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John                           Panepinto

John C. Panepinto PhD

Department of Microbiology and Immunology

Associate Professor

Specialty/Research Focus

Eukaryotic Pathogenesis; Gene Expression; Infectious Disease; Microbial Pathogenesis; Microbiology; RNA; Signal Transduction

Professional Summary:

There are estimated to be over one million species of fungi on the earth, yet very few of these species are capable of causing deadly systemic infections in humans. One of the major limiting factors for most fungi is their inability to grow at mammalian core body temperature. We utilize the fungal pathogen Cryptococcus neoformans var. grubii as a representative fungal pathogen to understand how these few fungi have adapted to growth at mammalian body temperature. C. neoformans is a worthy pathogen, as it is estimated to cause over 500,000 deaths from meningoencephalitis per year, primarily in Africa and Southeast Asia as an HIV/AIDS comorbidity. We use the temperature-limited Cryptococcus amylolentus as a comparator; it is an environmental strain that produces similar virulence factors to C. neoformans and is fully virulent in surrogate invertebrate hosts at permissive temperatures.

We have discovered that host temperature adaptation in C. neoformans is accompanied by a reprogramming of gene expression at the level of messenger RNA (mRNA) stability. In response to temperature stress, C. neoformans rapidly degrades mRNAs that encode energy consuming machinery such as ribosomes. At the same time, it prioritizes the translation of stress-responsive mRNAs on existing ribosomes.

Because mRNA synthesis and decay are coupled processes, we seek to identify the protein components of mRNA complexes that mediate the specificity of this decay process and posttranslational modifications, such as arginine methylation and phosphorylation, that modify their function. In addition, we are investigating the signaling pathways that accelerate or slow mRNA decay in response to specific environmental stimuli such as host temperature and nutrient deprivation.

Finally, mRNA decay not only alters gene expression at the posttranscriptional level, but the degradation of abundant mRNAs during stress releases nucleotide intermediates that can be utilized by the stressed cell to promote genome stability. We are investigating the process of mRNA degradation as well as nucleotide metabolic pathways as drug targets in C. neoformans and other fungal pathogens. Our goal is to define the unique attributes of C. neoformans that confer pathogenicity and to identify potential targets for novel therapeutics.

Each of my students has a project that contributes to the overall goals of my research team. Students in my laboratory work independently, though with frequent interaction with me regarding the direction of investigation and interpretation of data. Regular meetings allow us to provide input on each other’s projects. I expect my students to present their work at least once per year at a national or international meeting, and I expect them to do the bulk of the work in writing papers describing their findings for publication.

Education and Training:
  • PhD, Pathobiology and Molecular Medicine, University of Cincinnati (2002)
  • BS, Biology (Microbiology and Immunology), Virginia Tech (1997)
  • BS, Biochemistry, Virginia Tech (1997)
  • Associate Professor, Microbiology and Immunology, University at Buffalo, the State University of New York (2014-present)
  • Assistant Professor, Microbiology and Immunology, University at Buffalo, the State University of New York (2008–2014)
  • Postdoctoral Research Associate, Section of Infectious Diseases, Department of Medicine, University of Illinois at Chicago (2003–2008)
  • Postdoctoral Research Associate, Pathology and Laboratory Medicine, University of Cincinnati (2002–2003)
  • Adjunct Faculty, Biology, The College of Mount St. Joseph (2002)

Research Expertise:
  • Drug target discovery: Pathogenic fungi
  • Fungal Pathogenesis
  • Molecular mycology: Molecular mechanisms oof Cryptococcosis, C. neoformans stress adaptation and pathogenesis, mRNA decay in stress-responsive reprogramming of the translating mRNA pool, PUF-protein mediated post-transcriptional regulation, protein arginine methylation in C. neoformans stress response attenuation, mRNA 3’UTR G-quadruplexes in post-transcriptional regulation
Research Centers:
  • Witebsky Center for Microbial Pathogenesis and Immunology
UB 2020 Strategic Strengths:
  • Molecular Recognition in Biological Systems and Bioinformatics
Grants and Sponsored Research:
  • July 2011–June 2016
    R01 AI089920-01A1 Stress Responsive RNA Regulons in Cryptococcus neoformans
    Role: Principal Investigator

Journal Articles:
See All (29 Total) >

Clinical Specialties:
Clinical Offices:
Insurance Accepted:

Contact Information

117 Biomedical Research Building
Buffalo, NY 14214
Phone: (716) 829-2090

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