
Rachel Louise Moran
· ProfessorVerifiedTexas A&M University · History
Active 2013–2026
About
Rachel Louise Moran is a Professor of History at Texas A&M University. Her research focuses on health, medicine, gender, and politics in the modern United States. She is particularly interested in how political culture and institutions have influenced Americans' relationships with health and wellness, including areas such as nutrition and fitness, psychiatry, and reproductive and sexual health. Dr. Moran's first book, Governing Bodies: American Politics and the Shaping of the Modern Physique, published by the University of Pennsylvania Press in 2018, examines governmental efforts to manage and monitor citizen bodyweight throughout the 20th century. Her upcoming book, Blue: A History of Postpartum Depression in America, scheduled for publication by the University of Chicago Press in 2024, explores the history of postpartum depression diagnosis and women's activism to make postpartum suffering visible. This project also led to the creation of her Maternal Mental Health oral history collection. Dr. Moran's research has been supported by notable organizations including the National Science Foundation, the American College of Obstetricians and Gynecologists, and the Woodrow Wilson Foundation. She has received recognition for her teaching, including two university-wide awards at the University of North Texas, namely the J. H. Shelton Excellence in Teaching Award and the Teacher Scholar Award.
Research topics
- Evolutionary biology
- Genetics
- Biology
- Ecology
- Neuroscience
Selected publications
SSRN Electronic Journal · 2026-01-01
preprintOpen accessSenior authorHormones and Behavior · 2026-04-15
articleOpen accessSenior authorThe repeated evolution of parental care is often accompanied by shifts in the neural circuits and hormonal pathways that regulate motivation and aggression. Nonapeptides of the oxytocin/vasopressin family, including arginine vasotocin (AVT) in teleost fishes, modulate diverse social behaviors across vertebrates such as courtship, pair bonding, parental care, and territoriality. The mechanism behind conservation of these neuromodulators during behavioral diversification remains unclear. We used a comparative pharmacological approach across six darter species (Percidae: Etheostomatinae) by injecting either AVT, an AVT receptor antagonist (Manning's compound), or a vehicle control (saline), followed by physiological and behavioral monitoring in standardized intruder assays. AVT administration significantly increased respiration rate, quantifiable as opercular beats per minute (OBPM) across species, indicating conserved AVT-responsive physiology. In contrast, AVT-evoked aggression varied sharply among lineages: AVT robustly elevated fin flare displays in caregiving species (Etheostoma podostemone, E. nigrum, E. flabellare, and Nothonotus starnesi) and in one non-care species with intense male-male competition (N. rufilineatus), but had no effect in E. vitreum, which has secondarily lost paternal care and spawns communally. This implies that AVT signaling remains physiologically intact, but its behavioral coupling has been selectively strengthened or lost across evolutionary transitions in parental care. These results identify lineage-specific rewiring of nonapeptide control of aggression and establish a framework for cellular and molecular dissection of AVT receptor expression and circuit remodeling in the vertebrate social brain.
bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-03
articleOpen accessSimilar traits repeatedly evolve across independent populations in response to similar environmental conditions. For many repeatedly evolved traits it is unknown if populations evolve similar traits through the same or different genetic mechanisms. To address this question, we leveraged the Mexican tetra fish, Astyanax mexicanus , which has evolved repeatedly through altering many traits including reduced sleep duration, eye degeneration, and metabolic shifts to accommodate limited nutrient availability. We defined whether shared or independent genetic architecture govern the repeated evolution of sleep loss, increased food consumption, early onset adipose deposition, and eye loss in different evolutionary origins of the cavefish phenotype by using Quantitative Trait Locus (QTL) mapping across three cave x surface F2 mapping populations. We found that, among the traits evaluated, eye loss exhibits the most genetic repeatability, with ~43% of QTL shared across lineages. Sleep loss and metabolic traits (i.e., feeding, adiposity) were genetically less repeatable, with only ~25-33% of QTL shared across lineages. Next, we explored whether QTL for metabolism, eye loss, and sleep traits in cavefish co-localize in the cavefish genome and could be inherited together to facilitate potential cavefish adaptation. Although these traits have repeatedly co-evolved in cave populations, we did not find evidence for extensive genetic linkage among them. Overall, we found that genetic repeatability is a common feature in the repeated evolution of cave traits, the extent of genetic repeatability varies across cave traits, and that there is little evidence for widespread co-localization of sleep, eye loss, and metabolic traits within the genome.
