Necrotrophism Is a Quorum-Sensing-Regulated Lifestyle in <em>Bacillus thuringiensis</em>

<div><p>How pathogenic bacteria infect and kill their host is currently widely investigated. In comparison, the fate of pathogens after the death of their host receives less attention. We studied <em>Bacillus thuringiensis</em> (<em>Bt</em>) infection of an insect host, and show that NprR, a quorum sensor, is active after death of the insect and allows <em>Bt</em> to survive in the cadavers as vegetative cells. Transcriptomic analysis revealed that NprR regulates at least 41 genes, including many encoding degradative enzymes or proteins involved in the synthesis of a nonribosomal peptide named kurstakin. These degradative enzymes are essential <em>in vitro</em> to degrade several substrates and are specifically expressed after host death suggesting that <em>Bt</em> has an active necrotrophic lifestyle in the cadaver. We show that kurstakin is essential for <em>Bt</em> survival during necrotrophic development. It is required for swarming mobility and biofilm formation, presumably through a pore forming activity. A <em>nprR</em> deficient mutant does not develop necrotrophically and does not sporulate efficiently in the cadaver. We report that necrotrophism is a highly regulated mechanism essential for the <em>Bt</em> infectious cycle, contributing to spore spreading.</p>