Hometown:

Lake Villa, Illinois

Undergraduate Institution:

University of Iowa

Research Interests:

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder characterized by social deficits and is known to disproportionately affect males. The mechanism responsible for male vulnerability or female protection is unknown. Elucidating the molecular underpinnings of sociability could result in the development of new therapeutic targets for social deficits. Before joining the Abel lab, Pravda's work as a research intern included investigating the mechanisms of social deficits and sex differences in neurodevelopmental disorders. The lab had demonstrated basolateral amygdala (BLA) activation in C57BL/6J (B6) mice during social approach behavior. Alongside research scientist Dr. Ferri, Pravda worked on identifying the neural circuits in the BLA involved in social approach behavior using fiber photometry technology.

Research Description:

Sleep deprivation affects more than one-third of U.S adults, and its prevalence is increasing at an alarming rate. Chronic sleep loss has been associated with serious medical conditions such as cardiovascular disease, cancer, and diabetes. However, even acute bouts of sleep deprivation have been linked to cognitive deficits. Acute sleep deprivation disrupts gene expression at the level of transcription and translation. Notably, recovery sleep is sufficient to return many transcripts to their baseline levels of expression. Among the dysregulated transcripts, several components of the nonsense mediated mRNA-decay (NMD) pathway exhibit increased expression following sleep loss. Canonically, NMD has been considered a surveillance mechanism responsible for the degradation of defective mRNA transcripts, preventing the translation of faulty transcripts into potentially harmful proteins that could contribute to pathogenesis. However, emerging evidence suggests that NMD also regulates the expression of endogenous transcripts. Despite this, there is limited research exploring the involvement of NMD in the regulation of biological processes like sleep homeostasis. Our long-term objective is to identify the specific transcripts that undergo degradation after sleep loss and to gain insight into the functional implications of sleep. Our current overall objective is to investigate the post-transcriptional mechanisms that restore normal physiology that enable recovery from sleep deprivation. We hypothesize that conditions during sleep deprivation prime NMD factors to enhance degradation once translation is restored during recovery sleep, thereby normalizing gene expression and restoring homeostasis. To test this, we probe the protein abundance of core NMD factors through western blotting of hippocampal tissue obtained from sleep deprived, sleep recovered, and non-sleep deprived control animals. By developing a comprehensive understanding of how NMD influences mRNA turnover to maintain cellular and molecular homeostasis, we aim to uncover novel insights into the regulation of essential biological processes.

Awards:

• Howard Hughes Medical Institute Gilliam Fellowship, 2025-present
• Predoctoral Training Grant in the Pharmacological Sciences (NIH T32 GM144636), 2023-2025

Publications:

• Quiñones-Labernik, P., Blocklinger, K. L., Bruce, M. R., & Ferri, S. L. Excess neonatal testosterone causes male-specific social and fear memory deficits in wild-type mice. 2025. eNeuro, in press.
• Matasic, D. S., Yoon, J. Y., Haider, M., McLendon, J. M., Schmidt, M. S., Greiner, A. M., Quinones, P., Morgan, G. M., Boudreau, R., Irani, K., Brenner, C., & London, B. Modulation of the cardiac sodium channel NAV1.5 peak and late currents by NAD+precursors. J Mol Cell Cardio. 141:70-81, 2020. PMCID: PMC7234910

Outside Interests:

Pravda enjoys going on hikes with her husband and chihuahua.