Elevated DNA damage without signs of aging in the short-sleeping Mexican cavefish
eLife · 2025-11-14
articleOpen accessDysregulated sleep has widespread health consequences, including the accumulation of DNA damage. The Mexican tetra, Astyanax mexicanus , provides a powerful model to study the evolution and consequences of sleep loss. Multiple cave-adapted populations of this species have independently evolved reduced sleep compared to surface populations, yet show no obvious decline in healthspan or longevity. To examine whether evolved sleep loss is associated with DNA damage, we compared DNA damage response (DDR) and oxidative stress across populations. Cavefish exhibited elevated γH2AX in the brain and increased gut oxidative stress, consistent with chronic sleep deprivation. Following acute UV exposure, surface fish, but not cavefish, increased sleep and activated the photoreactivation repair pathway. Fibroblast cell lines derived from both populations confirmed diminished DDR and repair in cavefish, supporting an attenuated acute DNA damage response. Transcriptomic analysis revealed that many genes differentially expressed with aging in surface fish remain unchanged in cavefish, suggesting altered regulation of aging-related pathways. Together, these findings indicate that cavefish experience elevated cellular hallmarks of sleep deprivation yet exhibit resilience to its long-term consequences, highlighting an evolutionary model to investigate the mechanisms underlying sleep, DNA repair, and healthy aging.
Resetting the rules: Sex-chromosome turnover as an escape hatch for mitonuclear conflict
2025-10-08
articleOpen access1st authorCorrespondingMitochondrial and nuclear genomes must remain coadapted to sustain oxidative phosphorylation, yet their distinct inheritance often fosters conflict. Sex chromosomes are a key arena for these dynamics: by biasing co-transmission between nuclear-encoded mitochondrial (N-mt) genes and maternally inherited mtDNA, they can amplify or suppress mitonuclear incompatibilities. Existing syntheses emphasize stable XY (mammals) and ZW (birds) systems, where genomic context is conserved. In contrast, many fishes and amphibians undergo frequent shifts among XY, ZW, and polygenic or environmental sex determination, repeatedly resetting the linkage backdrop for mitonuclear interaction. I propose a comparative framework in which sex-chromosome turnover acts as an evolutionary “escape hatch” from Y- or W-linked deleterious N-mt alleles by entrapping N-mt loci into, or releasing them from, non-recombining sex-linked strata, thereby altering the sex bias and intensity of conflict through time. This hypothesis predicts cyclical pulses of hybrid dysfunction and genomic “scars’’ that record historical entrapment, offering testable predictions for when turnover entrenches versus relieves mitonuclear conflict. By integrating evidence from stable and labile vertebrate systems, this article outlines how sex-chromosome dynamics shape mitonuclear coadaptation, postzygotic isolation, and ultimately lineage diversification.
