Congratulations to the Penn Genetics Postdoc Booster Prize Winners – Bradley Lukasak (Korb Lab) and Joanna Medina (Zhou lab)

Esteemed congratulations to the two inaugural winners of the Penn Genetics Postdoc Booster Prize – Bradley Lukasak (Korb Lab) and Joanna Medina (Zhou lab)!

Titles and abstracts of winners:

Bradley Lukasak – Korb lab

TRAP Multiomics: Expanding the Toolkit for Profiling of Previously Activated Neurons

Our environment has a profound impact on our behavior and overall mental health. In response, our brains undergo constant molecular changes. At the simplest level, groups of neurons respond to our environment, allowing us to form memories of events and modulate future behavior. Following activation, neurons exhibit a rapid transcriptional and translation response. To date, work in these areas has largely focused on transcriptomics and understanding the neurophysiology of these processes. In contrast, the work done on identifying proteomic and epigenomic signatures of neuronal response is limited, primarily due to technological limitations. To address this gap, we are implementing a multidisciplinary approach to develop new workflows and mouse models that illuminate the molecular basis of neuronal response. Specifically, we utilize the targeted recombination in active populations (TRAP2) mouse model to examine neurons activated during behavioral paradigms. By combining established and novel mouse models, we are creating tools to investigate the proteomic and epigenomic signatures of neuronal response.

Joanna Medina – Zhou lab

Bridging the translational gap between preclinical and clinical studies of autism

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by deficits in social communication and restrictive or repetitive behaviors. Despite affecting approximately 1% of children worldwide, effective treatments remain limited, largely due to the heterogeneity of behavioral symptoms and the poor translatability of findings from animal models to clinical applications. Addressing these challenges requires identifying quantitative and translatable biomarkers that bridge the gap between preclinical studies and clinical applications. Among the most common comorbidities in ASD are sleep and circadian disturbances, occurring in ~80% of autistic individuals, as well as sensory processing deficits, including altered auditory evoked event-related potentials (ERPs) – patterns similarly observed in animal models of ASD. We have been investigating mouse models carrying different genetic alleles of Neurexin 1 (Nrxn1), a presynaptic protein involved in neurotransmitter release. Copy number variations in NRXN1 are among the most frequently observed single-gene variants associated with ASD, and our recent systematic behavioral phenotyping of an allelic series of Nrxn1 mouse models has demonstrated its critical role in autism-related behavioral phenotypes. However, sleep, circadian rhythms, and ERPs have yet to be examined in these models. By leveraging a recently developed reversible Nrxn1 mouse model, exon 9 Flex, I am assessing the potential reversibility of ASD-relevant phenotypes in adulthood via a comprehensive battery of behavioral and neurophysiological assessments, including motor learning with low- and high-speed rotarod testing, sleep and circadian activity monitoring through EEG/EMG and Continuous Open Mouse Phenotyping of Activity and Sleep Status (COMPASS), and sensory processing evaluation via auditory ERP recordings. By integrating these approaches, my goal is to establish robust biomarkers that enhance translational research and accelerate the development of effective ASD therapies.