Michael C. Golding
Associate ProfessorPhone: (979) 862-1332Email: firstname.lastname@example.org
Research and Scholarly Interests
Within the department, I serve as the lead instructor for two courses covering human embryology and the physiological events of pregnancy. My research is focused at the interface between pregnancy and epigenetics, trying to understand how environmental exposures before conception or early in development cause disease later in life. My lab works in the area of research known as Developmental Programming, which seeks to better understand the biochemical mechanisms by which chromatin structure is altered during development and how these epigenetic changes cause birth defects and disease.
- BSc in Honors Genetics, University of Western Ontario, London, Ontario Canada, 1996 – 2000
- PhD in Veterinary Physiology, Texas A&M University, College Station, Texas USA, 2000 – 2003
- Postdoctoral Fellowship, Cold Spring Harbor Laboratories, Cold Spring Harbour, New York USA, 2004 – 2006
- Canadian Institute of Health Postdoctoral Fellow, University of Western Ontario, London, Ontario Canada, 2006 – 2009
I am a tenured Associate Professor in 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. I am an associate editor for the scientific journal Environmental Epigenetics and have served on multiple NIH, NSF and CIHR study sections examining epigenetics and developmental programming. My research program focuses on understanding the biochemical mechanisms by which chromatin structure is altered during development, how these processes are influenced by environmental exposures, and the capacity of these heritable changes to influence physiological function.
My Ph.D. studies focused on deciphering the developmental basis to the structural, and placental defects observed in bovine fetuses conceived through somatic cell nuclear transfer or animal cloning. This work prompted me to begin examining embryonic patterns of DNA methylation and the role of epigenetic programming in the failed development of clones. In 2006, I received a fellowship to continue studies of developmental programming in the laboratory of Dr. Mellissa Mann, who examines the impacts of superovulation and embryo culture on the epigenetic regulation of imprinted genes.
- Cell Biology
- Reproductive and Developmental Biology
My long-term objective is to understand the mechanisms that control chromatin structure within the developing embryo and how environmental exposures, either before conception or during gestation, cause birth defects and disease. My laboratory studies environmentally-induced alterations in cellular patterns of DNA methylation and post-translational histone modifications within the developing fetus. As a model, my laboratory studies the growth defects associated with fetal alcohol spectrum disorders (FASDs) and how the cellular memory of alcohol exposures, either before conception or during gestation, influence the growth and development of the offspring. We suspect that disruptions in the epigenetic program of the early embryo alter the formation or function of the placenta, which leads to long-term alterations in developmental programming within the offspring.
Our studies have demonstrated lineage-specific sensitivities to ethanol-induced alterations in histone structure and that multiple embryonic cell types are susceptible to alcohol-induced perturbation of the histone code (Veazey et al., 2013). We have conducted basic research into the transcriptional consequences of alcohol exposure in vitro and identified a significant correlation between altered histone structure and alcohol-induced central nervous system birth defects in vivo (Veazey et al., 2015, Veazey et al., 2017). Recently, we have begun to examine the impacts alcohol exposures have on long-term developmental programming and the propensity of preconception paternal alcohol exposures to influence fetal development. Our most recent work (Cheng et al., 2017) demonstrates the capacity of chronic male alcohol exposure to induce fetal growth restriction and that these influences on offspring phenotype are not associated with heritable alterations in the DNA methylation profile of sperm.
Chang RC, Skiles WM, Chronister SS, Wang H, Sutton GI, Bedi YS, Snyder M, Long CR, Golding MC. DNA methylation-independent growth restriction and altered developmental programming in a mouse model of preconception male alcohol exposure. Epigenetics. 2017;12(10):841-853. PubMed PMID: 28816587; PubMed Central PMCID: PMC5788439.
Veazey KJ, Wang H, Bedi YS, Skiles WM, Chang RC, Golding MC. Disconnect between alcohol-induced alterations in chromatin structure and gene transcription in a mouse embryonic stem cell model of exposure. Alcohol. 2017 May;60:121-133. PubMed PMID: 28433419; PubMed Central PMCID: PMC5484046.
Veazey KJ, Parnell SE, Miranda RC, Golding MC. Dose-dependent alcohol-induced alterations in chromatin structure persist beyond the window of exposure and correlate with fetal alcohol syndrome birth defects. Epigenetics Chromatin. 2015;8:39. PubMed PMID: 26421061; PubMed Central PMCID: PMC4587584.
Veazey KJ, Carnahan MN, Muller D, Miranda RC, Golding MC. Alcohol-induced epigenetic alterations to developmentally crucial genes regulating neural stemness and differentiation. Alcohol Clin Exp Res. 2013 Jul;37(7):1111-22. PubMed PMID: 23488822; PubMed Central PMCID: PMC3688681.
Golding Lab Projects
Paternal Exposures Prior to Conception and Placental Development
Using a mouse model, our lab has associated preconception male alcohol exposure with fetal growth restriction and long-term alterations in the metabolic health of offspring. We believe these alterations in developmental programming are linked to placental defects caused by epigenetic errors in the alcohol-exposed sperm. Our current research is aimed at trying to decipher the mechanisms by which these epigenetic errors arise and are transmitted to the offspring.
Current and Past Funding
NIH – National Institute of Alcoholism and Alcohol Abuse – 1R21AA022484 (2014–2016)
NIH – Office of Research Infrastructure Programs 5T35OD010991 (2011–2015)
NIH – National Institute of Alcoholism and Alcohol Abuse – RO3AA020129 (2010–2012)
My undergraduate and graduate courses explore the physiological processes of pregnancy with a special emphasis on the formation of the body plan, the endocrine control growth and parturition, and the development of birth defects. These courses provide a framework upon which to build a basic understanding of the physiology of pregnancy and several developmental disorders that arise due to biomedical miss-regulation or environmental exposures.
Michael C. Golding is accepting trainees of these groups:
- Graduate Students
- Non-Thesis Masters
- Undergraduate Scholars
Richard Cheng-An Chang: Originally from Kaohsiung Taiwan, Richard received his Master’s degree from National Yang-Ming University, where his work focused on the molecular pathways leading to obesity. Richard is now a Ph.D. student in the Golding lab, where his research focuses on sperm-inherited alterations in epigenetic programming.