“…Presumably, it was Pba enzymes that cleaved Gal side chains of RG-I since three Pba β-galactosidase/endo-β-1,4-galactanase genes were upregulated in planta ( Table S3 ) and none of plant β-galactosidase genes were upregulated during the infection, while most of them were downregulated ( Table S2 ). Such kinds of low-Gal-substituted, 50–400 kDa RG-I fragments were previously shown to prime the assemblage of bacterial emboli, forming an initial extracellular matrix that was further substituted by Pba exopolysaccharides [ 10 , 34 ]. It should be noted that the bacterial polysaccharides were unlikely to contribute to the obtained data: first, we have previously shown that the portion of bacterial polysaccharides is negligible in the whole polysaccharide pool of the infected plant [ 10 ], and second, exopolysaccharides of Pba have the specific content and proportion of monosaccharides [ 34 ], and thus, their contribution to the whole carbohydrate pool would be evident if this was the case.…”