Biology subjects

Caterino, M.

Publications and source records attributed to Caterino, M..

2 recordsLinked to original sources

bioRxiv2025

Host and Microbe Scale Processes Shape Spatial Variation in Aphaenogaster (Hymenoptera: Formicidae) Genetics and Their Microbiota

Like all ecological communities, host-associated (HA) microbiota are shaped by environmental selection and dispersal limitation. However, unlike communities of free-living organisms, communities of HA microbes experience selection and dispersal at two separate scales - the scale of the microbes and the scale of their hosts. Thus, HA microbes must tolerate not only the environment created by their host (microbe-scale environment), but also, the environment in which their host resides (host-scale environment). Likewise, HA microbes can disperse between hosts through either horizontal or vertical transmission (microbe-scale dispersal) but can also disperse between locations through host movement (host-scale dispersal). In this paper, we examine how multiscale environmental selection and dispersal limitation shape the genetics and HA microbiota of ants in the Aphaenogaster fulva-rudis-texana (Hymenoptera: Formicidae) complex. We begin by showing how spatial variation in Aphaenogaster genetics is shaped by host-scale environmental selection and dispersal limitation. We then show how this allows both host- and microbe-scale environmental selection to govern spatial variation in Aphaenogaster microbiota. Finally, we discuss the possibility that microbe-scale dispersal limitation also impacts spatial variation in Aphaenogaster microbiota and that this, in turn, may contribute to spatial variation in Aphaenogaster genetics. Ultimately, our results help to shed light on the myriad of interacting factors governing spatial variation in HA microbiota, including the potential for complex, bidirectional interactions between host- and microbe-scale processes.

ecology↗

bioRxiv2024

Tbx1 haploinsufficiency causes brain metabolic and behavioral anomalies in adult mice which are corrected by vitamin B12 treatment

IntroductionThe brain-related phenotypes observed in 22q11.2 deletion syndrome (22q11.2DS) are highly variable and their origin is poorly understood. Changes in brain metabolism may cause or contribute to the phenotypes, given that many of the deleted genes (approx. 10%) are implicated in metabolic processes, but this is currently unknown. It is clearly important to address this knowledge gap, but in humans, the primary material required for studying brain metabolism is inaccessible. For this reason, we sought to address the issue using two mouse models of 22q11.2DS. MethodsWe used three independent approaches to investigate brain metabolism in young adult mice, namely, mass spectrometry, nuclear magnetic resonance spectroscopy and transcriptomics. We selected to study primarily Tbx1 single gene mutants because it is the primary candidate disease gene. We then confirmed key findings in the multi-gene deletion mutant Df1/+. ResultsWe found that Tbx1 mutants have alterations of specific brain metabolites, including methylmalonic acid, which is highly brain-toxic, as well as a more general metabolomic imbalance. We provide transcriptomic evidence of an interaction genotype-vB12 treatment, and behavioural evidence of a response to vB12 treatment, which rescued some of the behavioural anomaly observed in Tbx1 mutants. We conclude that Tbx1 haploinsufficiency causes extensive brain metabolic anomalies, which are partially responsive to vB12 treatment. We suggest that alterations of glutamine-glutamate metabolism and fatty acid metabolism are key components of the metabolic phenotype in these mutants.

genetics↗