Effector-mediated transcriptional rewiring resolves interbacterial conflict through conserved c-di-GMP antagonism

Area of Science:

• Microbiology
• Bacterial competition
• Evolutionary biology

Background:

• Microbial competition drives evolution of bacterial offensive and defensive strategies.
• Bacteria use secretion systems to deliver effectors, but hijacking competitor effectors is poorly understood.

Purpose of the Study:

• To investigate if bacteria can utilize competitor-derived effector proteins to resolve interspecies conflicts.
• To elucidate the mechanism by which Pseudomonas protegens hijacks the LtaE effector from Lysobacter enzymogenes.

Main Methods:

• Investigated interspecies conflict resolution in Pseudomonas protegens.
• Analyzed the hijacking of LtaE effector via type IV secretion system (T4SS).
• Utilized biochemical analyses to study LtaE-FleQ interactions and c-di-GMP binding inhibition.

Main Results:

• P. protegens hijacks LtaE to neutralize a toxin and reprogram signaling.
• LtaE binds FleQ, the flagellar master regulator, shielding it from inhibitory c-di-GMP.
• This interaction overrides sessility signals, activating flagellar gene expression and escape motility.
• LtaE broadly targets FleQ homologs, linking competitor detection to motility.

Conclusions:

• Established a novel bacterial conflict-resolution paradigm involving effector hijacking.
• Demonstrated how non-cytotoxic effectors act as molecular switches to reprogram transcriptional networks.
• Highlighted the role of effector hijacking in enhancing bacterial phenotypic plasticity and survival.