Abstract

(Core B, Barton) Core B of this Program Project Grant (P01) will maintain a colony of mouse strains with deficiencies in components of innate immunity or other genetic modifications useful for the study of innate immunity and the host response to pathogens. Core B also supports the generation of new mouse strains using Cas9-mediated genome editing. This new technology enables rapid and affordable generation of knock-out and knock-in mice. Core B will work with each of the Project Labs to develop new mouse strains that will facilitate hypothesis testing. Mice are cells from the mice maintained within Core B will be distributed to each of the projects within the P01. All mouse strains have been or will be backcrossed onto the C57BL/6J genetic background to equivalent degrees. Core B will reduce overall mouse costs due to economies of scale. In addition, each P01 project will benefit from using cells and mice with fewer genetic and experimental variations.

Public Health Relevance

(Core B, Barton) Core B will provide mice and cells lacking key immune genes to each of the projects within this P01 application. Experiments using these materials will dissect how the immune system detects and responds to a broad range of pathogens.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program Projects (P01)
Project #
5P01AI063302-15
Application #
9492771
Study Section
Special Emphasis Panel (ZAI1)
Project Start
Project End
Budget Start
2018-07-01
Budget End
2019-06-30
Support Year
15
Fiscal Year
2018
Total Cost
Indirect Cost

  Institution

Name
University of California Berkeley
Department
Type
DUNS #
124726725
City
Berkeley
State
CA
Country
United States
Zip Code
94704

  Publications

Price, April E; Shamardani, Kiarash; Lugo, Kyler A et al. (2018) A Map of Toll-like Receptor Expression in the Intestinal Epithelium Reveals Distinct Spatial, Cell Type-Specific, and Temporal Patterns. Immunity 49:560-575.e6
Cheng, Mandy I; Chen, Chen; Engström, Patrik et al. (2018) Actin-based motility allows Listeria monocytogenes to avoid autophagy in the macrophage cytosol. Cell Microbiol 20:e12854
Mitchell, Gabriel; Cheng, Mandy I; Chen, Chen et al. (2018) Listeria monocytogenes triggers noncanonical autophagy upon phagocytosis, but avoids subsequent growth-restricting xenophagy. Proc Natl Acad Sci U S A 115:E210-E217
Penn, Bennett H; Netter, Zoe; Johnson, Jeffrey R et al. (2018) An Mtb-Human Protein-Protein Interaction Map Identifies a Switch between Host Antiviral and Antibacterial Responses. Mol Cell 71:637-648.e5
Chen, Chen; Nguyen, Brittney N; Mitchell, Gabriel et al. (2018) The Listeriolysin O PEST-like Sequence Co-opts AP-2-Mediated Endocytosis to Prevent Plasma Membrane Damage during Listeria Infection. Cell Host Microbe 23:786-795.e5
Nguyen, Brittney N; Peterson, Bret N; Portnoy, Daniel A (2018) Listeriolysin O: a phagosome-specific cytolysin revisited. Cell Microbiol :e12988
Price, Jordan V; Jiang, Kallie; Galantowicz, Abigail et al. (2018) Legionella pneumophila Is Directly Sensitive to 2-Deoxyglucose-Phosphate via Its UhpC Transporter but Is Indifferent to Shifts in Host Cell Glycolytic Metabolism. J Bacteriol 200:
Light, Samuel H; Su, Lin; Rivera-Lugo, Rafael et al. (2018) A flavin-based extracellular electron transfer mechanism in diverse Gram-positive bacteria. Nature 562:140-144
Deng, Weiwen; Lira, Victor; Hudson, Thomas E et al. (2018) Recombinant Listeria promotes tumor rejection by CD8+ T cell-dependent remodeling of the tumor microenvironment. Proc Natl Acad Sci U S A 115:8179-8184
Whiteley, Aaron T; Ruhland, Brittany R; Edrozo, Mauna B et al. (2017) A Redox-Responsive Transcription Factor Is Critical for Pathogenesis and Aerobic Growth of Listeria monocytogenes. Infect Immun 85:

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