Ectopic expression of a truncated NLR gene from wild Arachis enhances resistance to Fusarium oxysporum

Front Plant Sci. 2024 Nov 13:15:1486820. doi: 10.3389/fpls.2024.1486820. eCollection 2024.

Abstract

Fusarium oxysporum causes devastating vascular wilt diseases in numerous crop species, resulting in substantial yield losses. The Arabidopsis thaliana-F. oxysporum f.sp. conglutinans (FOC) model system enables the identification of meaningful genotype-phenotype correlations and was applied in this study to evaluate the effects of overexpressing an NLR gene (AsTIR19) from Arachis stenosperma against pathogen infection. AsTIR19 overexpression (OE) lines exhibited enhanced resistance to FOC without any discernible phenotype penalties. To elucidate the underlying resistance mechanisms mediated by AsTIR19 overexpression, we conducted whole transcriptome sequencing of an AsTIR19-OE line and non-transgenic wild-type (WT) plants inoculated and non-inoculated with FOC using Illumina HiSeq4000. Comparative analysis revealed 778 differentially expressed genes (DEGs) attributed to transgene overexpression, while fungal inoculation induced 434 DEGs in the OE line, with many falling into defense-related Gene Ontology (GO) categories. GO and KEGG enrichment analysis showed that DEGs were enriched in the phenylpropanoid and flavonoid pathways in the OE plants. This comprehensive transcriptomic analysis underscores how AsTIR19 overexpression reprograms transcriptional networks, modulating the expression of stress-responsive genes across diverse metabolic pathways. These findings provide valuable insights into the molecular mechanisms underlying the role of this NLR gene under stress conditions, highlighting its potential to enhance resistance to Fusarium oxysporum.

Keywords: fungi; plant defense; stress; transcriptome; truncated-NLR.

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This research was supported by FAPDF (grant number 00193-00000771/2021) and The National Institute of Science and Technology (INCT) (grant numbers 465480/2014-4 and 193.001.265/2017)). AD was supported by a scholarship from CNPq (grant number 140588/2020-5). RM was supported by a fellowship from CNPq (Grant number 308165/2021-7).