Haynes:LitReviewNov2015

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JOURNAL ASSIGNMENTS:

JOURNAL WEBSITE Assigned to…
ACS Synthetic Biology http://pubs.acs.org/journal/asbcd6 Rene D.
Cell http://www.cell.com Ben N.
EMBO Molecular Systems Biology http://msb.embopress.org Daniel V.
Frontiers in Bioengineering and Biotechnology http://journal.frontiersin.org/journal/bioengineering-and-biotechnology David B.
Journal of Biological Engineering http://www.jbioleng.org Ben N.
Journal of Cell Biology http://jcb.rupress.org David T.
Molecular Biology of the Cell http://www.molbiolcell.org David B.
Molecular and Cellular Biology http://mcb.asm.org Rene D.
Nature http://www.nature.com/nature/index.html Ted K.
Nature Biotechnology http://www.nature.com/nbt/index.html Stefan T.
Nature Methods http://www.nature.com/nmeth/index.html Jan S.
Public Library of Science Biology (PLoS Biology) http://journals.plos.org/plosbiology/ Jiaqi W.
Proceedings of the National Academy of Sciences http://www.pnas.org Jan S.
Science http://www.sciencemag.org/journals Stefan T.
Miscellaneous Reviews and Media N/A Dr. Haynes


INSTRUCTIONS

  • Search for lab-relevant articles dated May 2015 up to today. You can use PubMed or go directly to the journal's website.
  • Be prepared to give a 3-minute summary of why the article should be read by the group.
  • Use the following text format EXACTLY as it is shown in the example below...

# (2011) Engineering a Photoactivated Caspase-7 for Rapid Induction of Apoptosis. Evan Mills, Xi Chen, Elizabeth Pham, Stanley Wong, and Kevin Truong et al. ACS Synthetic Biology, 1.3:75-82. Link.
Summary: A group from University of Toronto developed a protein that causes rapid apotosis (cell death) of targeted cells.

  • Open edit mode and THEN copy the template that is shown below. Do not use keyboard line returns to space out the numbered list, or else each item will start with the number 1.
# (year) Title. Author One, Author Two, and Author Three et al. Journal. Volume:pages. Link. 
Summary: Very short explanation of why this paper is relevant/ interesting.


Contents

FALL 2015, 11/16/2015

ACS Synthetic Biology

  1. (2015) BASIC: A New Biopart Assembly Standard for Idempotent Cloning Provides Accurate, Single-Tier DNA Assembly for Synthetic Biology. Storch M, Casini A, and Fleming T et al. ACS Synth Biol. 4(7):781-7. http://pubs.acs.org.ezproxy1.lib.asu.edu/doi/abs/10.1021/sb500356d. Summary: The authors propose a type IIs restriction enzyme based cloning standard, BASIC (Biopart Assembly Standard for Idempotent Cloning), that utilizes orthogonal linkers to build multi-gene constructs. A unique element of this strategy is the use of the linkers as small parts such as RBS sequences or fusion protein linkers.
  2. (2015) CRISPathBrick: Modular Combinatorial Assembly of Type II-A CRISPR Arrays for dCas9-Mediate Multiplex Transcriptional Repression in E. coli. Brady F. Cress, O. Duhan Toparlak, and Mattheos A. G. Koffas et al. ACS Synth Biol. 4(9):987-1000. http://pubs.acs.org.ezproxy1.lib.asu.edu/doi/10.1021/acssynbio.5b00012.Summary: This paper describes a vector system with rapid modular assembly that allows for the use of type II-A CRISPR arrays to simultaneously repress multiple gene loci in E. coli. Repression in the system is based on dCas9 binding.

Cell

  1. (2015) Crystal Structure of Staphylococcus aureus Cas9. Nishimasu H, Cong L, Yan WX, et al. Cell. 162:1113-1126. Link.
    Summary: Discovery of a new Cas9 protein from S. aureus, significantly smaller than currently used Cas9, for more efficient in vivo editing of genomes.

EMBO Molecular Systems Biology

  1. (2015) Tuning noise in gene expression Sanjay Tyagi. Molecular Systems Biology (2015) 11: 805 http://msb.embopress.org/content/11/5/805 Summary Noise from gene expression in this article was found to be more apparent at the single cell level than looking at all cells together. They used the DNase 1 sensitivity assay to determine that clones with more noise was always associated with less accessible chromatin.

http://msb.embopress.org/content/11/7/823

Frontiers in Microbiotechnology

  1. tba

Journal of Biological Engineering

  1. (2015) Artificial cell-cell communication as an emerging tool in synthetic biology applications. Stefan Hennig,corresponding author Gerhard Rödel, and Kai Ostermann. J Biol Eng. 9:13. Link.
    Summary: Review paper on cell signaling of interest to synthetic biologists, including quorum sensing, fungal pheromones, and communication systems in mammalian systems. Emphasis is on multiple cell subtypes within a networked population to reduce crosstalk and metabolic load of cell-cell communication system.
  2. (2015) No training required: experimental tests support homology-based DNA assembly as a best practice in synthetic biology. Afnan Azizi, Wilson Lam, and Hilary Phenix, et al. J Biol Eng. 9:8. Link.
    Summary: A bit of insider baseball, but the paper argues that the registry for standard biological parts and iGEM should include homology-based assembly methods in addition to the standard 3 antibiotic (3A) assembly method, due to the ease of setting up homology-based assembly.

