Mutations in the genetic sequences of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS CoV-2) has played a major part of the pandemic. This is evidenced by the increasing number of distinct strains that have appeared. Evaluating these mutations and their frequency within genetic sequences offers the opportunity to identify patterns that aid in increased virility for SARS CoV-2. We identified prevalent SARS CoV-2 strains in GISAID and downloaded genetic sequences from the NCBI nucleotide database. We used MAFFT (Multiple Alignment using Fast Fourier Transform) in Seaview to align SARS CoV-2 strains to the reference genome. We also built a custom python script to identify locations of mutations, and their potential effect on the proteins’ amino acid sequence. Preliminary work identified a mutation in the ORF1ab gene of the omicron strain. Part of this gene codes the typically conserved NSP-16, associated with the product 2’-O-ribose methyltransferase, an enzyme that catalyzes the transfer of a methyl group from a methyl donor molecule. The modification could affect the stability, localization, and function of RNA such as RNA splicing and post-transcriptional modification. We then generated a phylogenetic tree using BEAST/BEAuti to estimate the frequency and history of mutation across different strains. Our analysis identifies mutations accumulated over the course of the pandemic. Studying the effects of these mutations offers insights into SARS CoV-2 virology. These insights can be used to build a predictive model to aid in effective and efficient vaccine development.

Many age-related diseases in humans such as Parkinson's and Alzheimer's involve intracellular protein aggregation, but much is still unknown about the molecular mechanisms behind how this occurs. Characterizing these mechanisms is therefore important for developing effective treatments for age-related illnesses. Our work investigates the relationship between cell life span and aggregation of processing bodies (P-bodies), which are cytoplasmic ribonucleoprotein (RNP) granules that form inside cells experiencing stress and perform several molecular functions that appear to benefit cells experiencing stress. Using GFP-tagged Dcp2 as a P-body marker in S. cerevisiae and microfluidics to study single-cell lifespans, I demonstrated that P-bodies aggregated in aging cells that were not experiencing other forms of stress. P-body aggregation also correlated to the remaining lifespan of any given cell. To investigate this link further, I adjusted cytosol pH and observed a relationship between cytosolic pH and P-body aggregation rate. Slowing of P-body aggregation correlated to extension of cell lifespan. This suggests the need for additional research to determine whether there is a causal link between P-body aggregation and fatal single-cell pathogenesis and if so, whether these pathogenesis mechanisms are conserved in human cells and therefore a possible target for treatment for age-related illnesses.