水稻裂颖突变体sh1的鉴定及基因定位

[目的]本研究旨在定位和克隆水稻裂颖基因,为解析水稻裂颖性的遗传机制提供依据。[方法]从籼稻品种湘早籼6号突变体库中筛选出一个裂颖突变体(split husk 1, sh1),观察突变体的花器官和浆片形态,利用突变体与02428的F2群体定位目标基因,进一步通过定量 PCR 分析相关基因的表达情况。[结果]sh1 突变体的颖花形态与野生型基本一致,能正常开花,但不能正常闭颖,裂颖的主要原因是浆片不能在开颖后正常萎蔫。sh1突变体的有效穗数增加,但结实率和千粒重显著下降;遗传分析表明,sh1的裂颖表型受一对隐性核基因控制。将SH1 基因定位在ID19827与ID19884两个InDel标记之间,物理距离约为110 kb。定位区间测序发现,突变体中丙二烯氧化合酶编码基因OsAOS1发生单碱基突变,导致氨基酸发生改变;SH1基因的突变显著降低了花器官中的茉莉酸含量,进而影响了茉莉酸合成及信号转导相关基因的表达。[结论]SH1基因通过影响茉莉酸的合成和信号转导调控水稻闭颖,OsAOS1可能是 SH1基因的候选基因。

Identification and Genetic Analysis of Split Husk Mutant sh1 in Rice

【Objective】The objective of the research is to identify and clone a rice split-husk gene, providing support for elucidating the genetic mechanism of rice floret closing. 【Method】A split husk mutant, sh1, was isolated from an ethylmethylsulfone (EMS) mutagenic population of indica cultivar Xiangzaoxian 6. The morphological characteristics of florets and lodicules were observed. The SH1 gene was identified by map-based cloning using an F2 population of a cross between sh1 and 02428. In addition, expression levels of related genes were analyzed by quantitative PCR. 【Results】The sh1 mutant showed normal floral morphological characteristics, but failed to close the lemma and palea after floret opening, which was caused by delay of lodicule dehydration. The sh1 mutant was also featured by increased number of effective panicles, obviously decreased seed-setting rate and 1000-grain weight. Genetic analysis indicated that the mutant phenotype was controlled by a pair of recessive nuclear gene. The SH1 gene was fine-mapped to a 110 kb interval between markers ID19827 and ID19884 on the chromosome 3. After sequencing of this region, we found that there is a single base transition in the coding region of allene oxide synthase 1 (OsAOS1), which resulted in an amino acid substitution. Correspondingly, the mutant showed reduced content of jasmonic acid (JA) and differential expression of genes related to JA synthesis and signal transduction. 【Conclusion】The SH1 gene regulates rice floret closing through JA synthesis and signal transduction, and OsAOS1 is the candidate gene for SH1.