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Taylor, M. W.

Publications and source records attributed to Taylor, M. W..

4 recordsLinked to original sources

Capturing species-wide diversity of the gut microbiota and its relationship with genomic variation in the critically endangered kakapo

The gut microbiota plays an essential role in host health that has important implications for the conservation management of threatened wildlife. While factors such as diet, medication, and habitat are known to shape the microbiota, our understanding of the entirety of factors, including the complex role of the host genomic background, remains incomplete. Our research on the gut microbiota of the critically endangered k[a]k[a]p[o] (Strigops habroptilus), a flightless parrot species endemic to Aotearoa New Zealand, represents, to our knowledge, the first study to describe the gastrointestinal bacterial diversity for virtually an entire species and to assess the relationship between gut microbiota and host genomic diversity in a highly threatened population. Here we report a 16S rRNA gene-based analysis of k[a]k[a]p[o] faecal samples representing the gut microbiota for 84% of k[a]k[a]p[o] (n = 133). This survey was then leveraged with exceptional metadata to tease apart the impact of host genomic diversity and factors such as sex, diet, antibiotic treatment, disease status, habitat, and time of sampling on the k[a]k[a]p[o] gut microbiota, with sex being the only covariate significantly associated with gut microbiota diversity. We find evidence of a highly polygenic genomic architecture of the gut microbiota and further identify putative associations between gut bacterial diversity and functional biological pathways related to intestinal homeostasis, inflammation, immune response and metabolism. This improved understanding of the k[a]k[a]p[o] gut microbiota - and its relationship with host genomics - can directly benefit k[a]k[a]p[o] management and conservation by providing new insights into the role of the gut microbiome in k[a]k[a]p[o] health and disease mitigation. Overall, we anticipate that an integration of microbiome studies in conservation research and management will improve our understanding of how the concept of One Health with its implications for human, animal and environmental welfare can be achieved.

microbiology↗

Host Phylogeny Shapes Viral Transmission Networks in an Island Ecosystem

Viral transmission between host species underpins disease emergence. Both host phylogenetic relatedness and aspects of their ecology, such as species interactions and predator-prey relationships, may govern cross-species virus transmission and zoonotic risk, although their relative impact is unknown. By characterising the virome of a relatively isolated island ecological community linked through a food web we show that phylogenetic barriers result in distantly related host species sharing fewer viruses. Host ecology had a much smaller influence on overall virome composition. Network analysis revealed that hosts with a high diversity of viruses were more likely to gain new viruses, and that generalist viruses were more likely to infect new hosts. Such a highly connected ecological community heightens the risk of disease emergence, particularly among closely related species. One-Sentence SummarySequencing of an entire island virome reveals that closely related hosts have highly connected virus communities, increasing emergence risk.

microbiology↗

Effect of dietary zinc supplementation on the gastrointestinal microbiota and host gene expression in the Shank3B-/- mouse model of autism spectrum disorder

