Richard Novick, M.D.

Affiliations: 
Microbiology New York University, New York, NY, United States 
Area:
Staphylococcus aureus; superantigens; mobile genes; pathogenicity islands, signal transduction, regulation of virulence, microbial pathogenesis; MRSA; bacterial genetics
Website:
http://microbiology-parasitology.med.nyu.edu/richard-novick
Google:
"Richard Novick"
Bio:

http://www.nasonline.org/member-directory/members/20012496.html
http://skirball.med.nyu.edu/faculty/richard-p-novick/novick-lab
http://www.med.nyu.edu/biosketch/novicr01
http://dx.doi.org/10.1073/pnas.0707438104
RESEARCH INTERESTS: Our lab is focused on the study of staphylococcal virulence, its genetic and regulation. There are two major areas:

1. Global regulation of virulence genes by agr. Virulence in S. aureus is regulated by a complex network of regulatory determinants, the most important of which is the agr locus, which we have identified and characterized. The agr locus contains a two-component signaling module that is autoinduced by a small semi-cyclic peptide (AIP), that is encoded within the locus, is secreted, and then binds to AgrC, the signal receptor, activating the system. agr operates by autoinduction and is therefore a quorum sensor.

Agr has undergone a striking evolutionary differentiation into 4 specificity groups in S. aureus. Heterologous AIP-receptor interactions are generally inhibitory, blocking virulence gene expression (but not growth). This inhibition has been shown to block an experimental abscess in mice. We are currently developing one of the inhibitory peptides for potential therapeutic use. Additionally, we are purifying the receptor in collaboration with the Skirball Structural Biology Group, in order to determine its structure which will reveal the mechanism of signal transduction.

2. Mobile pathogenicity islands encoding superantigens. Our second major area is the study of mobile, phage-related pathogenicity islands (SaPIs) that encode and are responsible for the dissemination of genes encoding superantigens, such as toxic shock toxin and the enterotoxins. These elements, 15-20 kb in length, reside quiescently at specific chromosomal locations under the control of a repressor and are induced to excise and replicate by certain temperate phages, with which they severely interfere. Following replication, they are packaged in small, SaPI-induced infective phage-like particles that can infect other cells, thus spreading superantigen and other toxins. We have recently found that helper phages, but not non-helpers, produce specific bifunctional “moonlighting” proteins that induce SaPI reproduction by binding and inactivating the SaPI repressor. Current studies involve determination of the mechanism of SaPI interference with phage reproduction and identification of the SaPI genes involved. Additionally, we are very interested in similar elements carried by other bacteria, especially since an experiment to test for SaPI transfer to other species revealed efficient phage-mediated transfer, to Listeria monocytogenes, a serious food-borne pathogen, which is not known to produce superantigens.
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Children

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Jill E. Bargonetti grad student 1990 NYU
Nikola Vojtov grad student 2003 NYU
Gholson James Lyon grad student 1999-2003 Rockefeller
Katrina E. Traber grad student 2006 NYU
Brian C. Weinrick grad student 2006 NYU
Peter Barry grad student 2007 NYU
Edward Geisinger grad student 2008 NYU
Steven Projan post-doc New York University (Cell Biology Tree)
Emmanuelle Marie Charpentier research scientist 1999-2002 Skirball Institute of Biomolecular Medicine

Collaborators

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Gail Ellen Christie collaborator (Microtree)
Frank C. Hoppensteadt collaborator NYU Langone Medical Center (Neurotree)
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Publications

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Haag AF, Podkowik M, Ibarra-Chávez R, et al. (2021) A regulatory cascade controls Staphylococcus aureus pathogenicity island activation. Nature Microbiology
Xie Q, Wiedmann MM, Zhao A, et al. (2020) Discovery of quorum quenchers targeting the membrane-embedded sensor domain of the Staphylococcus aureus receptor histidine kinase, AgrC. Chemical Communications (Cambridge, England)
Novick R. (2019) Targeted killing of virulent Vibrio cholerae. Nature Biomedical Engineering
Xie Q, Zhao A, Jeffrey PD, et al. (2019) Identification of a Molecular Latch that Regulates Staphylococcal Virulence. Cell Chemical Biology
Wang B, Zhao A, Xie Q, et al. (2017) Functional Plasticity of the AgrC Receptor Histidine Kinase Required for Staphylococcal Virulence. Cell Chemical Biology. 24: 76-86
Wang B, Zhao A, Novick RP, et al. (2015) Key driving forces in the biosynthesis of autoinducing peptides required for staphylococcal virulence. Proceedings of the National Academy of Sciences of the United States of America. 112: 10679-84
Johnson JG, Wang B, Debelouchina GT, et al. (2015) Increasing AIP Macrocycle Size Reveals Key Features of agr Activation in Staphylococcus aureus. Chembiochem : a European Journal of Chemical Biology. 16: 1093-100
Wang B, Zhao A, Novick RP, et al. (2015) Key driving forces in the biosynthesis of autoinducing peptides required for staphylococcal virulence Proceedings of the National Academy of Sciences of the United States of America. 112: 10679-10684
Ram G, Chen J, Ross HF, et al. (2014) Precisely modulated pathogenicity island interference with late phage gene transcription. Proceedings of the National Academy of Sciences of the United States of America. 111: 14536-41
Wang B, Zhao A, Novick RP, et al. (2014) Activation and inhibition of the receptor histidine kinase AgrC occurs through opposite helical transduction motions. Molecular Cell. 53: 929-40
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