Javier Revollo Ph.D.

Research Biologist — Division of Genetic and Molecular Toxicology

Javier Revollo, Ph.D.
(870) 543-7121
NCTRResearch@fda.hhs.gov

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Background

Dr. Javier Revollo received a B.S. degree in genetics from the University of Wisconsin-Madison in 2000 and a Ph.D. from Washington University in St. Louis in 2006. He pursued postdoctoral studies at the National Institutes of Health (NIH) between 2007 and 2012. He joined FDA as a commissioner’s fellow in 2012. During his career, Dr. Revollo has studied several biomedical phenomena, including parasitology, NAD biosynthesis, mammalian aging, and glucocorticoid signaling. He has received numerous awards, including:

“Fellows Award for Research Excellence” (NIH, 2010)
“Rodbell Research Award” (NIH, 2010)
“Presidential Award” from The Endocrine Society in 2011.

Dr. Revollo was recruited to FDA because of his expertise in mammalian genetics and next generation sequencing (NGS).

Research Interests

The flow cytometry-based Pig-a assay detects cells deficient in Glycosylphosphatidylinositol (or GPI)-anchored surface markers and provides a rapid and cost-effective enumeration of cells that are presumed to contain mutations in the endogenous X-linked Pig-a gene. Dr. Revollo is currently working on the validation of the Pig-a assay by genetically characterizing presumed Pig-a mutants derived from the assay.

Another research area that interests Dr. Revollo is the direct detection of somatic mutations. Somatic mutations are genetic alterations in cells that increase cancer risk. They can occur spontaneously but also result from DNA damage induced by the environment (e.g., sunlight) or genotoxic compounds (e.g, carcinogens). Current genetic toxicology assays can only estimate somatic-mutation rates by assaying the function of certain gene markers (e.g., Pig-a) or transgenes. Dr. Revollo is developing NGS methods capable of directly and efficiently identifying somatic mutations in the whole genome — in any tissue, and in any species, or any established cell culture — without the need for selecting and expanding cells that have mutations in only a few specific reporter genes.

Professional Societies/National and International Groups

Environmental Mutagen and Genomics Society
Member
2014 – 2016

Applied Technologies Session Chair
2014

Transgenic and In Vivo Mutagenesis Special Interest Group New Investigator Co-chair
Current

Hispanic Organization of Toxicologists
Member
2016

Society for Advancement of Hispanics/Chicanos and Native Americans in Science
Member
2010 – 2012

Selected Publications

Whole Genome Sequencing of Mouse Lymphoma L5178Y-3.7.2C (TK+/-) Reveals Millions of Mutations and Genetic Markers.
McKinzie P.B. and Revollo J.R.
Mutat Res Genet Toxicol Environ Mutagen. 2017, 814:1-6. doi: 10.1016/j.mrgentox.2016.12.001. Epub 2016 Dec 5.

Mutation Analysis with Random DNA Identifiers (MARDI) Catalogs Pig-A Mutations in Heterogeneous Pools of CD48-Deficient T Cells Derived from DMBA-Treated Rats.
Revollo J.R., Crabtree N.M., Pearce M.G., Pacheco-Martinez M.M., and Dobrovolsky V.N.
Environ Mol Mutagen. 2016, 57(2):114-24.

Whole Genome and Normalized mRNA Sequencing Reveal Genetic Status of TK6, WTK1, and NH32 Human B-Lymphoblastoid Cell Lines.
Revollo J., Petibone D.M., McKinzie P., Knox B., Morris S.M., Ning B., and Dobrovolsky V.N.
Mutat Res Genet Toxicol Environ Mutagen. 2016, 795:60-9.

CD48-Deficient T-Lymphocytes from DMBA-Treated Rats have De Novo Mutations in the Endogenous Pig-A Gene.
Dobrovolsky V.N., Revollo J., Pearce M.G., Pacheco-Martinez M.M., and Lin H.
Environ Mol Mutagen. 2015, 56(8):674-83.

Confirmation of Pig-A Mutation in Flow Cytometry-Identified CD48-Deficient T-Lymphocytes from F344 Rats.
Revollo J., Pearce M.G., Petibone D.M., Mittelstaedt R.A., and Dobrovolsky V.N.
Mutagenesis. 2015, 30(3):315-24.

Draft Genome Sequence of a Methicillin-Resistant Staphylococcus aureus ST1413 Strain for Studying Genetic Mechanisms of Antibiotic Resistance.
Marasa B.S., Revollo J., Iram S., Sung K., Xu J., and Khan S.
Genome Announc. 2014, 2(2). pii:e00162-14.

HES1 is a Master Regulator of Glucocorticoid Receptor-Dependent Gene Expression.
Revollo J.R., Oakley R.H., Lu N.Z., Kadmiel M., Gandhavadi M., and Cidlowski J.A.
Sci Signal. 2013, 6(304):ra103.

The Ways and Means that Fine Tune Sirt1 Activity.
Revollo J.R. and Li X.
Trends Biochem Sci. 2013, 38(3):160-7.

Glucocorticoids Regulate Arrestin Gene Expression and Redirect the Signaling Profile of G Protein-Coupled Receptors.
Oakley R.H., Revollo J., and Cidlowski J.A.
Proc Natl Acad Sci U S A. 2012, 109(43):17591-6.

Mechanisms Generating Diversity In Glucocorticoid Receptor Signaling.
Revollo J.R. and Cidlowski J.A.
Ann N Y Acad Sci. 2009, 1179:167-78.

Nampt/PBEF/Visfatin Regulates Insulin Secretion in Beta Cells as a Systemic NAD Biosynthetic Enzyme.
Revollo J.R., Körner A., Mills K.F., Satoh A., Wang T., Garten A., Dasgupta B., Sasaki Y., Wolberger C., Townsend R.R., Milbrandt J., Kiess W., and Imai S.
Cell Metab. 2007, 6(5):363-75.

The Regulation of Nicotinamide Adenine Dinucleotide Biosynthesis by Nampt/PBEF/Visfatin in Mammals.
Revollo J.R., Grimm A.A., and Imai S.
Curr Opin Gastroenterol. 2007, 23(2):164-70.

Structure of Nampt/PBEF/Visfatin, a Mammalian NAD+ Biosynthetic Enzyme.
Wang T., Zhang X., Bheda P., Revollo J.R., Imai S., and Wolberger C.
Nat Struct Mol Biol. 2006, 13(7):661-2.

The NAD Biosynthesis Pathway Mediated by Nicotinamide Phosphoribosyltransferase Regulates Sir2 Activity in Mammalian Cells.
Revollo J.R., Grimm A.A., and Imai S.
J Biol Chem. 2004, 279(49):50754-63.

Sphingolipids are Essential for Differentiation but not Growth in Leishmania.
Zhang K., Showalter M., Revollo J., Hsu F.F., Turk J., and Beverley S.M.
EMBO J. 2003, 22(22):6016-26.

Lab Member

Contact information for all lab members:
(870) 543-7121
NCTRResearch@fda.hhs.gov

Lea Patrice McDaniel, M.S.
Biologist

Contact Information: Javier Revollo; (870) 543-7121

Expertise: Expertise

Approach

Domain

Technology & Discipline

Toxicology