Journal of Cell Biology

The articles weren't too relevant to our research so here are some interesting articles.

  1. (2015) Lamin A/C sustains PcG protein architecture, maintaining transcriptional repression at target genes. Elisa Cesarini, Chiara Mozzetta, and Fabrizia Marullo, et al. Journal of Cell Biology. 211.3:533-551. Link.
    Summary: The cross talk between lamin A/C and Polycomb group of proteins (epigenetic factors) and its effect were studied. Lamin A/C was found to be necessary for correct PcG protein nuclear compartmentalization; knock-down of lamin A/C lead to the disassembly and dispersion of PcG protein. These defects impair the repressive function of the epigenetic factors. Thus results suggest that lamin A/C can be used to maintain transcription by regulating PcG proteins.
  2. (2015) Live imaging and modeling of inner nuclear membrane targeting reveals its molecular requirements in mammalian cells. Andrea Boni, Antonio Politi, and Petr Strnad, et al. Journal of Cell Biology. 209.5:705-720. Link.
    Summary: Reporters Lamin B receptor and Lap2β were used to image membrane protein transport from the endoplasmic reticulum to the inner nuclear membrane in real-time. A mathematical model was created for the process which depends on the number and permeability of nuclear pores and the availability of nuclear binding sites. The mathematical model was proven to be accurate.

Molecular Biology of the Cell

  1. tba

Molecular and Cellular Biology

  1. (2015) The Lineage-Specific Transcription Factor PU.1 Prevents Polycomb Mediated Heterochromatin Formation at Macrophage-Specific Genes. Mohita Tagore, Michael J. McAndrew, Alison Gjidoda et al. Molecular and Cellular Biology. 35.22:3841-3853. Link.
    Summary: This paper argues that the pioneer transcription factor PU.1 is able to displace nucleosomes at its binding sites and prevent further nucleosome formation and PRC2 mediated silencing. They use a quantitative nucleosome occupancy assay to map nucleosomes to ~60bp resolution. This type of transcription factor could be useful for the openchrom project and the nucleosome assay could be used for many projects in the lab.

  2. (2015) Pluripotency and Epigenetic Factors in Mouse Embryonic Stem Cell Fate Regulation. Lluis Morey, Alexandra Santanach, and Luciano Di Croce. Molecular and Cellular Biology. 35.16:2716-2728. Link.
    Summary: Review on the roles of PRC1 and 2 complexes in mouse stem cell maintenance and differentiation. Discussion of non-canonical PRC1 (ncPRC1) and some mechanisms for how it might recruit PRC2 through H2AK119ub.

Nature

  1. (2015) Targeting Polycomb systems to regulate gene expression: modifications to a complex story. Neil Blackledge, Nathan Rose, Robert Kloseet et al. Nature. 16: 643-649 Link.
    Summary: A group from University of Oxford, UK have an alternative model for the Polyomb Repressive Complex, where initially complexes in PRC1 apart from chromobox (CBX) bind to chromatin, which then promotes the binding of PRC2. This initial process of binding is then independent from PRC2 and H3K27me3.

  2. (2015) Epigenetic regulation of ageing: linking environmental inputs to genomic stability. Elizabeth Pollina, Berenice Benayoun, Anne Brunet et al. Nature, 16:593-610. Link.
    Summary: A group from Stanford University finds that changes in H3K27me3 are correlated to longevity. Although in in different cells, up-regulation or down-regulation was needed to achieve longevity.
  3. (2015) In vivo genome editing using Staphylococcus aureus Cas9. Ran FA, Cong L, Yan WX, et al. Nature, 520:186-191.
    Summary: New Cas9 protein discovered with similar editing efficiency but over 1000 basepairs shorter. PAM sequence already identified.

