Battle between Gut Bacteria, Immune System, and Cry1Ac Toxin in Plutella xylostella

Research on Bacillus thuringiensis (Bt)-pest interactions has prioritized Cry toxin receptors, with
limited attention to gut bacteria’s role in modulating Bt sensitivity.
This study identified two Enterobacter strains in Plutella xylostella with
opposing effects on Cry1Ac susceptibility. Enterobacter
hormaechei (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 Enterobacter asburiae (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.