Characterization of Novel Anti-Programmed Cell Death human cDNA Sequences in Saccharomyces cerevisiaeVarious factors lead a cell to initiate genetically encoded forms of programmed cell death (PCD). PCD occurs as part of normal cellular processes such as homeostasis, aging, and development as well as in pathological situations such as ischemic events and Parkinson’s disease. In addition, a variety of stressors including chemicals (i.e., heavy metals), physical changes (i.e., temperature) as well as cellular damage (i.e., DNA damage) can induce PCD. Deficiencies in PCD are linked to other types of pathologies such as cancer. Ability to regulate PCD would thus have tremendous therapeutic applications. In my work, the yeast, Saccharomyces cerevisiae, was used to characterize novel negative regulators of PCD that were previously identified by screening a human heart cDNA expression library in yeast cells undergoing PCD in response to the expression of a pro-apoptotic murine Bax cDNA. My work focused on characterizing four of these human putative anti-apoptotic cDNA sequences, namely lactate dehydrogenase B (LDHB), thyroid cancer–1 (TC-1), 14-3-3β/α (YWHAB) and human ferritin (FTH1). Using spot assay and cell viability assays, I was able to show that these cDNA sequences prevent cell death due to multiple stresses including copper. In order to further examine the functions of anti-apoptotic genes in yeast, we challenged yeast heterologously expressing 14-3-3β/α with multiple stresses. My studies showed that iron and copper activate two different pathways that cross-talk in order to activate the appropriate stress specific response. 11:30-12:30 BioSci Rm. 3110Comments are closed.
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