4.7 Article

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

Journal

THEORETICAL AND APPLIED GENETICS
Volume 135, Issue 5, Pages 1493-1509

Publisher

SPRINGER
DOI: 10.1007/s00122-022-04049-4

Keywords

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Funding

  1. National Key Research and Development Program of China [2016YFD0101703]
  2. Key Research and Development Program of Shaanxi Province [2019ZDLNY03-05]

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The resistance gene Sl5R-1 interacts with the transcription factor SlTGA9 to regulate the SA and JA signaling pathways, providing resistance against Tomato spotted wilt virus.
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 F-2 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 F-2 population, with 1971 plants in 2020. This region encompassed 14 candidate genes, and in it was found a gene cluster consisting of three genes (S15R-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.

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