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A Silent Exonic Mutation in a Rice Integrin-? FG-GAP Repeat-Containing Gene Causes Male-Sterility by Affecting mRNA Splicing.


ABSTRACT: Pollen development plays crucial roles in the life cycle of higher plants. Here we characterized a rice mutant with complete male-sterile phenotype, pollen-less 1 (pl1). pl1 exhibited smaller anthers with arrested pollen development, absent Ubisch bodies, necrosis-like tapetal hypertrophy, and smooth anther cuticular surface. Molecular mapping revealed a synonymous mutation in the fourth exon of PL1 co-segregated with the mutant phenotype. This mutation disrupts the exon-intron splice junction in PL1, generating aberrant mRNA species and truncated proteins. PL1 is highly expressed in the tapetal cells of developing anther, and its protein is co-localized with plasma membrane (PM) and endoplasmic reticulum (ER) signal. PL1 encodes an integrin-? FG-GAP repeat-containing protein, which has seven ?-sheets and putative Ca2+-binding motifs and is broadly conserved in terrestrial plants. Our findings therefore provide insights into both the role of integrin-? FG-GAP repeat-containing protein in rice male fertility and the influence of exonic mutation on intronic splice donor site selection.

SUBMITTER: Zou T 

PROVIDER: S-EPMC7139555 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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A Silent Exonic Mutation in a Rice Integrin-α FG-GAP Repeat-Containing Gene Causes Male-Sterility by Affecting mRNA Splicing.

Zou Ting T   Zhou Dan D   Li Wenjie W   Yuan Guoqiang G   Tao Yang Y   He Zhiyuan Z   Zhang Xu X   Deng Qiming Q   Wang Shiquan S   Zheng Aiping A   Zhu Jun J   Liang Yueyang Y   Liu Huainian H   Wang Aijun A   Wang Lingxia L   Li Ping P   Li Shuangcheng S  

International journal of molecular sciences 20200316 6


Pollen development plays crucial roles in the life cycle of higher plants. Here we characterized a rice mutant with complete male-sterile phenotype, <i>pollen-less 1</i> (<i>pl1</i>). <i>pl1</i> exhibited smaller anthers with arrested pollen development, absent Ubisch bodies, necrosis-like tapetal hypertrophy, and smooth anther cuticular surface. Molecular mapping revealed a synonymous mutation in the fourth exon of <i>PL1</i> co-segregated with the mutant phenotype. This mutation disrupts the e  ...[more]

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