Jonathon Baker, PhD, joined the Department of Genomic Medicine at JCVI in 2018. 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.
In addition, since tooth enamel is the hardest surface in the human body, it is remarkable that S. mutans and other caries-causing bacteria are able to survive in conditions that are so acidic that they significantly demineralize enamel. One of the mechanisms employed by S. mutans to survive acid stress is increasing the proportion of unsaturated fatty acids (UFAs) in its cell membrane which occurs via the FabM isomerase enzyme. Although this adaptation is required for acid tolerance and virulence, it is not known how this shift is activated or controlled, or how the UFAs are protective. Dr. Baker’s research seeks to answer these questions, as well as determine how widespread this behavior is, since preliminary data indicates several other oral bacteria increase membrane UFAs in response to acid stress. The results obtained from this investigation are likely to open the door to development of novel anti-caries therapeutics.
Originally from Rochester, NY, Dr. Baker has a PhD in microbiology & immunology from the University of Rochester School of Medicine & Dentistry and a BS 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.
Investigating membrane alterations as a mechanism of acid tolerance in cavity-causing bacteria
- Determine what bacteria in the oral microbiota modify their membranes and/or cell walls in response to environmental acidification
- Determine how these membrane and cell wall alterations are effective at protecting disease-causing bacteria from acid
- Develop anti-caries therapeutics that disrupt caries-causing bacteria from altering their cell envelope and therefore prevent further acid damage to the tooth enamel
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