Genetic and molecular characterization of determinant of six-rowed spike of barley carrying vrs1.a4

文献类型： 外文期刊

第一作者： Wang, Jin-Hui

作者： Wang, Jin-Hui;Xu, Zhen-Mei;Qiu, Xue-Bing;Li, Li-Lan;Yu, Shui-Yang;Li, Tao;Tang, Yan-Yan;Pu, Xi;Zhang, Juan-Yu;Zhang, Hai-Li;Liang, Jun-Jun;Long, Hai;Deng, Guang-Bing;Wang, Jin-Hui;Li, Wei;Tang, Ya-Wei

作者机构：

期刊名称：THEORETICAL AND APPLIED GENETICS （ 影响因子：5.699； 五年影响因子：5.565 ）

ISSN： 0040-5752

年卷期： 2021 年 134 卷 10 期

页码：

收录情况： SCI

摘要： Key message Decisive role of reduced vrs1 transcript abundance in six-rowed spike of barley carrying vrs1.a4 was genetically proved and its potential causes were preliminarily analyzed. Six-rowed spike 1 (vrs1) is the major determinant of the six-rowed spike phenotype of barley (Hordeum vulgare L.). Alleles of Vrs1 have been extensively investigated. Allele vrs1.a4 in six-rowed barley is unique in that it has the same coding sequence as Vrs1.b4 in two-rowed barley. The determinant of row-type in vrs1.a4 carriers has not been experimentally identified. Here, we identified Vrs1.b4 in two-rowed accessions and vrs1.a4 in six-rowed accessions from the Qinghai-Tibet Plateau at high frequency. Genetic analyses revealed a single nuclear gene accounting for row-type alteration in these accessions. Physical mapping identified a 0.08-cM (similar to 554-kb) target interval on chromosome 2H, wherein Vrs1 was the most likely candidate gene. Further analysis of Vrs1 expression in offspring of the mapping populations or different Vrs1.b4 and vrs1.a4 lines confirmed that downregulated expression of vrs1.a4 causes six-rowed spike. Regulatory sequence analysis found a single 'TA' dinucleotide deletion in vrs1.a4 carriers within a 'TA' tandem-repeat-enriched region similar to 1 kb upstream of the coding region. DNA methylation levels did not correspond to the expression difference and therefore did not affect Vrs1 expression. More evidence is needed to verify the causal link between the 'TA' deletion and the downregulated Vrs1 expression and hence the six-rowed spike phenotype.

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