Responsiveness of different citrus genotypes to the Xanthomonas citri ssp. citri‐derived pathogen‐associated molecular pattern (PAMP) flg22 correlates with resistance to citrus canker. (27th October 2014)

• Record Type: Journal Article
• Authors: Shi, Qingchun; Febres, Vicente J.; Jones, Jeffrey B.; Moore, Gloria A.
• Is Part Of: Molecular plant pathology. Volume 16:Number 5(2015:Jun.)
• Page Start: 507
• Page End: 520
• Publication Date: 2014-10-27
• Subjects: Plant diseases -- Molecular aspects -- Periodicals; Plant-pathogen relationships -- Molecular aspects -- Periodicals; 571.936
• DOI: 10.1111/mpp.12206
• Languages: English
• ISSNs: 1464-6722

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>The bacterial agent of citrus canker disease (<italic>Xanthomonas citri</italic> ssp. <italic>citri</italic>, <italic>Xcc</italic>) has caused tremendous economic losses to the citrus industry around the world. Pathogen‐associated molecular pattern (PAMP)‐triggered immunity (PTI) is important to plant immunity. In this study, we compared the defence responses of citrus canker‐resistant and citrus canker‐susceptible genotypes to the <italic>Xcc</italic>‐derived PAMP flg22 (Xflg22) by analysing the expression of 20 citrus defence‐associated genes. We showed that, in the most resistant genotype, 'Nagami' kumquat, there was significant induction of several defence genes (<italic>EDS1</italic>, <italic>NDR1</italic>, <italic>PBS1</italic>, <italic>RAR1</italic>, <italic>SGT1</italic>, <italic>PAL1</italic>, <italic>NPR2</italic> and <italic>NPR3</italic>) as early as 6 h and up to 72 h after Xflg22 treatment. At the other end of the spectrum, highly susceptible 'Duncan' grapefruit showed no induction of the same defence genes, even 120 h after treatment. Citrus genotypes with partial levels of resistance showed intermediate levels of transcriptional reprogramming that correlated with their resistance level. Xflg22 also triggered a rapid oxidative burst in all genotypes which was higher and accompanied by the induction of PTI marker genes (<italic>WRKY22</italic> and <italic>GST1</italic>) only in the more resistant genotypes. Pretreatment with Xflg22 prior to <italic>Xcc</italic> inoculation inhibited bacterial growth in kumquat, but not in grapefruit. A flagellin‐deficient <italic>Xcc</italic> strain (<italic>XccΔfliC</italic>) showed greater growth increase relative to wild‐type <italic>Xcc</italic> in kumquat than in grapefruit. Taken together, our results indicate that Xflg22 initiates strong PTI in canker‐resistant genotypes, but not in susceptible ones, and that a robust induction of PTI is an important component of citrus resistance to canker.</p> </abstract>