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Bacillus anthracis , the causative agent of anthrax disease, elaborates a secondary cell wall polysaccharide (SCWP) that is essential for bacterial growth and cell division.B. anthracis SCWP is comprised of trisaccharide repeats with the structure, [→4)-β-ManNAc-(1→4)-β-GlcNAc(O 3-α-Gal)-(1→6)-α-GlcNAc(O 3-α-Gal,O 4-β-Gal)-(1→]6-12 . The genes whose products promote the galactosylation ofB. anthracis SCWP are not yet known. We show here that the expression ofgalE1 , encoding a UDP-glucose 4-epimerase necessary for the synthesis of UDP-galactose, is required forB. anthracis SCWP galactosylation. ThegalE1 mutant assembles surface (S) layer and S layer-associated proteins that associate with ketal-pyruvylated SCWP via their S layer homology domains similarly to wild-typeB. anthracis , but the mutant displays a defect in γ-phage murein hydrolase binding to SCWP. Furthermore, deletion ofgalE1 diminishes the capsulation ofB. anthracis with poly-d -γ-glutamic acid (PDGA) and causes a reduction in bacterial virulence. These data suggest that SCWP galactosylation is required for the physiologic assembly of theB. anthracis cell wall envelope and for the pathogenesis of anthrax disease.IMPORTANCE Unlike virulentBacillus anthracis isolates,B. anthracis strain CDC684 synthesizes secondary cell wall polysaccharide (SCWP) trisaccharide repeats without galactosyl modification, exhibits diminished growthin vitro in broth cultures, and is severely attenuated in an animal model of anthrax. To examine whether SCWP galactosylation is a requirement for anthrax disease, we generated variants ofB. anthracis strains Sterne 34F2 and Ames lacking UDP-glucose 4-epimerase by mutating the genesgalE1 andgalE2 . We identifiedgalE1 as necessary for SCWP galactosylation. Deletion ofgalE1 decreased the poly-d -γ-glutamic acid (PDGA) capsulation of the vegetative form ofB. anthracis and increased the bacterial inoculum required to produce lethal disease in mice, indicating that SCWP galactosylation is indeed a determinant of anthrax disease.

Galactosylation of the Secondary Cell Wall Polysaccharide of Bacillus anthracis and Its Contribution to Anthrax Pathogenesis