Sex chromosome turnover and mitonuclear conflict drive reproductive isolation
bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-04
preprintOpen access1st authorCorrespondingIdentifying the genetic basis of reproductive barriers is essential for understanding the origin and maintenance of biological diversity. While some hybrid incompatibilities evolve as incidental byproducts of divergence, those involving sex chromosomes and mitochondrial-nuclear interactions may arise through predictable pathways shaped by genomic conflict. Yet, the extent to which such interactions drive the evolution of reproductive barriers and speciation in natural populations remains unclear. Here, we use whole-genome resequencing in North American fishes to show that two hybridizing species possess distinct, nonhomologous sex chromosomes. These chromosomes exhibit strong associations with sex, reduced introgression in natural hybrid zones, segregation distortion in backcrosses, and an enrichment of nuclear-encoded mitochondrial genes, indicative of sex-linked mitonuclear incompatibilities. We identify a third, distinct sex chromosome in another hybridizing species, indicating repeated sex chromosome turnover within the clade. Parental crosses and genomic analyses suggest that at least one of these transitions was driven by a recessive female-determining mutation, a rare empirical example of a theoretically predicted but seldom observed mechanism of sex chromosome evolution. Together, these results link genomic architecture to hybrid dysfunction and behavioral isolation, providing strong empirical support for long-standing predictions about the role of sex-linked and cytonuclear incompatibilities in speciation.
Elevated DNA Damage without signs of aging in the short-sleeping Mexican Cavefish
eLife · 2025-02-10
preprintOpen accessAbstract Dysregulation of sleep has widespread health consequences and represents an enormous health burden. Short-sleeping individuals are predisposed to the effects of neurodegeneration, suggesting a critical role for sleep in the maintenance of neuronal health. While the effects of sleep on cellular function are not completely understood, growing evidence has identified an association between sleep loss and DNA damage, raising the possibility that sleep facilitates efficient DNA repair. The Mexican tetra fish, Astyanax mexicanus provides a model to investigate the evolutionary basis for changes in sleep and the consequences of sleep loss. Multiple cave-adapted populations of these fish have evolved to sleep for substantially less time compared to surface populations of the same species without identifiable impacts on healthspan or longevity. To investigate whether the evolved sleep loss is associated with DNA damage and cellular stress, we compared the DNA Damage Response (DDR) and oxidative stress levels between A. mexicanus populations. We measured markers of chronic sleep loss and discovered elevated levels of the DNA damage marker γH2AX in the brain, and increased oxidative stress in the gut of cavefish, consistent with chronic sleep deprivation. Notably, we found that acute UV-induced DNA damage elicited an increase in sleep in surface fish but not in cavefish. On a transcriptional level, only the surface fish activated the photoreactivation repair pathway following UV damage. These findings suggest a reduction of the DDR in cavefish compared to surface fish that coincides with elevated DNA damage in cavefish. To examine DDR pathways at a cellular level, we created an embryonic fibroblast cell line from the two populations of A. mexicanus. We observed that both the DDR and DNA repair were diminished in the cavefish cells, corroborating the in vivo findings and suggesting that the acute response to DNA damage is lost in cavefish. To investigate the long-term impact of these changes, we compared the transcriptome in the brain and gut of aged surface fish and cavefish. Strikingly, many genes that are differentially expressed between young and old surface fish do not transcriptionally vary by age in cavefish. Taken together, these findings suggest that cavefish have developed resilience to sleep loss, despite possessing cellular hallmarks of chronic sleep deprivation.
Environmental stress amplifies competitive asymmetry and drives divergent hybrid zone outcomes
bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-23
preprintOpen accessSenior authorAbstract Community persistence depends on the balance between abiotic constraints and biotic interactions. Environmental stress can either sort species by physiological limits or amplify competitive asymmetries, producing coexistence, exclusion, or collapse. We tested these alternatives in two replicate hybrid swarms between orangethroat and orangebelly darters ( Etheostoma pulchellum and E. radiosum spp. complex) with contrasting outcomes: long-term coexistence in the Blue River versus collapse in the Washita River. We combined critical-thermal-maximum (CT max ) assays with standardized feeding experiments to evaluate physiological tolerance, competitive exclusion, and stress-amplified competition. CT max varied with river, sex, and body size but not consistently between species, indicating that local history and demography outweighed intrinsic physiological differences. In contrast, competition trials revealed strong, temperature-dependent asymmetries: E. pulchellum dominated in the cooler, stable Blue River, whereas E. radiosum spp. gained a foraging advantage under high temperatures in the warmer Washita River drainage. These results support the prediction that abiotic stress amplifies competitive asymmetries, flipping dominance and explaining divergent hybrid zone outcomes. More broadly, our study links hybrid zone dynamics to coexistence theory, showing that climate extremes can shift competitive balance and determine whether secondary contact results in persistence or loss.
