# ZmNLR-7-Mediated Synergistic Regulation of ROS, Hormonal Signaling, and Defense Gene Networks Drives Maize Immunity to Southern Corn Leaf Blight

**Authors:** Bo Su, Xiaolan Yang, Rui Zhang, Shijie Dong, Ying Liu, Hubiao Jiang, Guichun Wu, Ting Ding

PMC · DOI: 10.3390/cimb47070573 · 2025-07-21

## TL;DR

This study shows how the ZmNLR-7 gene helps maize resist southern corn leaf blight by regulating stress responses and immune signals.

## Contribution

The study provides the first evidence that ZmNLR-7 confers resistance to southern corn leaf blight through synergistic regulation of ROS and defense genes.

## Key findings

- ZmNLR-7 mutants showed increased susceptibility to southern corn leaf blight with higher disease indices.
- ZmNLR-7 regulates ROS homeostasis and SA/ET signaling, impacting disease resistance in maize.
- Transcriptomic analysis revealed inhibited expression of key defense genes in ZmNLR-7 mutants.

## Abstract

The rapid evolution of pathogens and the limited genetic diversity of hosts are two major factors contributing to the plant pathogenic phenomenon known as the loss of disease resistance in maize (Zea mays L.). It has emerged as a significant biological stressor threatening the global food supplies and security. Based on previous cross-species homologous gene screening assays conducted in the laboratory, this study identified the maize disease-resistance candidate gene ZmNLR-7 to investigate the maize immune regulation mechanism against Bipolaris maydis. Subcellular localization assays confirmed that the ZmNLR-7 protein is localized in the plasma membrane and nucleus, and phylogenetic analysis revealed that it contains a conserved NB-ARC domain. Analysis of tissue expression patterns revealed that ZmNLR-7 was expressed in all maize tissues, with the highest expression level (5.11 times) exhibited in the leaves, and that its transcription level peaked at 11.92 times 48 h post Bipolaris maydis infection. Upon inoculating the ZmNLR-7 EMS mutants with Bipolaris maydis, the disease index was increased to 33.89 and 43.33, respectively, and the lesion expansion rate was higher than that in the wild type, indicating enhanced susceptibility to southern corn leaf blight. Physiological index measurements revealed a disturbance of ROS metabolism in ZmNLR-7 EMS mutants, with SOD activity decreased by approximately 30% and 55%, and POD activity decreased by 18% and 22%. Moreover, H2O2 content decreased, while lipid peroxide MDA accumulation increased. Transcriptomic analysis revealed a significant inhibition of the expression of the key genes NPR1 and ACS6 in the SA/ET signaling pathway and a decrease in the expression of disease-related genes ERF1 and PR1. This study established a new paradigm for the study of NLR protein-mediated plant immune mechanisms and provided target genes for molecular breeding of disease resistance in maize. Overall, these findings provide the first evidence that ZmNLR-7 confers resistance to southern corn leaf blight in maize by synergistically regulating ROS homeostasis, SA/ET signal transduction, and downstream defense gene expression networks.

## Linked entities

- **Genes:** NPR1 (natriuretic peptide receptor 1) [NCBI Gene 4881], acs-6 (fatty Acid CoA Synthetase family) [NCBI Gene 174156], ZFP36L1 (ZFP36 like 1 zinc finger CCCH-type) [NCBI Gene 677], TMEM37 (transmembrane protein 37) [NCBI Gene 140738]
- **Chemicals:** POD (PubChem CID 4369314), H2O2 (PubChem CID 784), MDA (PubChem CID 1614)
- **Species:** Bipolaris maydis (taxon 5016)

## Full-text entities

- **Genes:** PR1 [NCBI Gene 542352], POD [NCBI Gene 100384480], ERF1 [NCBI Gene 542184]
- **Diseases:** Southern Corn Leaf Blight (MESH:D002145), Bipolaris maydis infection (MESH:D007239)
- **Chemicals:** MDA (MESH:D015104), SA (MESH:D000077145), lipid peroxide (MESH:D008054), H2O2 (MESH:D006861), ROS (-)
- **Species:** Bipolaris maydis (southern corn leaf blight pathogen, species) [taxon 5016], Zea mays (maize, species) [taxon 4577]

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12293289/full.md

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Source: https://tomesphere.com/paper/PMC12293289