Current Scholars and Projects

      Herpes simplex virus 1 (HSV-1) is a common human pathogen that primarily causes oral sores during the lytic stage of its replication cycle. HSV-1 can significantly threaten human health, especially in immunocompromised individuals. Eye infections can lead to corneal scarring, which may cause blindness, and infections of the spinal cord or brain can lead to life-threatening conditions like herpes meningitis or encephalitis. The World Health Organization estimates that over 67% of people globally are infected with HSV-1. Current treatments reduce visible symptoms but do not eradicate the virus which lies dormant in sensory neurons. Reactivation of the virus from latency can be stimulated by stress, hormonal changes, and DNA damage, leading to further lytic replication.
      PARP14 is a host protein that has been found to have an antiviral effect against wild-type HSV-1. My project aims to determine whether PARP14 functions in a strain-specific manner by testing its impact on a more pathogenic strain of HSV-1 known as strain 17. This process involves performing plaque efficiency assays with strain 17 and five different A549 human lung carcinoma cell types (two controls and three PARP14 knockout variants). In addition, I will explore where in the viral replication cycle PARP14 exerts its inhibitory effects by using quantitative Polymerase Chain Reaction (qPCR) to measure viral mRNA transcripts and western blots to measure viral protein expression at various timepoints.
      It is expected that the results of this study will provide researchers with a better understanding of PARP14's antiviral mechanisms against HSV-1 and thus contribute to the development of potential treatments for HSV-1 infection, ultimately improving patient outcomes.

Chloroplasts are responsible for photosynthesis which requires a very different set of reactants than glucose-based metabolic systems. These reactions consequently need different import machineries for different reactants. The movement of substances in and out of the chloroplast needed to facilitate such reactions is understood to be accomplished by transmembrane beta barrels in the outer envelope. Yet to date, there is not a single chloroplast outer envelope protein that has been structurally solved and we remain unaware of the variety of proteins that participate in outer envelope import and export. Our laboratory has recently developed a computational algorithm to identify bacterial outer membrane beta barrels. Chloroplastic outer envelope beta barrels are likely related to bacterial beta barrels as chloroplasts most likely originated from a primitive prokaryotic cell that lived symbiotically within another cell. We are working to adapt our prokaryotic outer membrane beta barrel identifier for chloroplast. This will allow us to understand some sequence-based differences between bacterial and chloroplast outer membrane beta barrels, while also develop a database of chloroplast beta barrels that will further our understanding of chloroplast biology. So far, we have reimplemented a previous database of predicted chloroplast beta barrel sequences for all organisms in the kingdom Plantae. We have been able to describe important class-specific features of the 4,812 sequences of chloroplast outer envelope proteins we have collected so far. With this preliminary database, we have been able to test the performance of our computational algorithm against predicted chloroplast proteins, which will continue to give us insight on how to further modify our program for accurately predicting chloroplast beta barrels.

Chlamydia trachomatis has a characteristic biphasic developmental cycle. The signals and mechanisms that regulate it are still poorly understood. One of the signaling pathways that is believed to govern this cycle is the Rsb (Regulator of Sigma B) system. This pathway allows the cell to sense and respond to stress and starvation. This, in turn, prompts the organism to grow and develop. Because of its role in C. trachomatis' development, one of our lab's focuses is to understand this pathway's mechanisms.

In this system, several proteins interact with each other based on the phosphorylation state of an intermediate: RsbV1. This project seeks to determine the importance of RsbV1's phosphorylation state. To do so, I study a mutant form for RsbV1 called RsbV1S56A. RsbV1S56A's main feature is that it cannot be rephosphorylated during development, unlike the WT form. One of the methods used is to compare the growth of WT and mutant strains of C. trachomatis. I also examine the impact of the mutation in the organism's morphology. We expect that seeing the role of RsbV1's phosphorylation will help us better understand how the Rsb system affects C. trachomatis' development. C. trachomatis is the most prevalent sexually transmitted bacterial infection worldwide. Thus, understanding its development can help us determine better ways to combat infection.