The effect of environmental enrichment on whole-brain gene expression in an imperiled fish
bioRxiv (Cold Spring Harbor Laboratory) · 2025-10-20
preprintOpen accessWhen hatchery-reared fish are used to augment wild populations, phenotypic mismatch caused by differences between hatchery and wild environments can limit efforts to conserve fish species at risk of extinction. Some phenotypes adapted to or induced by hatchery environments are thought to be maladapted for life in the wild. Thus, enriching the hatchery environment (abiotically and biotically) to make it more similar to the wild may induce phenotypes, including gene expression profiles, that are better suited to the environments fish will experience after release. Here, we took a molecular approach (TagSeq) to elucidate how abiotic and biotic (predator training) enrichment impacts the whole-brain gene expression of a species of conservation concern, the Arkansas darter (Etheostoma cragini), comparing the effects in two hatchery populations to a wild reference population. While we found no effect of biotic enrichment, we found that numerous genes were differentially expressed between populations and abiotic enrichment treatments. Notably, we found that expression profiles of hatchery fish more closely resembled those of wild fish when reared with abiotic enrichment. Functional analysis revealed that many differentially expressed genes were related to feeding behavior, development, and reproduction. These results have implications for conservation, supporting the management of darters at the level of the population and the use of abiotic enrichment to reduce phenotypic mismatch between hatchery and wild fish.
Population Genomics of Premature Termination Codons in Cavefish With Substantial Trait Loss
Molecular Biology and Evolution · 2025-01-21 · 6 citations
articleOpen accessLoss-of-function alleles are a pertinent source of genetic variation with the potential to contribute to adaptation. Cave-adapted organisms exhibit striking loss of ancestral traits such as eyes and pigment, suggesting that loss-of-function alleles may play an outsized role in these systems. Here, we leverage 141 whole genome sequences to evaluate the evolutionary history and adaptive potential of single nucleotide premature termination codons (PTCs) in Mexican tetra. We find that cave populations contain significantly more PTCs at high frequency than surface populations. We also find that PTCs occur more frequently in genes with inherent relaxed evolutionary constraint relative to the rest of the genome. Using SLiM to simulate PTC evolution in a cavefish population, we show that the smaller population size and increased genetic drift is sufficient to account for the observed increase in PTC frequency in cave populations without positive selection. Using CRISPR-Cas9, we show that mutation of one of these genes, pde6c, produces phenotypes in surface Mexican tetra that mimic cave-derived traits. Finally, we identify a small subset of candidate genes that contain high-frequency PTCs in cave populations, occur within selective sweeps, and may contribute to beneficial traits such as reduced energy expenditure, suggesting that a handful of PTCs may be adaptive. Overall, our work provides a rare characterization of PTCs across wild populations and finds that they may have an important role in loss-of-function phenotypes, contributing to a growing body of literature showing genome evolution through relaxed constraint in subterranean organisms.
Frequent coauthors
- 74 shared
Nicolas Rohner
- 64 shared
Alex C. Keene
- 55 shared
Erik R. Duboué
Florida Atlantic University
- 54 shared
Wesley C. Warren
University of Missouri
- 52 shared
Aakriti Rastogi
Mitchell Institute
- 51 shared
Fanning Xia
Stowers Institute for Medical Research
- 51 shared
Robert A. Kozol
St. John's University
- 51 shared
Evan Lloyd
Texas A&M University
Awards & honors
- J. H. Shelton Excellence in Teaching Award
- Teacher Scholar Award
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