Please cite:
Barribeau SM, Schmid-Hempel P, Walser J-C, Zoller S, Berchtold M, Schmid-Hempel R, Zemp N.
More...Please cite:
Barribeau SM, Schmid-Hempel P, Walser J-C, Zoller S, Berchtold M, Schmid-Hempel R, Zemp N.. Genetic variation and microbiota in bumble bees cross-infected by different strains of C. bombi. PLoS ONE. 2023; in press .
The bumblebee Bombus terrestris is commonly infected by a trypanosomatid gut parasite Crithidia bombi. A feature of this host-parasite system is a striking degree of genetic specificity where genotypes of host are susceptible to particular genotypes of parasite. This relationship is determined, to a degree, by variation in host gene expression, however the coding genetic variation that underlies these expression differences on the part of either host or pathogen, or the relationship between genetic variation and microbial communities, has not been explored. Here we report on an extensive experiment where workers of twenty colonies of Bombus terrestris were infected by one of 20 strains of the intestinal parasite, Crithidia bombi. To elucidate the host's genetic bases of susceptibility to infection (infection intensity), we used a low-coverage (~2 x) GWAS , based on angsd, and a standard high-coverage (~15x) GWAS with a reduced set of a 8 x8 interaction matrix. The low-coverage approach remained ambiguous, but the high-coverage approach suggested that genetic variation in cell surface and adhesion processes are important, in particular, mucin, a surface mucoglycoprotein that potentially may affect parasite binding to the host gut epithelia emerged as an important candidate. As the gut bacterial community composition affects susceptibility to infection we further sequenced the gut microbial community of the same bees used in GWAS. The abundance of taxa, such as Gilliamella, Snodgrassella, or Lactobacillus, differed between susceptible and resistant microbiota, in line with earlier studies. Compared to studies of gene expression, that refer to the immediate responses to infection, our study suggests that the constitutive microbiota and binding processes at the cell surface are likely to also affect infection after the first response has run its course. We also note that a low-coverage approach may not be powerful enough to analyse such complex traits. Furthermore, testing large interactions matrices (as with the full 20 x 20 combinations) seems to blur the specific host x parasite interaction effects, likely because the outcome of an infection is a highly non-linear process dominated by individually different pathways of host defence (immune) responses.
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