Nature Biotechnology

  1. (2015) Epigenome editing by a CRISPR-Cas9-based acetyltransferase activates genes from promoters and enhancers. Hilton, I. B., D’Ippolito, A. M., Vockley, C. M., Thakore, P. I., Crawford, G. E., Reddy, T. E., & Gersbach, C. A. Nature Biotechnology, 33(5), 510–517. Link.
    Summary : This article describes a modular fusion protein consisting of a nuclease deficient Cas9 protein and an acetyltransferase. The fusion protein specifically acetylates H3K27 at sites determined by the Cas9 guide RNA, and is shown to greatly increase transcription at targeted genes (more so than dCas9-VP64). In addition, the acetyltransferase domain was shown to work as a fusion with other DNA binding domains (TALE (transcription activator like effector) and zinc finger protein).

Nature Methods

  1. (2015) DNA sense-and-respond protein modules for mammalian cells. Shimyn Slomovic & James Collins. Nature Methods 12, 1085–1090 (2015) Link.
    Summary: Using engineered zinc-finger proteins that bound a specific DNA sequence, researchers were able to induce apoptosis once cells transfected with the circuit recognized the target sequence, and also were able to have cells report via fluorescence when they were infected with viruses.

  2. (2015) Highly specific epigenome editing by CRISPR-Cas9 repressors for silencing of distal regulatory elements. Pratiksha I Thakore, Anthony M D'Ippolito... Charles Gersbach et al. Nature Methods. Link.
    Summary: Fusing the Cas9 protein to the KRAB repressor, researchers were able to target a single enhancer (HZ2) and observed repression via H3K9me3 methylation, which also reduced expression of the gene/promoter targets of the enhancer.

Nature Molecular Systems Biology

  1. tba

Public Library of Science Biology (PLoS Biology)

  • No new relevant articles

Proceedings of the National Academy of Sciences

  1. (2015) Genome-wide redistribution of H3K27me3 is linked to genotoxic stress and defective growth. Evelina Y. Basenko, Takahiko Sasaki... Zachary Lewis et al. PNAS. Link.
    Summary: Researchers examined H3K9me3-deficient bread mold cells and found that a mutation in PRC2 results in H3K27me3 accumulation in heterochromatin, resulting in genotoxic stress and increased sensitivity to drugs.

  2. (2015) Nanoscale spatial organization of the HoxD gene cluster in distinct transcriptional states. Pierre J. Fabre, Alexander Benke... Denis Duboule et al. PNAS vol. 112 no. 45 13964-13969. Link.
    Summary: Researchers found that the HoxD gene locus (the location of a Polycomb response element) physically elongated more in cells where it was highly expressed and at the boundary of two topological associating domains, suggesting links between the physical orientation and transcription of the HoxD locus.

Science

  1. (2015) Structural basis of histone H3K27 trimethylation by an active polycomb repressive complex 2. Jiao, L., & Liu, X. Science, 350(6258), aac4383-1 – aac4383-8. Link.
    Summary: A crystal structure of PRC2 was solved in an apo and bound state. The structure indicates that three of the subunits of PRC2 (Ezh2, Eed, Suz12) are closely associated when complexed. Although Ezh2 is the catalytic domain, Eed and Suz12 are minimally required for catalysis, as confirmed in the crystal structure through protein-protein contact. They also determined how an H3K27M cancer mutation directly inhibits PRC2 activity by allowing H3R26 to enter the active site.
  2. (2015) Epigenetics. Restricted epigenetic inheritance of H3K9 methylation. Audergon, P. N. C. B., Catania, S., Kagansky, A., Tong, P., Shukla, M., Pidoux, A. L., & Allshire, R. C. Science (New York, NY), 348(6230), 132–135. . Link.
    Summary: Yeast cells contain a single H3K9 methyltransferase (Clr4), which is involved in heterochromatin formation. However, epigenetic heritability has not been demonstrated. In this paper, releasable Clr4 was used in yeast cells to show that H3K9 methylation was an actively erased process. When the demethylase Epe1 was inactivated, H3K9 was maintained and was transmissible through meiosis through many generations. This indicates that H3K9 is a heritable epigenetic mark whose transmission is controlled by active removal by demethylases.
  3. (2015) Epigenetic inheritance uncoupled from sequence-specific recruitment. Ragunathan, K., Jih, G., & Moazed, D. Science, 348(6230),1258699-1 - 1258699-8 . Link.
    Summary: An inducible system for yeast heterochromatin establishment was made by fusing a Clr4 catalytic domain to a bacterial tet repressor. Tetracycline operators were introduced upstream of the target gene. Expression of the fusion gene resulted in targeted gene silencing via H3K9 methylation, which was demethylated within 10 generations after tetrecycline induced release. knockout of the demethylase Epe1 resulted in methylation for over 50 generations. Interestingly, the chromodomain of Clr4 does not seem to be required for establishment of heterochromatin, but it is required for maintenance of the repressed state.

Miscellaneous Reviews and Media

Reviews

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News

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iGEM 2015

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