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Bio

Jonathon Baker joined the Department of Genomic Medicine at JCVI in 2018.  Working in the oral microbiology group led by Dr. Anna Edlund, Dr. Baker’s research is focused primarily on the disease, dental caries, commonly referred to as “cavities” or “tooth decay.” Dental caries is the most common chronic infectious disease, globally, and will afflict roughly 90% of Americans at some point in their lives.  This extraordinary rate of infection, combined with high cost of treatment, translates to a massive global economic burden, approaching US$300 billion, annually. 

Historically, infection by the oral bacterium Streptococcus mutans was thought to be the primary cause of dental caries.  S. mutans causes disease by forming biofilms (dental plaque), firmly attached to the tooth surface, and generating large amounts of organic acids—by-products of its metabolism of the sugars it comes into contact with, thanks to the human diet.  These acids destroy the protective enamel coating on the tooth surface, and will lead to loss of the tooth if the disease process is unchecked.  In the era of next-generation sequencing, caries is increasingly recognized as a polymicrobial disease, caused by an ecological catastrophe in the plaque environment, rather than infection by a single species. Thus, the role of S. mutans as the keystone pathogen in caries progression has been called into question.  Dr. Baker’s research seeks to understand how S. mutans, and its bacterial neighbors in dental plaque, influence and interact with one another, and how these relationships affect the ability of these communities of bacteria to cause disease.

Originally from Rochester, NY, Dr. Baker has a Ph.D. in Microbiology & Immunology from the University of Rochester School of Medicine & Dentistry and a B.S. in Biology from SUNY Geneseo.  Prior to joining the team at JCVI, Dr. Baker conducted research in the Department of Oral Biology at the UCLA School of Dentistry and in the Vaccine Research and Early Development group at Pfizer, Inc. in Pearl River, NY.

Research Priorities

Identifying and characterizing interspecies interactions between S. mutans and other dental plaque bacteria that affect virulence of the community

  • Identifying contributing species
  • Discovering the mechanisms of interaction/signaling
  • Applying novel information to better understand how the plaque community interacts with the host and causes disease

Characterizing oral bacterial communities during ecological catastrophes and bottlenecks

  • Identifying which species survive and why
  • Applying this information to study how ecological catastrophes cause disease in the human host
Ecology of the Oral Microbiome: Beyond Bacteria.
Trends in microbiology. 2017-05-01; 25.5: 362-374.
PMID: 28089325
Acid-adaptive mechanisms of Streptococcus mutans-the more we know, the more we don't.
Molecular oral microbiology. 2017-04-01; 32.2: 107-117.
PMID: 27115703
A Modified Chromogenic Assay for Determination of the Ratio of Free Intracellular NAD+/NADH in Streptococcus mutans.
Bio-protocol. 2016-08-20; 6.16:
PMID: 28516115
Loss of NADH Oxidase Activity in Streptococcus mutans Leads to Rex-Mediated Overcompensation in NAD+ Regeneration by Lactate Dehydrogenase.
Journal of bacteriology. 2015-12-01; 197.23: 3645-57.
PMID: 26350138
Transcriptional profile of glucose-shocked and acid-adapted strains of Streptococcus mutans.
Molecular oral microbiology. 2015-12-01; 30.6: 496-517.
PMID: 26042838
Streptococcus mutans NADH oxidase lies at the intersection of overlapping regulons controlled by oxygen and NAD+ levels.
Journal of bacteriology. 2014-06-01; 196.12: 2166-77.
PMID: 24682329
Development and comparison of a quantitative TaqMan-MGB real-time PCR assay to three other methods of quantifying vaccinia virions.
Journal of virological methods. 2014-02-01; 196.126-32.
PMID: 24211297
Host factor SAMHD1 restricts DNA viruses in non-dividing myeloid cells.
PLoS pathogens. 2013-01-01; 9.8: e1003481.
PMID: 23825958