Microarrays are a powerful tool that allow us to take a snapshot of the current state of transcription for every gene inside of a cell.   A microarray chip is composed of synthesized genes from the yeast genome, where each spot on a microarray contains a series of around 70 nucleotides specific to that single gene. Before starting a microarray, RNA is stracted from cells and made into labeled cDNAs.  The cDNAs will specifically hybridize to the complementary genes on the microarray (National Center of Biotechnology Information).   Through the use of genetic knockouts we can analyze changes in transcription that are directly caused by genetic mutations.

  Baker's yeast or Saccharomyces cerevisiae is a model organism because of its short generation time, ease of genetic manipulation, and non-specific growth requirements it can be used to study a cell's processes in depth.  Due to common ancestry this knowledge of yeast can then be generalized to a wider variety of organisms including humans.  Our study looks specifically at oxidative stress in yeast and two genes that may help combat it are ZMS1 and ZMS2.  Knockouts of ZMS1 and ZMS2 are sensitive to oxidative stress.  Oxidative stress is problematic for cells; too many free radicals, such as hydrogen peroxide or superoxide, can cause damage to proteins, DNA and lipids. Oxidative stress has been associated with diseases such as cancer and cardiovascular disease (Bargagli et al).  Therefore it is important to understand how a cell keeps oxidative stress under control.  ZMS1 and ZMS2 are putative transcription factors with zinc finger binding motifs.  Previous studies have shown that zwf1, a gene that encodes the enzyme glucose-6-P-dehydrogenase, can suppress the phenotype of ZMS1 and ZMS2 knockouts when over expressed.  Glucose-6-P-dehydrogenase plays a key role in the Pentose Phosphate Pathway; it creates NADPH.  NADPH is used in reducing reactions throughout the oxidative stress pathway.  Theoretically in our microarray any change between ZMS2 and WT mRNA expression would be do to the lack of ZMS2 in the mutant strain. Analyzing the changes in expression will lead a better understanding of the ZMS1 and ZMS2 functions in the cell, including combating oxidative stress and its harmful effects.