Abstract
Major histocompatibility complex (MHC) genes determine immune repertoires and social preferences of vertebrates. Immunological regulation of microbial assemblages associated with individuals influences their sociality, and should also affect their life-history traits. We exposed Xenopus laevis tadpoles to water conditioned by adult conspecifics. Then, we analysed tadpole growth, development and survivorship as a function of MHC class I and class II peptide-binding region amino acid sequence similarities between tadpoles and frogs that conditioned the water to which they were exposed. Tadpoles approached metamorphosis earlier and suffered greater mortality when exposed to immunogenetically dissimilar frogs. The results suggest that developmental regulatory cues, microbial assemblages or both are specific to MHC genotypes. Tadpoles may associate with conspecifics with which they share microbiota to which their genotypes are well adapted.
Highlights
Pathogens and hosts are locked in antagonistic coevolution as increased fitness for one results in reduced fitness for the other
Host adaptations lag behind pathogens in this race owing to longer host generation times, hosts may be less susceptible to local pathogen repertoires to which they have had an opportunity to evolve defences [1]
We examined how tadpole development varied in response to the percentage of shared amino acids at major histocompatibility complex (MHC) class I and II loci peptide-binding region (PBR) domains [14,15] by quadratic regressions with tadpole snout–vent length (SVL) as a covariate
Summary
Pathogens and hosts are locked in antagonistic coevolution as increased fitness for one results in reduced fitness for the other. Adapted pathogens are more readily transmitted among and can be more virulent to genetically similar hosts [3]. Virulence of locally adapted microbiota may increase in new hosts [4]. Mating preferences for MHC-dissimilar partners should facilitate inbreeding avoidance and make offspring less vulnerable to disease by increasing their heterozygosity or by shuffling MHC alleles to confer protection against pathogens that successfully exploit parental genotypes [5]. Examples include communal nesting partner preferences in mice [9] and schooling preferences in tadpoles [10]. Social behaviour both influences and is influenced by the micro-organisms with which individuals live [11]
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