Abstract
Vascular plant pathogens spread through the veins of the host causing systemic infections whereas non vascular pathogens are confined to infection sites and cause localized symptom development. CbsA -1,4 beta cellobiosidase is a cell wall-degrading enzyme responsible for causing vascular infection and a mutant version of it is found in non vascular infection. Here, we investigate the sequence variation and structural changes accompanying a mutant CbsA gene present in some pathovars exhibiting non vascuar infection by Xanthomonas bacteria and also chalk out the evolutionary history of the non vascular phenotype. Among X.oryaze pv oryaze and X. oryzae pv oryzicola , X.oryzicola showed a number of large scale deletions and amino acid substitutions. Protein structure of X. oryaze pv oryaze showed 12 helices and X. oryzae pv oryzicola showed missing 2 helices. X. citri pv vignicola did not show the same large scale deletions however the sequence had accumulated large variation. The non vascular phenotype may have evolved in the ancestor of X. citri, X.oryzae and X. oryzicola pathovars, but may have reverted back in X. oryzae. We elaborate that sequence and structural changes accompanying just one gene might have had a major role in the phenotypic swift from vascular to nonvascular infection. This may have implications in plant disease because vascular infecting pathogens are efficient in invading the whole body of the plant while non vascuar infection is localized.