filler

Michael Golding

Professor Department of Veterinary Physiology & Pharmacology
Contact
9798621332
TAMU Mailstop: 4466

Research and Scholarly Interests

My long-term goals are to change the narrative on the origins of alcohol-induced birth defects, define epigenetic mechanisms of paternal inheritance, and provide an entertaining yet impactful learning experience to future professionals in the biomedical sciences.

The Golding Lab works in the area of research known as Developmental Programming and our research is focused at the interface between pregnancy and epigenetics. Our focus areas include physiology, genetics, neurology, neuroscience, toxicology, and cell, reproductive, and developmental biology.

As a model, we study development defects associated with paternal alcohol exposures, how these defects influence fetal alcohol spectrum disorders (FASDs), and how the cellular memory of alcohol exposures, either before conception or during gestation, influences the growth and development of the offspring.

Within the Texas A&M Department of Veterinary Pharmacology & Physiology, I'm the lead instructor for two courses covering human embryology and the physiological events of pregnancy.

Visit my lab's website at vetmed.tamu.edu/golding-lab and follow my lab on X at x.com/GoldingLab.

Education

  • BSc in Honors Genetics, University of Western Ontario, London, Ontario, Canada, 1996 – 2000
  • Ph.D. 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'm a tenured professor in the Department of Veterinary Physiology & Pharmacology. Here, I serve as the director of two courses studying human embryology and the physiological events of pregnancy.

I'm 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 is focused on defining biochemical mechanisms of epigenetic inheritance, determining how these processes are influenced by exposure to toxicants, and the capacity of these heritable changes to cause birth defects and disease, and contribute to the development of fetal alcohol spectrum disorders (FASDs). Currently, we are focused on understanding how male drinking, prior to conception, contributes to the development of alcohol-induced birth defects and disease. [https://research.tamu.edu/2019/10/21/fathering-a-child-dont-drink/]

My former trainees have successfully transitioned to the next phase of their careers and taken positions at the MD Anderson Cancer Center, the University of Washington, the University of California Irvine, or have successfully obtained employment at Epizyme pharmaceuticals and Seattle Children’s Hospital. Due to my research’s multidisciplinary nature, I accept Ph.D. trainees from the Biomedical Sciences, Genetics, and Toxicology programs.

Current Funding

NIH – National Institute of Alcoholism and Alcohol Abuse – R01AA028219 Heritable epigenetic effects of Paternal alcohol use on FASD phenotypes (2020 – 2025)

Past Funding (last 5 years)

Medical Research Grant – W.M. Keck Foundation – Paternal contributions to fetal alcohol spectrum disorders: questioning the prevailing paradigm. (2019 – 2023)

Learn more about me and my work at the Golding Lab website.

  • Cell Biology
  • Genetics
  • Neurology
  • Neuroscience
  • Physiology
  • Reproductive and Developmental Biology
  • Toxicology

Learn more about our work at the Golding Lab website.

My long-term goals are to change the narrative on the origins of alcohol-induced birth defects, define epigenetic mechanisms of paternal inheritance, and provide an entertaining yet impactful learning experience to future professionals in the biomedical sciences.

As a model, we study development defects associated with paternal alcohol exposures, how these defects influence fetal alcohol spectrum disorders (FASDs), and how the cellular memory of alcohol exposures, either before conception or during gestation, influences the growth and development of 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., 2013Veazey et al., 2015Veazey et al., 2017).

In late 2014, we began examining the epigenetic impact of preconception paternal alcohol exposures on offspring development.

Our work is among the first to demonstrate that alcohol-induced epigenetic changes in sperm contribute to the development of alcohol-related growth and structural birth defects. Specifically, our recent studies reveal that male alcohol use:

  • induces microcephaly and alcohol-related craniofacial abnormalities in offspring (Thomas et al., 2023);
  • compromises placental development, reducing in vitro fertilization-embryo development and pregnancy success rates (Roach et al., 2023);
  • impacts epigenetic programming in sperm, with some alterations persisting after alcohol withdrawal (Roach et al., 2024); and
  • causes lasting alterations in offspring mitochondrial function that persist into adulthood and cause disease (Basel et al., 2024).

