Literature DB >> 35179614

A new NLR gene for resistance to Tomato spotted wilt virus in tomato (Solanum lycopersicum).

Shiming Qi1,2, Yuanbo Shen1,2, Xinyu Wang1,2, Shijie Zhang1,2, Yushun Li1,2, Md Monirul Islam1,2, Jin Wang1,2, Pan Zhao1,2, Xiangqiang Zhan1, Fei Zhang1, Yan Liang3,4.   

Abstract

KEY MESSAGE: A typical NLR gene, Sl5R-1, which regulates Tomato spotted wilt virus resistance, was fine mapped to a region less than 145 kb in the tomato genome. Tomato spotted wilt is a viral disease caused by Tomato spotted wilt virus (TSWV), which is a devastating disease that affects tomato (Solanum lycopersicum) production worldwide, and the resistance provided by the Sw-5 gene has broken down in some cases. In order to identify additional genes that confer resistance to TSWV, the F2 population was mapped using susceptible (M82) and resistant (H149) tomato lines. After 3 years of mapping, the main quantitative trait locus on chromosome 05 was narrowed to a genomic region of 145 kb and was subsequently identified by the F2 population, with 1971 plants in 2020. This region encompassed 14 candidate genes, and in it was found a gene cluster consisting of three genes (Sl5R-1, Sl5R-2, and Sl5R-3) that code for NBS-LRR proteins. The qRT-PCR and virus-induced gene silencing approach results confirmed that Sl5R-1 is a functional resistance gene for TSWV. Analysis of the Sl5R-1 promoter region revealed that there is a SlTGA9 transcription factor binding site caused by a base deletion in resistant plants, and its expression level was significantly up-regulated in infected resistant plants. Analysis of salicylic acid (SA) and jasmonic acid (JA) levels and the expression of SA- and JA-regulated genes suggest that SlTGA9 interacts or positively regulates Sl5R-1 to affect the SA- and JA-signaling pathways to resist TSWV. These results demonstrate that the identified Sl5R-1 gene regulates TSWV resistance by its own promoter interacting with the transcription factor SlTGA9.
© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

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Year:  2022        PMID: 35179614     DOI: 10.1007/s00122-022-04049-4

Source DB:  PubMed          Journal:  Theor Appl Genet        ISSN: 0040-5752            Impact factor:   5.699


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