Link to home

Two type III effectors are sufficient to transform nonpathogenic or pathogenic bacteria into host-specific gall-forming pathogens

Isaac Barash: Tel Aviv University

<div><em>Pantoea agglomerans</em> (<em>Pa</em>), a widespread commensal bacterium, has evolved into host-specific gall-forming pathogens on beet (<em>Beta vulgaris</em>) and gypsophila (<em>Gypsophila paniculata</em>) by acquisition of a plasmid-born type III secretion system (T3SS) and effectors (T3Es). The pathovar <em>Pa </em>pv. <em>betae</em> (<em>Pab</em>) elicits galls on beet and gypsophila whereas <em>Pa </em>pv. <em>gypsophilae</em> (<em>Pag</em>) elicits galls on gypsophila and a hypersensitive response (HR) on beet. HsvB and HsvG are paralogous host specific T3Es that present in both pathovars and act as transcription factors in beet and gypsophila, respectively. PthG incites virulence in gypsophila and HR on beet, whereas PseB is exclusively present in <em>Pab</em>. The cosmid pHIR11 containing the T3SS of <em>Pseudomonas syringae</em> was mobilized by triparental mating into the nonpathogenic bacteria <em>Pa</em> 3-1 and <em>Pseudomonas fluorescenc</em>e (<em>Pf</em>). HsvB, HsvG, PthG and PseB were then mobilized either individually or in various combinations into <em>Pa</em>3-1 and <em>Pf</em>, as well as into the pathogenic bacteria <em>Erwinia amylovora,</em> <em>Dickeya solani</em> and <em>Xanthomonas euvesicatoria</em>, respectively, followed by inoculation into beet and gypsophila. Results obtained indicated that the assemblage of HsvB and PseB incited galls on beet, whereas the assemblage of HsvG and PthG caused galls on gypsophila in all the tested non-pathogenic or pathogenic bacteria. Thus, different combinations of two T3Es were sufficient to elicit galls on either beet or gypsophila in a host-specific manner.</div>