Battle between Gut Bacteria, Immune System, and Cry1Ac Toxin in <i>Plutella xylostella</i>

Research on <i>Bacillus thuringiensis</i> (Bt)-pest interactions has prioritized Cry toxin receptors, with limited attention to gut bacteria's role in modulating Bt sensitivity. This study identified two <i>Enterobacter</i> strains in <i><i>Plutella xylostella</i></i> with opposing effects on Cry1Ac susceptibility. <i>Enterobacter hormaechei</i> (PxG15) degraded Cry1Ac protoxin and activated the proPO-AS and JNK pathway, which reduced Cry1Ac's damage to the midgut while limiting the invasion of gut bacteria into the hemolymph. Although <i>Enterobacter asburiae</i> (PxG1) rapidly activated the proPO-AS, the JNK pathway was activated in a much slower and weaker mode when compared to PxG15, which attenuated the repairing efficiency of the midgut under the treatment of Cry1Ac, leading to death resulting from sepsis from the quick invasion of gut bacteria into the hemolymph. This study illustrates the intricate interrelationships among Cry1Ac, the pest's midgut bacteria, and its immune system, offering novel insights into how gut bacteria shape pest survival following Cry1Ac exposure.