The cellular stress response (CSR) is one of the most highly conserved mechanisms among all organisms. Cellular stress can be defined as damage or the threat of damage to proteins, macromolecules and/or DNA. The response to damage can involve cell cycle regulation, protein chaperoning, DNA repair or, if macromolecular damage is too severe, apoptotic mechanisms can be initiated. This thesis details experiments that were designed to examine the cellular response to non-lethal environmental stressors at the protein level, using two fish species as study models. Two proteins that can cause cell cycle arrest and apoptosis mechanisms were examined. Expression of the CCAAT enhancer binding protein-delta (C/EBP-δ) was examined in the zebrafish, Danio rerio, exposed to acute, non-lethal hypoxic conditions. While C/EBP-δ was expressed constitutively in control individuals during all time points, exposure to hypoxic conditions did not have a consistent significant effect on C/EBP-δ expression (two-way ANOVA, P>0.05) in zebrafish white muscle tissue. In a second study, the expression of the growth arrest and DNA damage 45-alpha protein (gadd45-α), a mediator of cell cycle arrest and perhaps apoptosis was examined in heat-stressed liver tissue of an extremely cold-adapted Antarctic fish, Trematomus bernacchii. Gadd45-α levels were higher in fish exposure to 2°C across all time points (one-way ANOVA; P<0.05). The findings in these two studies expand our understanding of the CSR and how two genes that are involved in cell cycle regulation respond to acute, non-lethal environmental stress.
|Advisor:||Buckley, Bradley A.|
|Commitee:||Eppley, Sarah M., Podrabsky, Jason E.|
|School:||Portland State University|
|School Location:||United States -- Oregon|
|Source:||MAI 51/05M(E), Masters Abstracts International|
|Subjects:||Biology, Molecular biology, Biophysics|
|Keywords:||Antarctica, Heat stress, Hypoxia, Stress, Zebrafish|
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