Shank genes are implicated in ~1% of people with autism and mice with Shank3 knock out mutations exhibit autism-like behaviours. Zinc deficiency and gastrointestinal problems can be common among people with autism, and zinc is a key element required for SHANK protein function and gut development. In Shank3B-/- mice, a supplementary zinc diet reverses autism behaviours. We hypothesise that dietary zinc may alter the gut microbiome, potentially affecting the gut-microbiome-brain axis, which may contribute to changes in autism-like behaviours. To test this, four types of gastrointestinal samples (ileum, caecum, colon, faecal) were collected from wild-type and knock-out Shank3B-/- mice on either control or supplemented-zinc diets. Cage, genotype and zinc diet each contributed significantly to bacterial community variation (accounting for 12.8%, 3.9% and 2.3% of the variation, respectively). Fungal diversity differed significantly between wild-type and knock-out Shank3B-/- mice on the control zinc diet, and the fungal biota differed among gut locations. RNA-seq analysis of host (mouse) transcripts revealed differential expression of genes involved in host metabolism that may be regulated by the gut microbiota and genes involved in anti-microbial interactions. By utilising the Shank3B-/- knock-out mouse model we were able to examine the influence of - and interactions between - dietary zinc and ASD-linked host genotype. These data broaden understanding of the gut microbiome in autism and pave the way towards potential microbial therapeutics for gastrointestinal problems in people with autism. ImportancePreviously, supplemental dietary zinc in the Shank3B-/- mouse model of autism spectrum disorder resulted in observations of ASD behaviours reversal; in this study we also used the Shank3B-/- mouse model to examine the influence of - and interaction between - dietary zinc and ASD-linked host genotype. Sample location along the gastrointestinal tract, genotype and zinc diet explained some of the variation in the microbiota data, with notable bacterial differences between treatment groups. Differential expression of host genes between treatment groups, including antimicrobial interaction genes and gut microbiota-regulated host metabolism genes, suggests that the interplay between gut microbes, the gastrointestinal tract and the brain may play a major role towards the observed amelioration of ASD behaviours seen previously with supplemented dietary zinc. These results widen the scope towards manipulating both dietary zinc and the microbiota itself to ameliorate ASD-related behaviours and associated gastrointestinal issues.

microbiology↗

Comparison of subtyping approaches and the underlying drivers of microbial signatures for chronic rhinosinusitis

Chronic rhinosinusitis (CRS) is a heterogeneous condition characterised by persistent sinus inflammation and microbial dysbiosis. This study aimed to identify clinically relevant sub-groups of CRS patients based on distinct microbial signatures, with a comparison to the commonly used phenotypic subgrouping approach. The underlying drivers of these distinct microbial clusters were also investigated, together with associations with epithelial barrier integrity.\n\nSinus biopsies were collected from CRS patients (n=23), and disease controls (n=8). Expression of 42 tight junction genes was evaluated using quantitative PCR, together with microbiota analysis and immunohistochemistry for measuring mucosal integrity and inflammation.\n\nCRS patients clustered into two distinct microbial sub-groups using probabilistic modelling Dirichlet (DC) multinomial mixtures. DC1 exhibited significantly reduced bacterial diversity, increased dispersion, and was dominated by Pseudomonas, Haemophilus, and Achromobacter. DC2 had significantly elevated B-cells, incidence of nasal polyps, and higher numbers of Anaerococcus, Megasphaera, Prevotella, Atopobium, and Propionibacterium. In addition, each DC exhibited distinct tight junction gene and protein expression profiles compared with controls. Stratifying CRS patients based on clinical phenotypic subtypes (absence or presence of nasal polyps (CRSsNP or CRSwNP respectively) or with cystic fibrosis (CRSwCF)) did account for a larger proportion of the variation in the microbial dataset compared with DC groupings. However, no significant differences between CRSsNP and CRSwNP cohorts were observed for inflammatory markers, beta-dispersion and alpha diversity measures.\n\nIn conclusion, both approaches used for stratifying CRS patients had benefits and pitfalls, but DC clustering did provide greater resolution when studying tight junction impairment. Future studies in CRS should give careful consideration into the patient subtyping approach used.\n\nImportanceChronic rhinosinusitis (CRS) is a major human health problem that significantly reduces quality of life. While various microbes have been implicated, there is no clear understanding of the role they play in CRS pathogenesis. Another equally important observation made for CRS patients is that the epithelial barrier in the sino-nasal cavity is defective. Finding a robust approach to subtype CRS patients would be the first step towards unravelling the pathogenesis of this heterogeneous condition. Previous work has explored stratification based on clinical presentation of the disease (with or without polyps), inflammatory markers, pathology, or microbial composition. Comparing between the different stratification approaches used in these studies has not been possible due to different cohorts, analytical methods, or sample sites used. In this study, two approaches of subtyping CRS patients were compared and the underlying drivers of the heterogeneity in CRS were also explored.

microbiology↗