水稻卷叶突变体rl76的表型和组织分析及基因定位
作者:
作者单位:

湖南农业大学农学院, 长沙 410128

作者简介:

研究方向为种子科学与技术,E-mail : 1409589858@qq.com

通讯作者:

肖应辉,研究方向为水稻遗传育种,E-mail : xiaoyh@hunau.edu.cn

中图分类号:

基金项目:

湖南省重点领域研发计划项目(2023NK2003)


Histomorphological Analysis and Gene Mapping of the Rolled Leaf Mutant rl76 in Rice
Author:
Affiliation:

Agronomy College of Hunan Agricultural University, Changsha 410128

Fund Project:

Foundation project: Key Research and Development Program Projects in Hunan Province(2023NK2003)

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    摘要:

    叶片是水稻(Oryza sativa L.)进行光合作用的主要器官,叶片形态是影响水稻群体光合效率的首要因素,不断挖掘控制叶片卷曲的基因并揭示其遗传机理,可为培育叶片适度卷曲的理想株型水稻品种提供基因资源。本研究以卷叶突变体rl76为材料,开展了农艺性状调查、叶绿素a、叶绿素b、总叶绿素、类胡萝卜素、纤维素、半纤维素和木质素含量测定及组织学分析,并用水稻GSR40K芯片技术对卷叶基因进行定位。表型鉴定发现,从分蘖期开始,突变体rl76与野生型相比,叶片极度内卷成葱状且直立,叶片卷曲指数极显著增加,株高和有效分蘖数显著降低,叶宽、剑叶长和穗长无明显差异。突变体rl76叶绿素含量显著高于野生型,类胡萝卜素含量无明显差异,纤维素含量和木质素含量均低于野生型。石蜡切片结构显示,rl76突变体叶片气腔消失、远轴面厚壁细胞发育缺陷及泡状细胞面积和个数减少。遗传分析表明卷叶性状符合不完全显性单基因遗传规律;采用水稻GSR40K芯片技术将rl76基因初步定位在第9染色体上12.179~16.436 Mb的区段;进一步利用F2群体中的949株极端卷叶植株进行精细定位,将卷叶基因定位在第9染色体上SSR标记T5904-7和T5904-9物理距离为30.26 kb的染色体区段,在该染色体区间内含有3个注释基因,其中LOC_Os09g23200是已报道控制水稻叶片卷曲的基因SLL1,因此推测rl76的卷叶表型可能是SLL1基因在发挥作用。综上所述,突变体 rl76的卷叶表型是由9号染色体上的一个不完全显性单基因通过调控泡状细胞及远轴面厚壁细胞的发育所致。

    Abstract:

    Leaves are the main organs for photosynthesis in rice (Oryza sativa L.), and leaf morphology affects the photosynthetic efficiency of rice plants. Identification of genes that control leaf curling and revealing their genetic mechanisms, could provide genetic resources for optimizing the architecture of rice varieties with moderately curled leaves. In this study, the spontaneous rolled leaf mutant rl76 was measured on their agronomic traits, content of leaf cellulose and chlorophyll, histomorphological observation was carried out as well. In addition, the rice GSR40K chip was applied to map the mutant gene rl76. At the seedling stage, there was no significant difference between the mutant rl76 and the wild type on their leaf rolling severity, both of which showed slightly rolled leaves; through the tillering to the maturity stages, the leaves of rl76 severely rolled into shallot-like shape and erect, while the leaves of wild type were flat and slightly drooping. Comparing with wild type, the leaf rolling index of rl76 increased significantly, while the plant height and effective tiller number decreased significantly, there was no significant difference on leaf width, flag leaf length and panicle length. The chlorophyll content in leaves of rl76 was significantly higher than that of the wild type, the carotenoid content did not significantly vary; nevertheless, the content of cellulose and lignin were lower in rl76 than those in the wild type. The leaf histomophology was observed by paraffin sectioning, in the leaves of rl76 mutant, the two air cavities disappeared, the development of the sclerenchymatous cells on the abaxial surface was defective, and the area and number of the bulliform cells decreased. Genetic analysis showed that the rolled leaf was determined by a single gene inheritance pattern with incomplete dominant. By use of the rice GSR40K chip, the mutant gene rl76 was preliminarily mapped within the region of 12.179-16.436 Mb on chromosome 9. With 949 plants showing severely rolled leaf in an F2 population, the gene rl76 was further fine mapped within the chromosomal segment delimiting by the SSR markers T5904-7 and T5904-9, corresponding to a physical distance of 30.26 Kb. It contains three annotation genes within this chromosomal segment, among which the gene LOC_Os09g23200 encoding SHALLOT-LIKE 1 (SLL1) has been reported, it determines leaf curling by regulating the development of leaf distal surface cells. Therefore it is speculated that the rolled leaf in the mutant rl76 may be regulated by the gene SLL1. In summary, the rolling leaf in the rl76 mutant was resulted from abnormal development of the bulliform cells and abaxial sclerenchymatous cells that were regulated by a single incompletely dominant gene on chromosome 9.

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何虎强,邓秋雨,罗丽华,等.水稻卷叶突变体rl76的表型和组织分析及基因定位[J].植物遗传资源学报,2024,25(11):1934-1944.

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  • 收稿日期:2024-02-20
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  • 在线发布日期: 2024-11-07
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