Skip Navigation

Michael Golding

Associate Professor

Send Email

Phone: (979) 862-1332

Mailstop: 4466

Department: VTPP

Photo of Golding, Michael

Golding Lab

    I am an Associate Professor within the department of Veterinary Physiology at Texas A&M University. Here, I serve as the instructor of record for two courses studying human embryology and the physiological events of pregnancy. My research program focuses on understanding how exposures to various environmental chemicals alters the developmental program and cause birth defects. My lab is interested in the area of research known as Developmental Programming and Epigenetics. We seek to better understand the biochemical mechanisms by which chromatin structure is altered during development, and how these processes can be influenced by environmental factors. We currently employ a mouse model of developmental programming and study the abnormalities induced by prenatal alcohol exposure. I am interested in understanding the mechanisms that recruit epigenetic modifiers to specific cohorts of genes, identifying the biochemical machinery directing these processes, and determining how these events are impacted by environmental toxins and teratogens. I currently serve as an associate editor for the scientific journal Environmental Epigenetics, and have served as the PI for an R03, an R21, as well as a co-PI on university- and NIH-funded grants examining Epigenetics and Developmental Programming.

    Epigenetics & Fetal Alcohol Syndrome

      Work from my laboratory has demonstrated that alcohol has the capacity to act as a powerful epigenetic disruptor and can derail the transcriptional processes directing mammalian development. Our studies have shown that mice encountering an acute exposure to alcohol on gestational Day-7 exhibit significant alterations in chromatin structure (histone 3 lysine 9 dimethylation, lysine 9 acetylation, and lysine 27 trimethylation) at Day-17, and that these changes strongly correlate with the development of craniofacial and central nervous system defects. Our work to date indicates that alcohol-induced modifications to chromatin structure persist beyond the window of exposure, and likely contribute to the development of fetal alcohol syndrome-associated congenital abnormalities. My lab was among the first in the country to receive federal funding to examine an epigenetic basis for fetal alcohol syndrome, and we continue to make significant inroads into understanding the developmental origins of alcohol-induced birth defects. Today we are currently working to identify mechanisms by which ethanol influences epigenetic programming and ultimately test nutritional or small molecule interventions. Through this research, I seek to ultimately determine how alcohol and nutrition interact at the level of chromatin structure, and train future scientists to examine epigenetic mechanisms in the etiology of alcohol related birth defects.

Education

  • Postdoc Epigenetics, Childrens Health Research Institute - UWO 2009
  • Postdoc RNA Interference, Cold Spring Harbor Labs 2006
  • Ph.D. Veterinary Physiology, Texas A&M University 2003
  • BSc. Molecular Genetics, University of Western Ontario 2000

Job Functions

  • Teaching Undergraduate & Graduate Fetal Physiology. Conducting Research Examining Mammalian Pregnancy & Development

Scholarly Interests

Epigenetics; Developmental Programming; DOHaD; Birth Defects; Fetal Physiology; Congenital Defects; Fetal Alcohol Spectrum Disorders; Chromatin Structure; DNA Methylation; Placentation; Genomic Imprinting; Developmental Biology

Publications

Histone-lysine N-methyltransferase SETDB1 is required for development of the bovine blastocyst
Golding MC, Snyder M, Williamson GL, Veazey KJ, Peoples M, Pryor JH, Westhusin ME and Long CR.
Theriogenology.


Request Update