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A putative E3 ubiquitin ligase substrate receptor degrades transcription factor SmNAC to enhance bacterial wilt resistance in eggplant

Authors :
Yan, Shuangshuang
Wang, Yixi
Yu, Bingwei
Gan, Yuwei
Lei, Jianjun
Chen, Changming
Zhu, Zhangsheng
Qiu, Zhengkun
Cao, Bihao
Source :
Horticulture Research; January 2024, Vol. 11 Issue: 1
Publication Year :
2024

Abstract

Bacterial wilt caused by Ralstonia solanacearumis a severe soil-borne disease globally, limiting the production in Solanaceae plants. SmNAC negatively regulated eggplant resistance to Bacterial wilt (BW) though restraining salicylic acid (SA) biosynthesis. However, other mechanisms through which SmNAC regulates BW resistance remain unknown. Here, we identified an interaction factor, SmDDA1b, encoding a substrate receptor for E3 ubiquitin ligase, from the eggplant cDNA library using SmNAC as bait. SmDDA1bexpression was promoted by R. solanacearuminoculation and exogenous SA treatment. The virus-induced gene silencing of the SmDDA1bsuppressed the BW resistance of eggplants; SmDDA1boverexpression enhanced the BW resistance of tomato plants. SmDDA1b positively regulates BW resistance by inhibiting the spread of R. solanacearumwithin plants. The SA content and the SA biosynthesis gene ICS1and signaling pathway genes decreased in the SmDDA1b-silenced plants but increased in SmDDA1b-overexpression plants. Moreover, SmDDB1 protein showed interaction with SmCUL4 and SmDDA1b and protein degradation experiments indicated that SmDDA1b reduced SmNAC protein levels through proteasome degradation. Furthermore, SmNAC could directly bind the SmDDA1bpromoter and repress its transcription. Thus, SmDDA1b is a novel regulator functioning in BW resistance of solanaceous crops via the SmNAC-mediated SA pathway. Those results also revealed a negative feedback loop between SmDDA1b and SmNAC controlling BW resistance.

Details

Language :
English
ISSN :
26626810 and 20527276
Volume :
11
Issue :
1
Database :
Supplemental Index
Journal :
Horticulture Research
Publication Type :
Periodical
Accession number :
ejs65202553
Full Text :
https://doi.org/10.1093/hr/uhad246