Meeghan Gray

My research interests have focused on the behavioral ecology of large mammals, particularly the interactions between males and females, especially in the context of sex and reproduction. I have always been fascinated with why individuals mate with certain individuals and how those decisions impact levels of parental investment, offspring survival, and future conflict between the sexes. The majority of my research has stemmed from management based projects that I use to examine major themes in behavioral ecology. Currently, I am studying bobcat health and presence in suburban West Reno.

Monika Gulia-Nuss

The long-term interest of my research program is to understand the biology of disease vectors to identify novel strategies for vector control and pathogen transmission. My lab focuses on two arthropod vectors of human diseases: mosquitoes and ticks. Our research spans multiple disciplines, including ecology, biochemistry and physiology, genetics, genomics, and computational biology, to investigate questions related to arthropod biology. We employ techniques that encompass molecular, cellular, and organismal levels of studies. Since setting up my lab at UNR in 2016, the most significant research contributions of my program have been 1) pioneering an embryo injection protocol for ticks, 2) the first successful use of CRISPR/Cas9-based genome editing in ticks, 3) producing the first chromosome-level genome assembly for a tick species, and 4) adapting and optimizing a RADseq protocol (Rapture) for genome-wide markers to understand population genetic structure of mosquitoes and ticks. In addition, we have recently initiated a project for the identification of biomarkers for early diagnostics of Lyme disease.

Edwin Oh

We are a research group that thrives on collaboration. Through our interactions with collaborators, public health labs, and patients we have developed a research program that interrogates the following themes:

1) Wastewater genomics and COVID-19

Wastewater testing has been used for years to investigate viral infections, to study illicit drug use, and to understand the socioeconomic status of a community based on its food consumption. While tools are in place in many states to evaluate the presence of specific viral strains, the community has not needed previously to collaborate on a global scale to standardize procedures to detect and manage COVID-19 transmission. In response to this challenge, our laboratories in Arizona, Nevada, and Washington have developed collection techniques and genomic and bioinformatic approaches to harmonize and visualize the impact of SARS-CoV-2 infection and viral mutation rates in communities populated by local citizens and international tourists. Our findings will contribute to the development of best practices in sampling and processing of wastewater samples and genomic techniques to sequence viral strains, an area required for environmental surveillance of infectious diseases, and has the strong potential to improve the clinically predictive impact of the viral genotype on patient care and vaccine utility.

2) Rare neurological conditions

An association between the 16p13.2 copy number variation deletion and seizures has suggested that a) systematic suppression of each of genes in the loci might yield similar neurological phenotypes seen in the 16p13.2 deletion; and b) such genes might be strong candidates for harboring rare pathogenic point mutations. Through these studies, we discovered USP7 as a message capable of inducing abnormal neurological activity in brain organoids, cultured neurons, and loss-of-function mouse models. Together with collaborators at the Foundation for USP7-Related Diseases (www.usp7.org), our studies are centered on the mechanism by which USP7 gene dosage and rare variants can induce pathology. In addition, we have also identified other gene loci that mimic USP7-related disorders in human and animal models.

3) Ciliary biology and neurodevelopmental conditions

Large-scale studies have begun to map the genetic architecture of Schizophrenia. We now know that the genetic contribution to this condition arises from a variety of lesions that include a) rare copy number variants (CNVs) of strong effect; b) common non-coding alleles of mild effect; and c) rare coding alleles that cluster in biological modules. The challenge that has emerged from these studies is the requirement for large sample sizes to detect significant genetic signals. These findings intimate that SZ is genetically heterogeneous and manifesting potentially as a clinically heterogeneous group of phenotypes with discrete physiological drivers. To address this challenge and to complement the ongoing sequencing effort of cross-sectional SZ, we propose to sample individuals with extreme phenotypes (i.e., resistant to treatment: TRS) to potentially discover an enrichment of causal rare variants which would have otherwise not been observed or been difficult to detect in a large, random sampling of SZ. In addition, we will focus on the role of a specific biological module, the pericentriolar material (including the centrosome, basal body, and primary cilium) and how it relates to the development of the brain and behavior through the genomic and functional dissection of PCM1.