Today, we are expanding our model to examine interactions between maternal gestational and preconception paternal alcohol exposures, testing the hypothesis that dual-parental exposures exacerbate alcohol-related outcomes.

Current Funding

NIH – National Institute of Alcoholism and Alcohol Abuse – R01AA028219 Heritable epigenetic effects of Paternal alcohol use on FASD phenotypes (2020 – 2025)

Past Funding (last 5 years)

Medical Research Grant – W.M. Keck Foundation – Paternal contributions to fetal alcohol spectrum disorders: questioning the prevailing paradigm. (2019 – 2023)

Learn more about our research at the Golding Lab website.

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 to build a basic understanding of the physiology of pregnancy and several developmental disorders that arise due to biomedical misregulation or environmental exposures.

Learn more about our teaching at the Golding Lab website.

Our lab welcomes trainees from these groups and programs:

  • Graduate Students
  • Non-Thesis Masters
  • Postdoctoral Fellow
  • Undergraduate Scholars
  • Biomedical Sciences (BIMS)
  • Genetics (GENE)
  • Toxicology (TOXI)

Learn more about our Current Lab Members and our Lab Alumni at the Golding Lab website.

Comprehensive lists of our publications can be found at the following research databases:
ORCID | PubMed | Google Scholar | Scholars @ TAMU

Selected Publications

Aging in a Mouse Model. Aging and Disease. 2024 Jul 27. doi: 10.14336/AD.2024.0722. PMID: 39122451.

Roach AN, Bhadsavle SS, Higgins SL, Derrico DD, Basel A, Thomas KN, Golding MC. Alterations in sperm RNAs persist after alcohol cessation and correlate with epididymal mitochondrial dysfunction. Andrology. 2024 Jul;12(5):1012-1023. doi: 10.1111/andr.13566. Epub 2023 Dec 3. PMID: 38044754; PMCID: PMC11144833.

Thomas KN, Srikanth N, Bhadsavle SS, Thomas KR, Zimmel KN, Basel A, Roach AN, Mehta NA, Bedi YS, Golding MC. Preconception paternal ethanol exposures induce alcohol-related craniofacial growth deficiencies in fetal offspring. Journal of Clinical Investigation. doi: 10.1172/JCI167624. 2023 Apr PMID: 37040180.

Roach AN, Zimmel KN, Thomas KN, Basel A, Bhadsavle SS, Golding MC. Preconception paternal alcohol exposure decreases IVF embryo survival and pregnancy success rates in a mouse model. Molecular Human Reproduction. 2023a Jan 31;29(2):gaad002. doi: 10.1093/molehr/gaad002. PMID: 36637195; PMC9907225.

Chang RC, Thomas KN, Bedi YS, Golding MC. Programmed increases in LXRα induced by paternal alcohol use enhance offspring metabolic adaptation to high-fat diet-induced obesity. Mol Metab. 2019;30:161–172. doi: 10.1016/j.molmet.2019.09.016. PubMed ID: 31767168. PMCID: PMC6807343.

Bedi Y, Chang RC, Gibbs R, Clement TM, Golding MC. Alterations in sperm-inherited noncoding RNAs associate with late-term fetal growth restriction induced by preconception paternal alcohol use. Reproductive Toxicology. 2019 Apr 30;87:11-20. doi: 10.1016/j.reprotox.2019.04.006. PubMed ID: 31051257. PMCID: PMC6783280

Chang RC, Wang H, Bedi Y, Golding MC. Preconception paternal alcohol exposure exerts sex-specific effects on offspring growth and long-term metabolic programming. Epigenetics & Chromatin. 2019 Jan 22;12(1):9. doi: 10.1186/s13072-019-0254-0. PubMed ID: 30670059. PMC6341619

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. doi: 10.1080/15592294.2017.1363952. 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. doi: 10.1016/j.alcohol.2017.01.007. 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. doi: 10.1186/s13072-015-0031-7. 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. doi: 10.1111/acer.12080. PubMed PMID: 23488822; PubMed Central PMCID: PMC3688681.

Learn more about our research at the Golding Lab website.