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AbstractHoneybees host a specialised gut microbiota composed of five ever-present bacteria, which undergo seasonal variation in their proportions. The objective of this study was to investigate how host genetics can affect the microbial composition of the honeybee gut over a 5-month sampling period. Seventy-seven colonies from eight maternal genetic lines were sampled from a breeding population located in Lombardy, Italy. The colonies have been selected since 2015 for three different traits, using isolated mating stations for reproduction. Worker bees were sampled three times: June, July and October 2021. From each colony, gut from ten worker bees were pooled, and the V3-V4 region of the 16S rRNA gene was amplified and sequenced. Statistical analyses were conducted in the R environment to assess the impact of genetic lines, timepoints, and their interaction on α-diversity and β-diversity. Results for α-diversity showed a significant effect of genetic line on the Simpson index, as well as a consistent effect of the timepoint. Specifically, genetic line H showed a lower Simpson index, and this line also produced less honey in the same years, suggesting a genetic influence on both microbiota richness and honey yield. For β-diversity, results revealed that the month of sampling had the strongest effect, while no significant differences were identified for the genetic line or their interaction.

The P-Glycoprotein is an ATP-dependent drug transponder (P-gp) encoded by the MDR1 gene, also known as ABCB1. Lack of the P-gp protein causes multidrug resistance 1 in the hematoencephalic barrier, leading to neurotoxicosis after administration of several drugs (ex: ivermectin and P-glycoprotein substates). Within this study we analyzed a 4 bp deletion mutation that causes the introduction of several stop codons that eventually lead to the premature truncation of P-gp. In the absence of mutations, the P-Gp protein binds to a variety of compounds/drugs in the endothelial cells, transporting them back into the bloodstream and consequently preventing their diffusion in the brain. The aim of the present work was to analyze the frequency of the mutant MDR1 allele in the four recognized Collie breeds (FCI; Canis familiaris). The four collie breeds analyzed where: Bearded C. (BEA), Border C. (BOR), Rough C. (ROU) and Smooth C. (SMO) for a total of 135 individuals (mean sex ratio M/F = 3/4). Allelic frequencies in the four breeds and their comparison were calculated using the SAS software. In the BEA group 100% of the subject were wt/wt, in the BOR 98.53 were wt/wt and 1.47% wt/del. In the ROU breed we recorded 16.13% wt/wt, 48.39% of wt/del and 35.48% of del/del. The tested SMO was wt/del. The differences were significantly different (P≤ 0.05), however the BEA and SMO where represented only by 5 individuals in total. No differences were recorded in frequency of mutation in tested males and females analyzing the entire population. In conclusion, our results demonstrated that notwithstanding the common phylogenetic origin of the breeds analyzed the MDR1 mutation has significant different, leading to differential risk of drug response. These results further demonstrate, that the deletion can be easily tracked in pure breed collie of the different breeds allowing the planning of selective strategies aimed to improve animal health and genetic variability in small size canine populations.