Biology subjects

Dean, M. D.

Publications and source records attributed to Dean, M. D..

3 recordsLinked to original sources

bioRxiv2024

Sexual size dimorphism correlates with the number of androgen response in mammals, but only in small-bodied species

Sexual size dimorphism (SSD) is common throughout the animal kingdom. "Renschs Rule" was proposed nearly 80 years ago, named for the observation that the magnitude of SSD in male-larger species increased with average body size. Here we re-examine this trend across 268 mammalian species with full genome assemblies and annotations, and place the evolution of SSD in the context of androgen response elements or estrogen response elements, the DNA motifs to which sex hormone receptors bind. Hormone receptors provide intuitive mechanisms for sex-specific regulation of the genome and could greatly impact SSD. We find that the three relatively large-bodied lineages (orders Carnivora, Cetartiodactyla, and Primates) follow Renschs Rule, and SSD does not correlate with the number of receptor elements. In contrast, SSD in small-bodied lineages (Chiroptera and Rodentia) correlates with the number of androgen response elements, but SSD does not correlate with overall body size. One hypothesis to unify our observations is that small-bodied organisms like bats and rodents tend to reach peak reproductive fitness quickly and are more reliant on hormonal signaling to achieve SSD over relatively short time periods. Our study uncovers a previously unappreciated relationship between SSD, body size, and hormone signaling that likely varies in ways related to life history.

evolutionary biology↗

bioRxiv2024

GPSA2: combining landmark-free and landmark-based methods in geometric morphometrics

Geometric Morphometrics (GM) revolutionized the way that biologists quantify shape variation among individuals, populations, and species. Traditional GM methods are based on homologous landmarks that can be reliably identified across all specimens in a sample. However, landmark-based studies are limited by the intensive labor required of anatomical experts, and regions of interest are often devoid of landmarks. These limitations inspired the development of many "landmark-free" approaches, but unreliable homology estimation and complicated underlying mathematical bases can make biological interpretation challenging. Here we present GPSA2, a novel method for analyzing surface meshes that combines landmark-based and landmark-free methodology within the familiar framework of Generalized Procrustes Analysis. In a major innovation, our method can incorporate user-defined landmarks into otherwise landmark-free analysis by transforming the landmarks into pointwise shape descriptors that are exploited during iterative homology estimation and superimposition (i.e. "alignment" of objects). GPSA2 also addresses a longstanding issue in morphometrics - the impact of variability in the distribution of sampled points over an object - by introducing a surface area-weighted shape distance metric and superimposition cost function. The improved homology approximation, together with the application of Taubin smoothing and an optional resistant-fit superimposition technique, ensure robust analysis even when a dataset exhibits regions of intense shape variation. We apply GPSA2 to two empirical datasets: 15 primate skulls and 369 mouse bacula. Our analyses show that inclusion of landmarks increases biological accuracy, and that GPSA2 produces summaries of shape variation that are easy to visualize and interpret.

bioinformatics↗

bioRxiv2022

Complex genetics cause and constrain fungal persistence in different parts of the mammalian body

Determining how genetic polymorphisms enable certain fungi to persist in mammalian hosts can improve understanding of opportunistic fungal pathogenesis, a source of substantial human morbidity and mortality. We examined the genetic basis of fungal persistence in mice using a cross between a clinical isolate and the lab reference strain of the budding yeast Saccharomyces cerevisiae. Employing chromosomally-encoded barcodes, we tracked the relative abundances of 822 genotyped, haploid segregants in multiple organs over time and performed linkage mapping of their persistence in hosts. Detected loci showed a mix of general and antagonistically pleiotropic effects across organs. General loci showed similar effects across all organs, while antagonistically pleiotropic loci showed contrasting effects in the brain and the kidneys, liver, and spleen. Persistence in an organ required both generally beneficial alleles and organ-appropriate pleiotropic alleles. This genetic architecture resulted in many segregants persisting in the brain or in non-brain organs, but few segregants persisting in all organs. These results show complex combinations of genetic polymorphisms collectively cause and constrain fungal persistence in different parts of the mammalian body.

genetics↗