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Avalos, A.

Publications and source records attributed to Avalos, A..

4 recordsLinked to original sources

Metatranscriptomic Profiling Reveals Species-Level Microbial Shifts and Metabolic Remodeling in Feline Oral Inflammatory Disease

Progressive oral mucosal inflammatory diseases are common among mammals. Cats are a valuable natural model for these conditions because they frequently develop oral diseases with varying severity, yet causative microbes remain unidentified in part because longitudinal studies are challenging and sampling is difficult. The lack of individual pathobionts suggests community-scale taxonomic and functional remodeling of the microbiome may be a contributor to oral disease. This study evaluated the microbiome composition and function of 33 cats across three cohorts with different levels of inflammation: healthy, aggressive periodontitis, and feline gingivostomatitis. Ultradeep metatranscriptomic sequencing was used to assign microbial taxonomy and examine functional changes via differential gene expression analysis to reveal genera that maintained stable relative abundance across all three disease states, including Porphyromonas and Treponema, while others had more subtle shifts in species activity, including multiple members of Moraxella and Mycoplasmopsis. Disease status was marked by co-occurring changes in low activity species accompanied by microbiome-level changes in protein, arginine, and nitrogen metabolism. Cats with aggressive periodontitis and gingivostomatitis displayed microbiome shifts in species that correlated to disease state. Microbial differential expression analysis revealed induction of stress-related genes and metabolic genes involved in amino acid metabolism, polyamine production, and nitric oxide production. Together, species identification and functional profiling suggest oral inflammation was correlated to shifts in the activity of multiple species that were involved with NO and polyamines. These coordinated metabolic signatures represent potential diagnostic targets for feline oral inflammatory disease.

microbiology↗

Molecular analyses of individual variation in honey bee sociability

Individual variation in sociability is a central feature of every society. This includes honey bees, with some individuals well-connected and sociable, and others at the periphery of their colonys social network. However, the genetic and molecular bases of sociability are poorly understood. Trophallaxis - a behavior involving sharing liquid with nutritional and signaling properties - comprises a social interaction and a proxy for sociability in honey bee colonies: more sociable bees engage in more trophallaxis. Here we identify genetic and molecular mechanisms of trophallaxis-based sociability by combining genome sequencing, brain transcriptomics, and automated behavioral tracking. A genome-wide association study (GWAS) identified 18 single-nucleotide polymorphisms (SNPs) associated with variation in sociability. Several SNPs were localized to genes previously associated with sociability in other species, including in the context of human autism, suggesting shared molecular mechanisms of sociability. Variation in sociability also was linked to differential brain gene expression, particularly genes associated with neural signaling and development. Using comparative genomic and transcriptomic approaches, we also detected evidence for divergent mechanisms underpinning sociability across species, including those related to reward sensitivity and encounter probability. These results highlight both potential evolutionary conservation of the molecular roots of sociability and points of divergence.

genomics↗

Evolution of decreased aggression in honey bees targeted brain cell gene regulatory networks

Understanding how genotypic variation results in phenotypic variation, a major challenge in biology, is especially difficult for collective behaviour because collective group phenotypes arise from complex interactions between group members1. Honeybees aggressively defend their colony from attacks with highly integrated collective behaviour in which different groups of bees play specific roles, giving rise to distinct colony-level differences in aggression. A previous genome-wide association study of a population of Africanized honeybees (Apis mellifera scutellata) from Puerto Rico that recently evolved decreased aggression identified hundreds of genes with single nucleotide polymorphisms (SNPs) that associated with colony-level variation in aggression2. Many of these SNPs also showed strong signals of selection for decreased aggression2,3, but their influence on brain function was unknown. Using brain single-cell (sc) transcriptomics and sc gene regulatory network analysis, we show here that variants of these genes give rise to genetic differences in transcription factor-target gene relationships. These differences involved the activity of several TFs, some that have been previously associated with aggression, like single stranded-binding protein c31A, and some that have been associated with tissue morphogenesis but not behaviour, like apontic. The activity of these and other TFs was located in specific brain cell populations related to olfaction and vision, the two sensory modalities that bees use in colony defence. They also implicate metabolism of serotonin, a neurochemical already known to influence honeybee aggression, but not from a genetic perspective. Surprisingly, genetic differences were more pronounced in the brains of forager bees than in similarly aged but more aggressive soldier bees, pointing to an evolutionary change in division of labour for colony defence. Our results demonstrate how group genetics can shape a collective phenotype by modulating individual brain gene regulatory network architecture.

genomics↗

Parallel mechanisms of visual memory formation across distinct regions of the honey bee brain

Visual learning is vital to the behavioral ecology of the Western honey bee (Apis mellifera). Honey bee workers forage for floral resources, a behavior that requires the learning and long-term memory of visual landmarks, but how these memories are mapped to the brain remains poorly understood. To address this gap in our understanding, we collected bees that successfully learned visual associations in a conditioned aversion paradigm and compared gene expression correlates of memory formation in the mushroom bodies, a higher-order sensory integration center classically thought to contribute to learning, as well as the optic lobes, the primary visual neuropil responsible for sensory transduction of visual information. We quantitated expression of CREB and CaMKii, two classical genetic markers of learning and fen-1, a gene specifically associated with punishment learning in vertebrates. As expected, we report substantial involvement of the mushroom bodies for all three markers but additionally demonstrate an unexpected involvement of the optic lobes across a similar time course. Our findings imply the molecular involvement of a sensory neuropil during visual associative learning parallel to a higher-order brain region, furthering our understanding of how a tiny brain processes environmental signals.

animal behavior and cognition↗