Background 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. Results 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. Conclusions 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.

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

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2025年12月2日

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Huai-Xia Zhang,
Shuang Wu,
Yu-Ting Yang,
Abid Khan,
Chun-Hui Wu,
Fei-Fei Pan,
Bi-Hua Chen,
Xin-Zheng Li,
Bing Hu,
Zhen-Hui Gong

摘要

Background

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.

Results

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.

Conclusions

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.