CaSBP12 is implicated in pepper’s defense resistance to Phytophthora capsici infection associated with the SA signaling pathway

TL;DR

This study explores how the gene CaSBP12 helps peppers resist a harmful fungus by influencing specific defense genes and signaling pathways.

Contribution

The study reveals that CaSBP12 regulates pepper resistance to Phytophthora capsici through the salicylic acid signaling pathway.

Findings

Silencing CaSBP12 increases defense gene expression in pepper plants.

CaSBP12 influences the SA and JA signaling pathways in Arabidopsis.

CaSBP12 may regulate PR gene expression by modulating NPR1 and NPR3/NPR4.

Abstract

Pepper is a crucial vegetable crop with significant economic value, yet its yield and quality are severely affected by pepper Phytophthora Blight. Our previous research indicated that CaSBP12 negatively regulates pepper resistance to Phytophthora capsici (P. capsici) infection. However, the precise role of CaSBP12 in the defense response against P. capsici remains unclear. Thus, it is essential to investigate the defense mechanisms by which CaSBP12 contributes to pepper resistance against P. capsici infection.

In this study, silencing CaSBP12 significantly increased the expression of defense-related genes (CaBPR1, CaSAR8.2, CaDEF1, CaPO1) in CaSBP12-silenced plants compared to controls after P. capsici inoculation. Even under normal conditions, these genes exhibited higher expression levels in CaSBP12-silenced plants relative to controls. Conversely, these genes were downregulated in CaSBP12-overexpressing pepper plants under stress-free conditions. Therefore, we hypothesized that CaSBP12 mediates the P. capsici defense response through these genes. Further research involved salicylic acid (SA) and jasmonic acid (JA) signaling pathway mutants (sid2, coi1-21, coi1-22) and the NahG gene (salicylate hydroxylase, inhibiting SA accumulation in plants). Without treatment, SA pathway genes AtNPR1, AtTGA6, AtPR1, and AtSARD1 were significantly higher in CaSBP12-overexpressing Arabidopsis thaliana lines than in wild-type, while AtNPR3, AtTGA5, AtPAD4, AtNPR4, and AtNDR1 were lower. In the sid2 mutant, CaSBP12 promoted the expression of SA pathway genes except for AtPR1, which was suppressed. In coi1-21 and coi1-22 mutants, CaSBP12 promoted AtPR1 expression and suppressed the JA pathway gene AtPDF1.2. In NahG and CaSBP12 co-expression lines, SA pathway genes were higher compared to NahG-overexpressing lines, while AtPR1, AtNDR1, AtSARD1, and AtCBP60g levels were lower.

CaSBP12 may participate in plant defense responses by regulating the expression of defense-related genes. It may inhibit upstream SA signaling genes NDR1, PAD4, and EDS5 while promoting NPR1 expression and inhibiting NPR3 and NPR4, thereby regulating PR gene expression to participate in plant defense responses. These findings lay the foundation for further elucidating the molecular mechanisms of CaSBP12 in pant defense response against P. capsici infection.

The online version contains supplementary material available at 10.1186/s12870-025-07858-z.

Figures