Biology subjects

Andrews, E. R.

Publications and source records attributed to Andrews, E. R..

3 recordsLinked to original sources

bioRxiv2026

Early resource scarcity drives persistent transcriptional changes and vascular remodeling in the female prefrontal cortex

Early childhood poverty is an environmental risk factor for psychiatric and neurodegenerative disorders, yet the cellular mechanisms by which resource scarcity produces persistent brain vulnerability remain poorly understood. The medial prefrontal cortex (mPFC), which regulates executive function and motivated behavior, is sensitive to early environmental conditions. To identify mechanisms linking early resource scarcity to lasting mPFC dysfunction, we used the rat limited bedding and nesting (LBN) model, which recapitulates key features of poverty. Prior work shows LBN disrupts mPFC-mediated behaviors in adulthood, often in a sex-specific manner. Here, we used single-nucleus RNA sequencing (snRNAseq) to identify sex- and cell-type-specific transcriptional alterations in the adult mPFC following brief postnatal LBN exposure or control housing. LBN induced more differentially expressed genes (DEGs) across multiple pyramidal neuron clusters in females than in males. Unexpectedly, the largest transcriptional changes due to LBN occurred in vascular cells in females, whereas male vascular cells exhibited no DEGs. These female-specific vascular genes were enriched for alterations of transcriptional programs regulating angiogenesis and endothelial structure. This molecular profile was orthogonally validated with 3D vascular reconstruction, revealing LBN reduced vascular coverage in the adult female mPFC, driven by decreased vessel volume and shortened vessel length, while males were unaffected. Reduced vascular coverage may constrain metabolic support to this region. The postnatal period is a critical window for vascular maturation, and, taken together, these findings identify persistent, female-specific vascular alterations as a novel and previously unrecognized mechanism through which early resource scarcity may persistently affect brain function and vulnerability.

neuroscience↗

bioRxiv2025

Microbiome evolution plays a secondary role in host rapid adaptation

Understanding how populations adapt to environmental change is a central goal in evolutionary biology. Microbiomes have been proposed as a source of heritable variation that is central to rapid adaptation in hosts, yet empirical evidence supporting this remains limited, particularly in naturalistic settings. We combined a field evolution experiment in Drosophila melanogaster exposed to an insecticide with microbiome manipulations to disentangle the contributions of host standing genetic variation and microbiome evolution to adaptation. Within three generations, independent populations rapidly and repeatedly evolved increased survivorship, a defining feature of resistance evolution. Adaptive changes in sub-lethal traits such as reproductive output, stress tolerance, and body size occurred with a delayed response following the evolution of resistance. Core microbiome taxa declined following insecticide exposure, and resistant populations evolved to house lower microbial abundances. Axenic rearing and microbiome transplant experiments demonstrated that adaptation via host standing genetic variation was the mechanism for resistance evolution. Microbiome evolution played a secondary and cryptic role in host adaptation by masking slowed development rates that evolved in resistant populations. Together, these results reinforce the primacy of adaptation occurring through selection on host standing genetic variation while also demonstrating the contributions of microbiome evolution in host adaptation. SignificanceIdentifying the mechanisms that allow organisms to adapt to environmental stress is a foundational goal in biology. Using field experimental evolution and microbiome manipulations in Drosophila melanogaster, we directly tested the relative contributions of host genomic evolution and microbiome evolution to adaptation. We found that adaptation to environmental stress occurred rapidly and repeatedly, driven primarily by selection on host standing genetic variation, with microbiome evolution acting as a secondary contributor. These findings reinforce the importance of host genetic variation in rapid adaptation and demonstrate that microbiome evolution can contribute to host evolutionary trajectories in a cryptic manner.

evolutionary biology↗

bioRxiv2024

A test for microbiome-mediated rescue via host phenotypic plasticity in Daphnia

Phenotypic plasticity is a primary mechanism by which organismal phenotypes shift in response to the environment. Host-associated microbiomes often exhibit considerable shifts in response to environmental variation and these shifts could facilitate host phenotypic plasticity, adaptation, or rescue populations from extinction. However, it is unclear how much shifts in microbiome composition contribute to host phenotypic plasticity, limiting our knowledge of the underlying mechanisms of plasticity and, ultimately, the fate of populations inhabiting changing environments. In this study, we examined phenotypic responses and microbiome composition in 20 genetically distinct Daphnia magna clones exposed to non-toxic and toxic diets containing Microcystis, a cosmopolitan cyanobacteria and common stressor for Daphnia. Daphnia exhibited significant plasticity in survival, reproduction, and population growth rates in response to Microcystis exposure. However, the effects of Microcystis exposure on the Daphnia microbiome were limited, with the primary effect being differences in abundance observed across five bacterial families. Moreover, there was no significant correlation between the magnitude of microbiome shifts and host phenotypic plasticity. Our results suggest that microbiome composition played a negligible role in driving host phenotypic plasticity or microbiome-mediated rescue. One sentence summaryDaphnia exhibits considerable plasticity in individual and population-level responses to a cosmopolitan stressor, yet shifts in microbiome composition are not correlated with the magnitude of this plasticity.

ecology↗