Harsh environmental factors have continuous negative effects on plant growth and development, leading to metabolic disruption and reduced plant productivity and quality. However, filamentation temperature-sensitive H protease (FtsH) plays a prominent role in helping plants to cope with these negative impacts. In the current study, we examined the transcriptional regulation of the CaFtsH06 gene in the R9 thermo-tolerant pepper (Capsicum annuum L.) line. The results of qRT-PCR revealed that CaFtsH06 expression was rapidly induced by abiotic stress treatments, including heat, salt, and drought. The CaFtsH06 protein was localized to the mitochondria and cell membrane. Additionally, silencing CaFtsH06 increased the accumulation of malonaldehyde content, conductivity, hydrogen peroxide (H₂O₂) content, and the activity levels of superoxide dismutase and superoxide (·O₂⁻), while total chlorophyll content decreased under these abiotic stresses. Furthermore, CaFtsH06 ectopic expression enhanced tolerance to heat, salt, and drought stresses, thus decreasing malondialdehyde, proline, H₂O₂, and ·O₂⁻ contents while superoxide dismutase activity and total chlorophyll content were increased in transgenic Arabidopsis. Similarly, the expression levels of other defense-related genes were much higher in the transgenic ectopic expression lines than WT plants. These results suggest that CaFtsH06 confers abiotic stress tolerance in peppers by interfering with the physiological indices through reducing the accumulation of reactive oxygen species, inducing the activities of stress-related enzymes and regulating the transcription of defense-related genes, among other mechanisms. The results of this study suggest that CaFtsH06 plays a very crucial role in the defense mechanisms of pepper plants to unfavorable environmental conditions and its regulatory network with other CaFtsH genes should be examined across variable environments.

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.