The Field Laboratory, in the Division of nutritional Sciences at Cornell University, studies gene-nutrient interactions that lead to development of disease.  It is clear that what we eat can be associated with disease onset, and some individuals are more likely to be affected based on certain genetic, or inherited, characteristics.  We investigate these interactions at a molecular level, with the ultimate goal of designing interventions that prevent disease and improve human health.  

It is clear that what we eat can be associated with disease onset, and some individuals are more likely to be affected based on certain genetic, or inherited, characteristics.

Martha Field, PhD

Impaired folate-dependent one-carbon metabolism is associated with adverse physiological outcomes that include certain cancers, cardiovascular disease, neurological impairments, and birth defects.  Our laboratory uses several in vitro and in vivo model systems to study the mechanisms that underlie physiological outcomes associated with perturbed one-carbon metabolism. More specifically, we are interested in understanding the contributions of folate and/or vitamin B12 nutrition and enzyme localization in supporting mitochondrial DNA precursor synthesis, with a focus on understanding how folate nutrition affects mitochondrial DNA integrity and pathogenesis of metabolic diseases such as mitochondrial DNA depletion syndromes, chronic disease, and age-related decline in mitochondrial function. 

Recently, our research has also focused on the metabolism of erythritol, which is a product of the pentose phosphate pathway and which has recently emerged as a predictive biomarker of weight gain, type 2 diabetes, and cardiovascular disease.  We have identified the enzymes responsible for endogenous production of erythritol and are currently using animal models to understand the metabolic pathways underlying the association between erythritol exposure, genetic variants that affect endogenous erythritol synthesis, and central adiposity.

  • Schlicker, L., Szebenyi, D.M.E., Ortiz, S.R., Heinz, A., Hiller, K., and Field, M.S. (2019) Unexpected roles for ADH1 and SORD in catalyzing the final step of erythritol biosynthesis.  J. Biol. Chem., 294, 16095-16108.
  • Chon, J., Field, M.S., and Stover, P.J. (2019) Deoxyuracil in DNA and disease:  genomic signal or managed situation?  DNA Repair, 77:  36-44.
  • Tiani, K.A., Stover, P.J., and Field, M.S. (2019) Nutrition and the blood-brain barrier.  Ann. Rev. Nutr., 39:  147-173.
  • Misselbeck, K., Marchetti, L., Priami, C.,  Stover, P.J., and Field, M.S. (2018) An extended hybrid-stochastic model of folate-mediated one-carbon metabolism: 5-formyltetrahydrofolate futile cycle regulates de novo purine synthesis and reduces pathway stochasticity.  Sci Rep., 9:  4322.
  • Garza, C., Stover, P.J., Ohlhorst, S.D., Field, M.S., Steinbrook, R., Rowe, S., Woteki, C., and Campbell, E., (2019)  Best practices in nutrition science to earn and keep the public’s trust.  Amer. J. Clin. Nutr., 0:  1-19.
  • Alonzo, J.R., Venkataraman, C., Field, M.S., and Stover, P.J.  (2018) The mitochondrial inner membrane protein MPV17 prevents uracil accumulation in mitochondrial DNA.  J. Biol. Chem., 293:  20285-20294.
  • Lan, X., Field, M.S., and Stover, P.J. (2018) Cell Cycle Regulation of Folate-Mediated One-Carbon Metabolism.  Wiley Interdisciplinary Reviews: Systems Biology and Medicine, 10:e1426.
  • Field, M.S., Kamynina, E., Chon, J., and Stover, P.J. (2018) Nuclear Folate Metabolism.  Ann. Rev. Nutr., 38:  219-43.
  • Field, M.S., Lan, X., Stover, D.M., and Stover, P.J. (2018) Uridine modifies tumorigenesis in the ApcMin/+model of intestinal cancer.  Curr. Dev. Nutr., 2:  nzy013
  • Field, M.S. and Stover, P.J. (2017) Safety of folic acid.  Ann. NY Acad. Sci., 1414:  59-71.
  • Stover, P.J., Durga, J., and Field, M.S. (2017) Folate and blood-brain barrier dysfunction.  Curr. Opin. Biotechnol., 44:  146-152.
  • Palmer, A.M., Kamynina, E., Field, M.S., and Stover, P.J. (2017) Folate rescues vitamin B12 depletion-induced inhibition of nuclear thymidylate biosynthesis and genome instability.  Proc. Natl. Acad. Sci., 114:  E4095-4102 
  • Kamynina, E., Lachenauer, E., DiRisio, A.C., Liebenthal, R.P., Field, M.S., and Stover, P.J. (2017) Arsenic trioxide targets MTHFD1 and SUMO-dependent nuclear de novo thymidylate biosynthesis.  Proc. Natl. Acad. Sci., 114:  E2319-E2326.
  • Misselbeck, K., Marchetti, L., Field, M.S., Scotti, M., Priami, C.,  and Stover, P.J. (2017) A hybrid stochastic model of folate-mediated one-carbon metabolism: Effect of the common C677T MTHFR variant on de novo thymidylate biosynthesis.  Sci Rep., 11:  797.
  • Bae, S., Chon, J., Field, M.S., and Stover, P.J. (2017) Alcohol dehydrogenase 5 is a source of formate for de novo purine biosynthesis in HepG2 cells.  J. Nutr., 147:  499-505.
  • Chon, J., Stover, P.J., and Field, M.S. (2017) Targeting Nuclear Thymidylate Biosynthesis.  Molecular Aspects of Medicine, 53:  48-56.
  • Stover, P.J., Berry, R.J., and Field, M.S. (2016) Time to think about nutrient needs in chronic disease.  JAMA Internal Medicine, 176:  1451-1452
  • Field, M.S., Stover, P.J., and Kisliuk, R. (2016) Thymidylate Synthesis.  In: eLS. John Wiley & Sons, Ltd: Chichester. DOI: 10.1002/9780470015902.a0001397.pub3
  • Field, M.S., Kamynina E., Watkins, D., Rosenblatt, D.S., Stover, P.J. (2016) MTHFD1 regulates nuclear de novo thymidylate biosynthesis and genome stability.  Biochimie, 126: 27-30.
  • Field, M.S., Kamynina E., Watkins, D., Rosenblatt, D.S., Stover, P.J. (2015) New insights into the metabolic and nutritional determinants of severe combined immunodeficiency.  Rare Diseases, 3: 1, e1112479.
martha field

Martha Field, PhD, Field Lab PI
113 Savage Hall
Division of Nutritional Sciences at Cornell University
244 Garden Avenue, Ithaca NY, 14853
mas246@cornell.edu
(607)255-6081

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