LACCASE35 enhances lignification and resistance against Pseudomonas syringae pv. actinidiae infection in kiwifruit
文献类型: 外文期刊
作者: Li, Yawei 1 ; Zhang, Dongle 1 ; Wang, Xiaojie 1 ; Bai, Fuxi 3 ; Li, Rui 4 ; Zhou, Rongrong 2 ; Wu, Shunyuan 1 ; Fang, Zemin 2 ; Liu, Wei 4 ; Huang, Lili 4 ; Liu, Pu 1 ;
作者机构: 1.Anhui Agr Univ, Sch Hort, Anhui Key Lab Hort Crop Qual Biol, Hefei 230036, Peoples R China
2.Anhui Univ, Sch Life Sci, Hefei 230039, Peoples R China
3.Hubei Acad Agr Sci, Res Inst Fruit & Tea, Wuhan 430064, Peoples R China
4.Northwest A&F Univ, Coll Plant Protect, State Key Lab Crop Stress Biol Arid Areas, Yangling 712100, Peoples R China
期刊名称:PLANT PHYSIOLOGY ( 影响因子:6.9; 五年影响因子:7.7 )
ISSN: 0032-0889
年卷期: 2025 年 197 卷 2 期
页码:
收录情况: SCI
摘要: Kiwifruit bacterial canker, a highly destructive disease caused by Pseudomonas syringae pv. actinidiae (Psa), seriously affects kiwifruit (Actinidia spp.) production. Lignin deposition in infected cells serves as a defense mechanism, effectively suppressing pathogen growth. However, the underlying process remains unclear. In this study, we determined that Psa infection leads to a significant increase in S-lignin accumulation in kiwifruit. The S/G ratio in lignin was higher in a Psa-resistant cultivar than in a Psa-sensitive cultivar. Furthermore, kiwifruit laccase 35 (AcLac35), encoding an enzyme in the lignin biosynthesis pathway with characteristic laccase activity, showed tissue-specific expression in plants and was upregulated following infection by Psa. Overexpressing AcLac35 in kiwifruit leaves resulted in greater lignin content than in wild-type leaves, leading to the formation of thicker cell walls, and also activated plant-pathogen interactions and MAPK pathways, thereby enhancing resistance against Psa infection. Yeast 1-hybrid assays, dual-LUC reporter assays, electrophoretic mobility shift assays, and transient injection experiments indicated that SQUAMOSA PROMOTER-BINDING PROTEIN-LIKE 9 (AcSPL9) can bind to the AcLac35 promoter, thereby positively regulating its expression. Moreover, overexpression of AcSPL9 increased lignin accumulation in kiwifruit leaves, enhancing resistance to Psa, while virus-induced gene silencing of AcSPL9 expression reduced this resistance. Our findings reveal the function of AsSPL9-AcLac35 in kiwifruit, providing insight into enhancing resistance against Psa in kiwifruit. The transcription factor AcSPL9 promotes expression of a laccase-encoding gene AcLac35, enhancing kiwifruit disease resistance and providing potential breeding targets for enhanced disease resistance.
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