Submitted to: Molecular Plant Microbe International Symposium
Publication Type: Abstract Only
Publication Acceptance Date: 2/6/2016
Publication Date: 7/17/2016
Citation: Burbank, L.P., Stenger, D.C. 2016. The DinJ/RelE toxin-antitoxin system suppresses virulence in Xylella fastidiosa. Molecular Plant Microbe International Symposium. Presented at the International Society for Molecular Plant-Microbe Interactions XVII Congress, July 17-21, 2016, Portland, OR
Technical Abstract: Xylella fastidiosa, the causal agent of a number agriculturally important plant diseases, encodes multiple toxin-antitoxin (TA) systems. TA modules consist of a toxin protein co-expressed with a specific antitoxin, and are often acquired through horizontal gene transfer. Antitoxin molecules (RNA or protein) are generally unstable and require continued synthesis to neutralize existing toxin molecules. TA systems function as plasmid stability elements and, in some cases, contribute to growth regulation, biofilm development, and cell dormancy. Xf toxin RelE is an endoribonuclease which is inhibited by antitoxin DinJ. A knockout mutant of DinJ/RelE ('dinJ/relE) in Xf strain Stag’s Leap exhibits faster and more severe symptom development in inoculated grapevines, although in vitro growth rate is unaffected. There is evidence that some TA systems perform specific regulatory functions in addition to the general growth arrest caused by unbound toxin molecules. In Xf, expression of csp1 (encoding an RNA chaperone which is important for virulence) is increased in 'dinJ/relE. RNA degradation by RelE in vitro is enhanced by addition of purified Csp1, possibly due to reduction in RNA secondary structure by Csp1 binding activity. It is possible that the DinJ/RelE TA system plays a role in gene expression control during infection of the plant host, in part through regulation of Csp1 chaperone activity. Exploring the broader functions of chromosomally encoded TA systems during plant colonization will provide valuable insight into the growth dynamics of Xf during the infection process.