Bacteriophages of the Podoviridae family often exhibit so-called depolymerases as structural components of the virion. These enzymes appear as tail spike proteins (TSPs). After specific binding to capsular polysaccharides (CPS), exopolysaccharides (EPS) or lipopolysaccharide (LPS) of the host bacteria, polysaccharide-repeating units are specifically cleaved. Finally, the phage reaches the last barrier, the cell wall, injects its DNA, and infects the cell. Recently, similar enzymes from bacteriophages of the Ackermannviridae, Myoviridae, and Siphoviridae families were also described. In this mini-review the diversity and function of phage encoded CPS-, EPS-, and LPSdegrading depolymerases is summarized. The function of the enzymes is described in terms of substrate specificity and applications in biotechnology.

Phages vB_EamP-S2 (S2) and vB_EamM-Bue1 (Bue1) infect the plant pathogen Erwinia amylovora. S2 has a genome size of 45,495 bp and belongs to the genus SP6virus.

Summary Bacteriophages are highly selective in targeting bacteria. This selectivity relies on the specific adsorption of phages to the host cell surface. In this study, a Tn5 transposon mutant library of Erwinia amylovora, the causative agent of fire blight, was screened to identify bacterial receptors required for infection by the podovirus S6. Phage S6 was unable to infect mutants with defects in the bacterial cellulose synthase operon (bcs). The Bcs complex produces and secretes bacterial cellulose, an extracellular polysaccharide associated with bacterial biofilms. Deletion of the bcs operon or associated genes (bcsA, bcsC and bcsZ) verified the crucial role of bacterial cellulose for S6 infection. Application of the cellulose binding dye Congo Red blocked infection by S6. We demonstrate that infective S6 virions degraded cellulose and that Gp95, a phage‐encoded cellulase, is involved to catalyse the reaction. In planta S6 did not significantly inhibit fire blight symptom development. Moreover, deletion of bcs genes in E. amylovora did not affect bacterial virulence in blossom infections, indicating that sole application of cellulose targeting phages is less appropriate to biologically control E. amylovora. The interplay between cellulose synthesis, host cell infection and maintenance of the host cell population is discussed.