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论文类型： 期刊论文

发表时间： 2019-01-01

发表刊物： PLANT CELL REPORTS

收录刊物： SCIE、PubMed、Scopus

卷号： 38

期号： 1

页面范围： 1-13

ISSN号： 0721-7714

关键字： MiR482b; Overexpressing; Phytophthora infestans; RNA-Seq; Tomato; Regulatory network

摘要： Key messageThe transcriptomic profile in the leaves of miR482b-overexpressing tomato plants revealed that miR482b may suppress alpha-linolenic acid metabolism, cysteine and methionine metabolism, plant-pathogen interaction, and the MAPK pathway to reduce resistance to Phytophthora infestans.AbstractOur previous study showed that tomato miR482b acted as a negative regulator during tomato resistance to Phytophthora infestans by silencing NBS-LRR genes. To investigate pathways related to miR482b, the transcriptomic profile of tomato plants that overexpressed miR482b was constructed. A total of 47,124,670 raw sequence reads from the leaves of miR482b-overexpressing tomato plants were generated by Illumina sequencing. A total of 746 genes in miR482b-overexpressing tomato plants were found to show significantly differential expression relative to those in wild-type tomato plants, including 132 up-regulated genes and 614 down-regulated genes. GO and KEGG enrichment analyses showed that plant-pathogen interaction, the MAPK pathway, and the pathways related to JA and ET biosynthesis were affected by miR482b in tomato. qRT-PCR results showed that all the enriched genes in these pathways were down-regulated in tomato plants that overexpressed miR482b and up-regulated in tomato plants that overexpressed an NBS-LRR gene (Soly02g036270.2, the target gene of miR482b). After P. infestans infection, the expression of the enriched genes showed a time-dependent response, and the genes played different roles between resistant tomato (Solanum pimpinellifolium L3708) and tomato susceptible to P. infestans (S. lycopersicum Zaofen No. 2). Our results have, therefore, demonstrated that miR482b is an important component of defense response network. This will also help to identify candidate genes involved in plant-pathogen interaction.