A novel metalloproteinase virulence factor is involved in B acillus thuringiensis pathogenesis in nematodes and insects

Abstract

Summary The Gram‐positive soil bacterium B acillus thuringiensis has been developed as the leading microbial insecticide for years. The pathogenesis of B . thuringiensis requires common extracellular factors that depend on the PlcR regulon, which regulates a large number of virulence factors; however, the precise role of many of these proteins is not known. In this study, we describe the complete lifecycle of a nematicidal B . thuringiensis strain in the free living nematode C aenorhabditis elegans using in vitro and in vivo molecular techniques to follow host and bacterial effectors during the infection process. We then focus on the metalloproteinase ColB , a collagenase, which was found highly important for destruction of the intestine thereby facilitates the adaptation and colonization of B . thuringiensis in C . elegans. In vivo green fluorescent protein ( GFP ) reporter‐gene studies showed that ColB expression is highly induced and regulated by the global activator PlcR . Finally, we demonstrated that ColB also takes part in B . thuringiensis virulence in an insect model following injection and oral infection. Indeed, addition of purified ColB accelerates the action of Cry toxin proteins in insects, too . These results give novel insights into host adaptation for B . thuringiensis and other B . cereus group bacteria and highlight the role of collagenase metalloproteases to synergize infection process.

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