Research Faculty of Agriculture, Hokkaido University, N-9, W-9, Kita-ku, Sapporo, 060-8589, Japan.
Hokkaido Agricultural Research Center, National Agriculture and Food Research Organization, Shinsei Minami 9-4, Memuro, 082-0081, Japan.
Theor Appl Genet. 2019 Jan;132(1):227-240. doi: 10.1007/s00122-018-3211-6. Epub 2018 Oct 19.
The sugar beet Rf1 locus has a number of molecular variants. We found that one of the molecular variants is a weak allele of a previously identified allele. Male sterility (MS) caused by nuclear-mitochondrial interaction is called cytoplasmic male sterility (CMS) in which MS-inducing mitochondria are suppressed by a nuclear gene, restorer-of-fertility. Rf and rf are the suppressing and non-suppressing alleles, respectively. This dichotomic view, however, seems somewhat unsatisfactory to explain the recently discovered molecular diversity of Rf loci. In the present study, we first identified sugar beet line NK-305 as a new source of Rf1. Our crossing experiment revealed that NK-305 Rf1 is likely a semi-dominant allele that restores partial fertility when heterozygous but full fertility when homozygous, whereas Rf1 from another sugar beet line appeared to be a dominant allele. Proper degeneration of anther tapetum is a prerequisite for pollen development; thus, we compared tapetal degeneration in the NK-305 Rf1 heterozygote and the homozygote. Degeneration occurred in both genotypes but to a lesser extent in the heterozygote, suggesting an association between NK-305 Rf1 dose and incompleteness of tapetal degeneration leading to partial fertility. Our protein analyses revealed a quantitative correlation between NK-305 Rf1 dose and a reduction in the accumulation of a 250 kDa mitochondrial protein complex consisting of a CMS-specific mitochondrial protein encoded by MS-inducing mitochondria. The abundance of Rf1 transcripts correlated with NK-305 Rf1 dose. The molecular organization of NK-305 Rf1 suggested that this allele evolved through intergenic recombination. We propose that the sugar beet Rf1 locus has a series of multiple alleles that differ in their ability to restore fertility and are reflective of the complexity of Rf evolution.
糖用甜菜 Rf1 基因座有许多分子变体。我们发现其中一个分子变体是之前鉴定的等位基因的弱等位基因。核-线粒体相互作用引起的雄性不育称为细胞质雄性不育(CMS),其中诱导雄性不育的线粒体被核基因恢复育性所抑制。Rf 和 rf 分别是抑制和非抑制等位基因。然而,这种二分法观点似乎不太令人满意,无法解释最近发现的 Rf 基因座的分子多样性。在本研究中,我们首先鉴定了糖用甜菜 NK-305 品系为 Rf1 的新来源。我们的杂交实验表明,NK-305 Rf1 可能是一个半显性等位基因,在杂合子时恢复部分育性,但在纯合子时恢复完全育性,而来自另一个糖用甜菜品系的 Rf1 似乎是一个显性等位基因。花药绒毡层的适当退化是花粉发育的前提条件;因此,我们比较了 NK-305 Rf1 杂合体和纯合体绒毡层的退化。两种基因型都发生了退化,但杂合体的退化程度较小,这表明 NK-305 Rf1 剂量与绒毡层退化不完全导致部分育性之间存在关联。我们的蛋白质分析表明,NK-305 Rf1 剂量与由诱导雄性不育的线粒体编码的 CMS 特异性线粒体蛋白组成的 250 kDa 线粒体蛋白复合物积累减少之间存在定量相关性。Rf1 转录本的丰度与 NK-305 Rf1 剂量相关。NK-305 Rf1 的分子组织表明,该等位基因是通过基因间重组进化而来的。我们提出,糖用甜菜 Rf1 基因座有一系列不同的等位基因,它们在恢复育性的能力上存在差异,反映了 Rf 进化的复杂性。