6-orf79 的转录谱与通过将雄性不育植物与 T65(T)杂交获得的可育恢复植物的转录谱。在恢复植物中,未加工的 B-atp6-orf79 RNA 的细胞水平降低,但未检测到加工效率或 B-atp6-orf79 DNA 的数量发生变化。这些结果表明,Ifr1 通过降低 B-atp6-orf79 的转录率或其初级转录本的稳定性来恢复育性,这一机制与 Rf1 介导的 BT 型 CMS 育性恢复的机制不同。