Genome-wide identification and expression patterns of the laccase gene family in response to kiwifruit bacterial canker infection

Autor: Zhuzhu Zhang, Youhua Long, Xianhui Yin, Weizhen Wang, Wenzhi Li, Lingli Jiang, Xuetang Chen, Bince Wang, Jiling Ma
Jazyk: angličtina
Rok vydání: 2023
Předmět:
Zdroj: BMC Plant Biology, Vol 23, Iss 1, Pp 1-15 (2023)
Druh dokumentu: article
ISSN: 1471-2229
DOI: 10.1186/s12870-023-04606-z
Popis: Abstract Background Kiwifruit bacterial canker, caused by Pseudomonas syringae pv. actinidiae (Psa), is a destructive disease worldwide. Resistance genes that respond to Psa infection urgently need to be identified for controlling this disease. Laccase is mainly involved in the synthesis of lignin in the plant cell wall and plays a prominent role in plant growth and resistance to pathogen infection. However, the role of laccase in kiwifruit has not been reported, and whether laccase is pivotal in the response to Psa infection remains unclear. Results We conducted a bioinformatics analysis to identify 55 laccase genes (AcLAC1–AcLAC55) in the kiwifruit genome. These genes were classified into five cluster groups (I–V) based on phylogenetic analysis, with cluster groups I and II having the highest number of members. Analysis of the exon–intron structure revealed that the number of exons varied from 1 to 8, with an average of 5 introns. Our evolutionary analysis indicated that fragment duplication played a key role in the expansion of kiwifruit laccase genes. Furthermore, evolutionary pressure analysis suggested that AcLAC genes were under purifying selection. We also performed a cis-acting element analysis and found that AcLAC genes contained multiple hormone (337) and stress signal (36) elements in their promoter regions. Additionally, we investigated the expression pattern of laccase genes in kiwifruit stems and leaves infected with Psa. Our findings revealed that laccase gene expression levels in the stems were higher than those in the leaves 5 days after inoculation with Psa. Notably, AcLAC2, AcLAC4, AcLAC17, AcLAC18, AcLAC26, and AcLAC42 showed significantly higher expression levels (p
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