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Insects lack the adaptive, antibody mediated responses of vertebrates, yet they possess a robust innate immune system capable of defending themselves against pathogens. Immune priming has been observed in multiple insect species, wherein exposure to a pathogen provides protection against subsequent infections by the pathogen. Heterologous immune priming has also been described, where presence of one bacterial species provides protection against another. We determined thatRhodococcus rhodnii, a gut symbiont of the kissing bugRhodnius prolixus,induces strong heterologous immune priming, while axenic bugs lacking gut bacteria are highly susceptible to pathogens. CommensalEscherichia coliprovides less robust protection.R. rhodniimust be alive within the insect as dead bacteria do not stimulate immune priming and pathogen resistance. Removal ofR. rhodniifrom the gut reduces resistance to pathogens while restoring it to axenic bugs improves pathogen resistance, though not completely. Unlike most other examples of symbiont-mediated immune priming, we find no evidence thatR. rhodniiever leaves the gut, despite activating a potent immune response in the hemocoel and fat body.R. rhodniiandE. coliactivate both the IMD and Toll pathways indicating cross-activation of the pathways, while silencing of either pathway leads to a loss of the protective effect. Several antimicrobial peptides are induced in the fat body by presence of gut bacteria. WhenE. coliis in the gut, expression of antimicrobial peptides is often higher than whenR. rhodniiis present, whileR. rhodniiinduces proliferation of hemocytes and induces a stronger melanization response thanE. coli. Hemolymph fromR. rhodniibugs has a greater ability to convert the melanin precursor DOPA to melanization products than axenic orE. coli-harboring bugs. These results demonstrate thatR. rhodnii’sbenefits to its host extend beyond nutritional provisioning, playing an important role in the host immune system. 

Hydrahas a tubular bilayered epithelial body column with a dome-shaped head on one end and a foot on the other.Hydralacks a permanent mouth: its head epithelium is sealed. Upon neuronal activation, a mouth opens at the apex of the head which can exceed the body column diameter in seconds, allowingHydrato ingest prey larger than itself. While the kinematics of mouth opening are well characterized, the underlying mechanism is unknown. We show thatHydramouth opening is generated by independent local contractions that require tissue-level coordination. We model the head epithelium as an active viscoelastic nonlinear spring network. The model reproduces the size, timescale and symmetry of mouth opening. It shows that radial contractions, travelling inwards from the outer boundary of the head, pull the mouth open. Nonlinear elasticity makes mouth opening larger and faster, contrary to expectations. The model correctly predicts changes in mouth shape in response to external forces. By generating innervated : nerve-free chimera in experiments and simulations, we show that nearest-neighbour mechanical signalling suffices to coordinate mouth opening.Hydramouth opening shows that in the absence of long-range chemical or neuronal signals, short-range mechanical coupling is sufficient to produce long-range order in tissue deformations.