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SCAN: Arsenic poisoning in eukaryotic cells: insights into the adaptation mechanisms of Saccharomyces cerevisiae

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Regina Menezes, Genomics and stress Laboratory

When 01 Oct, 2008 from
12:00 pm to 01:00 pm
Where Auditorium ITQB II
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Metals are of the most important environmental toxics that cause acute and chronic adverse health effects. Among these, arsenic is considered the greatest single-cause of ill-health in the world. Its ubiquity in the environment allowed the evolution of very similar defense mechanisms in organisms ranging from bacteria to man. To address the molecular mechanisms of arsenic adaptation in eukaryotic cells we take advantage of the use of the model yeast Saccharomyces cerevisiae, since that it is tractable by classical genetic techniques enabling rapid progress in molecular studies. Furthermore, yeast and metazoan genome comparative studies have proved to be an excellent tool to identify mammalian orthologs. Both yeast and mammalian cells utilize proteins that span cellular membranes, acting as pumps to reduce the cellular concentrations of arsenic to sub-toxic levels. S. cerevisiae counteract increased levels of arsenic in the environment by mediating the expression of the ACR (Arsenic Compound Resistance) cluster, composed by the genes YAP8 (ACR1), ACR2 and ACR. Yap8 is an AP-like bZIP transcription factor belonging to the YAP family (Yeast Activator Proteins) and a key regulator of the expression of the arsenate-reductase Acr2 and the plasma membrane arsenite efflux transporter Acr3. Yap1, the master regulator of the cell antioxidant defenses, contributes to arsenic stress responses by regulating the expression of a vacuolar GSH-conjugated arsenite detoxification pathway encoded by YCF1, a gene which shares a great sequence similarity with the human ATP transporter super-family genes MRP1 and CFTR1. We have recently shown that the most important role of Yap1 in arsenic adaptation is through the maintenance of the redox homeostasis disturbed by inorganic arsenic compounds. Both Yap1 and Yap8 share a common activation mechanism through nuclear accumulation and recognize the same cis-element TGATTAATAATCA in the promoter of the ACR genes. To analyze whether they use general mechanisms to transduce the stress signals to the basal transcription machinery, we are addressing the effect of mutations in specific subunits of the tail module of the mediator complex.
Post-Doc at ITQB/Genomics and Stress Laboratory under the supervision of Prof. Claudina Rodrigues-Pousada, since 01/2003
PhD – Biological Sciences: Genetics, Heinrich-Heine Düsseldorf Universitaet (HHUD) – Germany / Universidade Federal do Rio de Janeiro (UFRJ) - Brazil, 06/1997 – 03/2002
M.Sc. - Biological Sciences: Genetics – UFRJ, Brazil, 08/1994 – 03/1997
B.Sc. – Biological Sciences – UFRJ, Brazil, 08/1987 – 12/1993

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