Northern Kentucky University
Exploring the Roles of the bZIP Transcription Factors Met28 and Gcn4 in Saccharomyces cerevisiae
Grade Level at Time of Presentation
Sophomore
Major
Biological Sciences
Minor
Chemistry and Honors
Institution 24-25
Northern Kentucky University
KY House District #
67
KY Senate District #
24
Faculty Advisor/ Mentor
Erin D. Strome, PhD
Department
Department of Biological Sciences
Abstract
In Saccharomyces cerevisiae, the genes SAM1 and SAM2 encode the enzyme responsible for AdoMet synthesis. Losses of these genes impacts genome stability and AdoMet levels. AdoMet regulates methionine and sulfur networks, within which bZIP transcription factors (TFs) play a role. The bZIP family of TFs are basic leucine zippers that regulate gene expression by binding to DNA and can regulate stress responses such as to oxidative stress. The SAM1 and SAM2 genes have a common bZIP TF binding site in their promoter, most strongly recognized by the bZIP TF Met28. This common region indicates that bZIP TFs play a specific role in regulating the SAM genes. To investigate this role, we created gene knockout (KO) strains for two bZIP TFs of interest: Met28 and Gcn4. We then tested these strains for reactive oxygen species (ROS), genome instability, and growth to understand the impact of bZIP TFs on the oxidative stress response and cell health. We found that the deletions of met28 and gcn4 have opposite impacts on ROS levels. The current data collected points to the possibility that the deletion of gcn4 leads to cells having less ROS than the wildtype strain while the deletion of met28 leads to cells having more ROS than the wildtype. Regarding genome stability, the current data points to gcn4 deletant strains being more stable than wildtype and the met28 deletant strain having no significant difference from the wildtype. When growth was measured it was found that the deletion of met28 led to strains growing slower compared to the wildtype and gcn4 deletant strain. This slower growth indicates that the loss of met28 negatively impacts cell health. This research indicates that the family of bZIP TFs do not all necessarily impact stress response and genome stability in the same way.
Exploring the Roles of the bZIP Transcription Factors Met28 and Gcn4 in Saccharomyces cerevisiae
In Saccharomyces cerevisiae, the genes SAM1 and SAM2 encode the enzyme responsible for AdoMet synthesis. Losses of these genes impacts genome stability and AdoMet levels. AdoMet regulates methionine and sulfur networks, within which bZIP transcription factors (TFs) play a role. The bZIP family of TFs are basic leucine zippers that regulate gene expression by binding to DNA and can regulate stress responses such as to oxidative stress. The SAM1 and SAM2 genes have a common bZIP TF binding site in their promoter, most strongly recognized by the bZIP TF Met28. This common region indicates that bZIP TFs play a specific role in regulating the SAM genes. To investigate this role, we created gene knockout (KO) strains for two bZIP TFs of interest: Met28 and Gcn4. We then tested these strains for reactive oxygen species (ROS), genome instability, and growth to understand the impact of bZIP TFs on the oxidative stress response and cell health. We found that the deletions of met28 and gcn4 have opposite impacts on ROS levels. The current data collected points to the possibility that the deletion of gcn4 leads to cells having less ROS than the wildtype strain while the deletion of met28 leads to cells having more ROS than the wildtype. Regarding genome stability, the current data points to gcn4 deletant strains being more stable than wildtype and the met28 deletant strain having no significant difference from the wildtype. When growth was measured it was found that the deletion of met28 led to strains growing slower compared to the wildtype and gcn4 deletant strain. This slower growth indicates that the loss of met28 negatively impacts cell health. This research indicates that the family of bZIP TFs do not all necessarily impact stress response and genome stability in the same way.