Open AccessRevealing the inventory of type III effectors in Pantoea agglomerans gall‐forming pathovars using draft genome sequences and a machine‐learning approach
Author(s) -
Nissan Gal,
Gershovits Michael,
Morozov Michael,
Chalupowicz Laura,
Sessa Guido,
ManulisSasson Shulamit,
Barash Isaac,
Pupko Tal
Publication year - 2018
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12528
Subject(s) - pantoea agglomerans , biology , effector , microbiology and biotechnology , pathogenicity island , virulence , pantoea , genome , bacteria , gall , genetics , botany , gene , 16s ribosomal rna
Summary Pantoea agglomerans , a widespread epiphytic bacterium, has evolved into a hypersensitive response and pathogenicity ( hrp )‐dependent and host‐specific gall‐forming pathogen by the acquisition of a pathogenicity plasmid containing a type III secretion system (T3SS) and its effectors (T3Es). Pantoea agglomerans pv. betae ( Pab ) elicits galls on beet ( Beta vulgaris ) and gypsophila ( Gypsophila paniculata ), whereas P. agglomerans pv. gypsophilae ( Pag ) incites galls on gypsophila and a hypersensitive response (HR) on beet. Draft genome sequences were generated and employed in combination with a machine‐learning approach and a translocation assay into beet roots to identify the pools of T3Es in the two pathovars. The genomes of the sequenced Pab 4188 and Pag 824‐1 strains have a similar size (∼5 MB) and GC content (∼55%). Mutational analysis revealed that, in Pab 4188, eight T3Es (HsvB, HsvG, PseB, DspA/E, HopAY1, HopX2, HopAF1 and HrpK) contribute to pathogenicity on beet and gypsophila. In Pag 824‐1, nine T3Es (HsvG, HsvB, PthG, DspA/E, HopAY1, HopD1, HopX2, HopAF1 and HrpK) contribute to pathogenicity on gypsophila, whereas the PthG effector triggers HR on beet. HsvB, HsvG, PthG and PseB appear to endow pathovar specificities to Pab and Pag , and no homologous T3Es were identified for these proteins in other phytopathogenic bacteria. Conversely, the remaining T3Es contribute to the virulence of both pathovars, and homologous T3Es were found in other phytopathogenic bacteria. Remarkably, HsvG and HsvB, which act as host‐specific transcription factors, displayed the largest contribution to disease development.