Canker disease caused by Pseudomonas syringae pv. actinidiae (Psa) is a severe bacterial infection threatening global kiwifruit production. Psa causes lignin degradation, cell wall rupture, leaf wilting, and canker formation on branches and trunks, often leading to plant death. The plant cell wall serves as a structural barrier against pathogens, with its thickness, composition, and cell density influencing disease resistance. Comparative studies between resistant germplasms Actinidia eriantha "Maohuaxiong" (A. eriantha 'MHX') and Actinidia latifolia "Kuoye" (A. latifolia 'KY') and susceptible cultivars Actinidia chinensis "Hongyang" (A. chinensis 'HY') and "Donghong" (DH) indicate that the resistant lines developed smaller lesions and slower disease progression after Psa infection, compared with susceptible cultivars. Histological and biochemical analyses revealed that "MHX" and "KY" had denser mesophyll cells and higher lignin deposition. Transcriptomic analysis and transient overexpression screening identified AcLFYL1 as a positive regulator of Psa resistance. AcLFYL1 overexpression increased cell density, lignin content, and disease resistance, while RNAi silencing produced the opposite phenotypes. Yeast one-hybrid, dual-luciferase reporter, and ChIP-qPCR assays confirmed that AcLFYL1 directly activates AcCSE, a key gene in lignin biosynthesis. Consistent with this, overexpression of AcCSE similarly increased cell density and lignin content and improved Psa resistance, whereas knockdown of AcCSE in both wild-type (WT) and AcLFYL1 overexpression lines significantly reduced lignin accumulation and compromised disease resistance. These findings demonstrate that AcLFYL1 enhances resistance by promoting lignin biosynthesis and increasing mesophyll cell density through direct regulation of AcCSE, offering valuable genetic targets for breeding Psa-resistant kiwifruit varieties.
Song et al. (Mon,) studied this question.