CaNAC61, CaNAC79, and CaNAC92 Act as Negative Regulators in Pepper Defense Response Against Phytophthora capsici

Phytophthora blight, caused by the oomycete pathogen Phytophthora capsici, is a devastating disease that severely constrains pepper (Capsicum annuum) production, leading to significant yield reduction and quality deterioration. Pathogen infection elicits a host immune response that involves extensive transcriptional reprogramming, during which transcription factors (TFs) act as key regulatory hubs linking upstream signaling cascades to downstream defense gene expression networks. NAC TFs represent a plant-specific gene family and play crucial roles in plant growth, development, and response to various stresses. However, the infection-responsive transcriptional dynamics and functions of NAC TFs during pepper–P. capsici interactions remain poorly elucidated. In this study, transcriptome profiling and RT-qPCR analysis of pepper plants challenged with P. capsici identified three NAC TF genes—CaNAC61, CaNAC79, and CaNAC92—that were consistently upregulated at the infection stages. Subcellular localization assays demonstrated that all these three proteins localize to the nucleus. Silencing of CaNAC61, CaNAC79, or CaNAC92 in pepper conferred enhanced resistance to P. capsici. In contrast, their transient overexpression in pepper leaves significantly promoted lesion expansion and suppressed transcript levels of the defense marker genes CaPR1, CaDEF1, and CaLOX1. Consistently, heterologous overexpression in transgenic Nicotiana benthamiana further validated CaNAC61, CaNAC79, and CaNAC92 as negative regulators in resistance to P. capsici. Collectively, our findings demonstrated that CaNAC61, CaNAC79, and CaNAC92 negatively regulate plant resistance to P. capsici, expanding the functional diversity of NAC TFs in plant immune responses and providing valuable candidate targets for genetic improvement against Phytophthora blight.