CAJ | 학술논문

叶序和出叶间隔期是叶片生长发育的基本生物学特性和水稻的重要农艺性状之一。对叶序或出叶间隔期突变体的研究，可以帮助我们了解叶片的形成机制。本研究通过甲基磺酸乙酯(EMS)诱变粳稻品种日本晴，获得一个稳定遗传的类树状突变体s2-21。该突变体出叶间隔期变短、节间缩短、植株矮化、分蘖数减少、叶片数增加、不能正常进行生殖生长。将该突变体与籼稻品种Dular杂交，遗传分析表明该突变体性状受1对隐性基因控制。通过InDel分子标记对s2-21/Dular F2群体进行遗传定位，将该基因初步定位在第1染色体InDel标记C1-15和S1-17之间。利用本实验已测序的籼稻品种Dular全基因组序列与NCBI (http：//www.ncbi.nlm.nih.gov/)上提供的粳稻品种日本晴基因组序列比对，开发了6个新的InDel标记，最终将该基因定位在W25和W26之间约88 kb的区间内。测序结果表明该突变体中PLA2基因的第4个内含子的第5位碱基由G突变为A。
협서화출협간격기시협편생장발육적기본생물학특성화수도적중요농예성상지일。대협서혹출협간격기돌변체적연구，가이방조아문료해협편적형성궤제。본연구통과갑기광산을지(EMS)유변갱도품충일본청，획득일개은정유전적류수상돌변체s2-21。해돌변체출협간격기변단、절간축단、식주왜화、분얼수감소、협편수증가、불능정상진행생식생장。장해돌변체여선도품충Dular잡교，유전분석표명해돌변체성상수1대은성기인공제。통과InDel분자표기대s2-21/Dular F2군체진행유전정위，장해기인초보정위재제1염색체InDel표기C1-15화S1-17지간。이용본실험이측서적선도품충Dular전기인조서렬여NCBI (http：//www.ncbi.nlm.nih.gov/)상제공적갱도품충일본청기인조서렬비대，개발료6개신적InDel표기，최종장해기인정위재W25화W26지간약88 kb적구간내。측서결과표명해돌변체중PLA2기인적제4개내함자적제5위감기유G돌변위A。
Phyllotaxy and plastochron are basic aspects of leaf development and the important agronomic traits of rice. The study of phyllotaxy or plastochron mutant will help us to understand the mechanism of leaf formation. In this study, a leafy head mutant s2-21 was isolated from an EMS (ethyl methane sulfonate) mutagenized japonica cultivar Nipponbare. It was characterized by shorter intervals between leaves, shortened internodes, dwarf plants, decreased tiller number, and increased leaf number. It was also unable to transit from vegetative to reproductive growth. Genetic analysis with a F2 population of the mutant and an indica cultivar Dular showed that this trait is controlled by a single recessive nucleus gene, which was primarily mapped between two insertion-deletion (InDel) markers C1-15 and S1-17 on chromosome 1. For the fine mapping, new InDel markers were designed by utilizing information of genomic sequences from Nipponbare (http://www.ncbi.nlm.nih.gov/) and Dular (our unpublished data), and eventually the gene was localized within the region of 88 kb between W25 and W26. Sequence analysis indicated the mutant was caused by mutation of the fifth base from G to A in the fourth intron of the PLA2 gene.