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.

Research Priorities

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


mSystems. 2022-10-26; 7.5: e0049122.
Using Nanopore Sequencing to Obtain Complete Bacterial Genomes from Saliva Samples
Baker JL
PMID: 35993719
Microbiology resource announcements. 2022-05-19; 11.5: e0002322.
Complete Genome Sequence of "Candidatus Nanosynbacter" Strain HMT-348_TM7c-JB, a Member of Saccharibacteria Clade G1
Baker JL
PMID: 35404101
Journal of bacteriology. 2022-04-11; e0004222.
mucG, mucH, and mucI Modulate Production of Mutanocyclin and Reutericyclins in Streptococcus mutans B04Sm5
Baker JL, Tang X, LaBonte S, Uranga C, Edlund A
PMID: 35404110
Frontiers in oral health. 2022-01-07; 2.796140.
Tetramic Acids Mutanocyclin and Reutericyclin A, Produced by Streptococcus mutans Strain B04Sm5 Modulate the Ecology of an in vitro Oral Biofilm
Uranga C, Nelson KE, Edlund A, Baker JL
PMID: 35048077
International journal of molecular sciences. 2021-11-07; 22.21:
Multi-Omics Study of Keystone Species in a Cystic Fibrosis Microbiome
Silveira CB, Cobián-Güemes AG, Uranga C, Baker JL, Edlund A, Rohwer F, Conrad D
PMID: 34769481
Microbiology resource announcements. 2021-06-10; 10.23: e0051721.
Complete Genome Sequence of Strain JB001, a Member of Saccharibacteria Clade G6 ("Candidatus Nanogingivalaceae")
Baker JL
PMID: 34110243
Methods in molecular biology (Clifton, N.J.). 2021-01-01; 2327.161-189.
Identification of Oral Bacterial Biosynthetic Gene Clusters Associated with Caries
Baker JL, Edlund A
PMID: 34410645
Genome research. 2021-01-01; 31.1: 64-74.
Deep metagenomics examines the oral microbiome during dental caries, revealing novel taxa and co-occurrences with host molecules
Baker JL, Morton JT, Dinis M, Dinis M, Alvarez R, Tran NC, Knight R, Edlund A
PMID: 33239396
Journal of dental research. 2020-07-01; 99.8: 969-976.
Caries-Associated Biosynthetic Gene Clusters in Streptococcus mutans
Momeni SS, Beno SM, Baker JL, Edlund A, Ghazal T, Childers NK, Wu H
PMID: 32298190
Molecular oral microbiology. 2020-06-01; 35.3: 118-128.
Streptococcus mutans SpxA2 relays the signal of cell envelope stress from LiaR to effectors that maintain cell wall and membrane homeostasis
Baker JL, Saputo S, Faustoferri RC, Quivey RG
PMID: 32043713
ACS infectious diseases. 2020-04-10; 6.4: 563-571.
Cariogenic Streptococcus mutans Produces Tetramic Acid Strain-Specific Antibiotics That Impair Commensal Colonization
Tang X, Kudo Y, Baker J, Baker JL, LaBonte S, Jordan P, Jordan PA, McKinnie SMK, McKinnie S, Guo J, Huan T, Moore BS, Edlund A
PMID: 31906623
Frontiers in microbiology. 2020-03-04; 11.327.
Development of a Bacteriophage Cocktail to Constrain the Emergence of Phage-Resistant Pseudomonas aeruginosa
Yang Y, Shen W, Zhong Q, Chen Q, He X, Baker JL, Xiong K, Jin X, Wang J, Hu F, Le S
PMID: 32194532
Advances in dental research. 2019-11-01; 30.2: 34-39.
Precision Reengineering of the Oral Microbiome for Caries Management
Baker JL, He X, Shi W
PMID: 31633390
Proceedings of the National Academy of Sciences of the United States of America. 2019-04-23; 116.17: 8499-8504.
Klebsiella and Providencia emerge as lone survivors following long-term starvation of oral microbiota
Baker JL, Hendrickson EL, Tang X, Lux R, He X, Edlund A, McLean JS, Shi W
PMID: 30975748
mBio. 2019-04-16; 10.2:
Identification of the Bacterial Biosynthetic Gene Clusters of the Oral Microbiome Illuminates the Unexplored Social Language of Bacteria during Health and Disease
Aleti G, Baker JL, Tang X, Alvarez R, Dinis M, Tran NC, Melnik AV, Zhong C, Ernst M, Dorrestein PC, Edlund A
PMID: 30992349
Frontiers in microbiology. 2019-01-11; 9.3323.
Exploiting the Oral Microbiome to Prevent Tooth Decay: Has Evolution Already Provided the Best Tools?
Baker JL, Edlund A
PMID: 30687294
Journal of bacteriology. 2018-06-15; 200.12:
Characterization of the Trehalose Utilization Operon in Streptococcus mutans Reveals that the TreR Transcriptional Regulator Is Involved in Stress Response Pathways and Toxin Production
Baker JL, Lindsay EL, Faustoferri RC, To TT, Hendrickson EL, He X, Shi W, McLean JS, Quivey RG
PMID: 29632089
Trends in microbiology. 2017-05-01; 25.5: 362-374.
Ecology of the Oral Microbiome: Beyond Bacteria
Baker JL, Bor B, Agnello M, Shi W, He X
PMID: 28089325
Molecular oral microbiology. 2017-04-01; 32.2: 107-117.
Acid-adaptive mechanisms of Streptococcus mutans-the more we know, the more we don't
Baker JL, Faustoferri RC, Quivey RG
PMID: 27115703
Bio-protocol. 2016-08-20; 6.16:
A Modified Chromogenic Assay for Determination of the Ratio of Free Intracellular NAD+/NADH in Streptococcus mutans
Baker JL, Faustoferri RC, Quivey RG
PMID: 28516115
Molecular oral microbiology. 2015-12-01; 30.6: 496-517.
Transcriptional profile of glucose-shocked and acid-adapted strains of Streptococcus mutans
Baker JL, Abranches J, Faustoferri RC, Hubbard CJ, Lemos JA, Courtney MA, Quivey R
PMID: 26042838
Journal of bacteriology. 2015-12-01; 197.23: 3645-57.
Loss of NADH Oxidase Activity in Streptococcus mutans Leads to Rex-Mediated Overcompensation in NAD+ Regeneration by Lactate Dehydrogenase
Baker JL, Derr AM, Faustoferri RC, Quivey RG
PMID: 26350138
Journal of bacteriology. 2014-06-01; 196.12: 2166-77.
Streptococcus mutans NADH oxidase lies at the intersection of overlapping regulons controlled by oxygen and NAD+ levels
Baker JL, Derr AM, Karuppaiah K, MacGilvray ME, Kajfasz JK, Faustoferri RC, Rivera-Ramos I, Bitoun JP, Lemos JA, Wen ZT, Quivey RG
PMID: 24682329
Journal of virological methods. 2014-02-01; 196.126-32.
Development and comparison of a quantitative TaqMan-MGB real-time PCR assay to three other methods of quantifying vaccinia virions
Baker JL, Ward BM
PMID: 24211297
PLoS pathogens. 2013-01-01; 9.6: e1003481.
Host factor SAMHD1 restricts DNA viruses in non-dividing myeloid cells
Hollenbaugh JA, Gee P, Baker J, Daly MB, Amie SM, Tate J, Kasai N, Kanemura Y, Kim DH, Ward BM, Koyanagi Y, Kim B
PMID: 23825958
When Starved, Dangerous Oral Bacteria Hang On