Imacarae Week 11
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Contents
Purpose
- To create our team's home page and to get ourselves organized for the final project.
- To learn how to search the primary literature.
- To prepare and give a journal club presentation.
10 definitions
Research article Quantitative transciptome, proteome, and sulfur metabolite profiling of the Saccharomyces cerevisiae response to arsenitecan be found here
- Metabolite: A substance that is a product of metabolic action or that is involved in a metabolic process [1]
- Glutathione: Tripeptide: glutamylcysteinylglycine. It is an important cofactor for the enzyme glutathione peroxidase in the uptake of amino acids and participates in leucotriene synthesis [2]
- Promyelocytic leukemia: A nuclear structure (promyelocytic leukaemia body, Kremer body) containing multimers of promyelocytic leukaemia (PML) protein and a range of other nucleoproteins which assists in repair of double-strand breaks in DNA. PML protein is a RING finger motif protein that acts as a tumour suppressor and is implicated in the pathogenesis of a variety of tumours [3]
- Chelation: the combination of a metal ion with a chemical compound, forming a ring [4]
- Northern blot analysis: used to separate and identify RNA fragments; transfers RNA from an agarose gel to a nitrocellulose filter followed by probe detection [5]
- Ortholog/orthologous:genes or proteins found in different species that are so similar in their amino acid sequences that they are assumed to have originated from a single ancestral gene [6]
- Permease: a membrane-bound protein in bacteria that is responsible for transport of a specific substance in or out of the cell [7]
- Ubiquitination: the post-translational modification of one or more ubiquitin monomers (regulatory proteins) by covalent attachment [8]
- Homocysteine: a sulphur-containing amino acid that is an intermediate in the synthesis of cysteine [9]
- Hybridize: The process of forming a double stranded nucleic acid from joining two complementary strands of DNA [10]
Journal Outline
- What is the main result presented in this paper?
- Toxins, such as arsenic, will change the transcription of important genes in Saccharomyces cerevisiae cells and lead to an increase of sulfur metabolites and glutathoine levels.
- These important genes encode for survival metabolic pathways such as protein synthesis, stress defense, or redox maintenance.
- Yap1p and Met4p are essential to controlling the cells' response to arsenic exposure.
- What is the importance or significance of this work?
- What were the limitations in previous studies that led them to perform this work?
- How did they treat the yeast cells (what experiment were they doing?)
- What strain(s) of yeast did they use? Were the strain(s) haploid or diploid?
- What media did they grow them in? What temperature? What type of incubator? For how long?
- What controls did they use?
- How many replicates did they perform per treatment or timepoint?
- What method did they use to prepare the RNA, label it and hybridize it to the microarray?
- What mathematical/statistical method did they use to analyze the data?
- Are the data publicly available for download? From which web site?
- Briefly state the result shown in each of the figures and tables, not just the ones you are presenting.
- What do the X and Y axes represent?
- How were the measurements made?
- What trends are shown by the plots and what conclusions can you draw from the data?
- How does this work compare with previous studies?
- What are the important implications of this work?
- What future directions should the authors take?
- Give a critical evaluation of how well you think the authors supported their conclusions with the data they showed. Are there any major flaws to the paper?
Annotated Bibliography
- Will be done next Tuesday.
Data/files
Conclusion
Acknowledgments
References
- Thorsen, M., Lagniel, G., Kristiansson, E., Junot, C., Nerman, O., Labarre, J., & Tamás, M. J. (2007). Quantitative transcriptome, proteome, and sulfur metabolite profiling of the Saccharomyces cerevisiae response to arsenite. Physiological genomics, 30(1), 35-43. DOI: 10.1152/physiolgenomics.00236.2006