Michael Golding

Assistant Professor
Department of Veterinary Physiology & Pharmacology College of Veterinary Medicine Texas A&M University
Room 332 VMA College Station, TX 77843-4466

Research Interests: Fetal Physiology, Epigenetic Programming and Fetal Alcohol Syndrome.

Teaching: My undergraduate and graduate courses (VTPP 489/689 Fetal & Embryo Physiology VTPP 689 - Epigenetics & Development) explore the molecular mechanisms of developmental programing and the impact of nutrition & environmental toxins on the development of disease.

Summary: My laboratory is interested in epigenetic mechanisms controlling early mammalian development and the impact of dietary / environmental agents on developmental programming.

Mammalian Development and Epigenetics

Mammalian development consists of a series of carefully orchestrated changes in gene expression that occur as stem or progenitor cells differentiate to form the tissues and organs making up the growing fetus. These dynamic changes in gene expression arise from cell-specific alterations in the way in which the DNA encoding each gene becomes packaged within the nucleus. Much like a closed book cannot be read while an open book can, genes can either be tightly wound up and silent or in a relaxed, open, active state. As development proceeds, the DNA of each cell becomes packaged in a way that is unique to that cell type and thus "programmed" to express a specific cohort of genes, which confer its individual identity and physiological function. During fetal development, the processes of developmental programming are profoundly influenced by maternal nutrition and exposure to environmental toxins. My lab is interested in understanding how the maternal consumption of alcohol during pregnancy alters fetal developmental programming resulting in disease.

Three enzymatic mechanisms control the assembly and regulation of chromatin structure: DNA methylation, post-translational histone modification and ATP-dependent chromatin remodeling. These fundamental processes, which control gene packaging, are heritable through cell division and referred to as epigenetic as they impart a level of regulation that is above or "epi" to genetics. As development proceeds, changes to the epigenetic profile of a cell reflect various lineage commitment and differentiation events along the path to obtaining the specialized cell types making up the growing fetus. Defects in the capacity of the embryo to properly program differentiating cells result in developmental failure or structural/functional defects due to inappropriate patterns of gene expression. This is especially true during development of the fetal nervous system wherein carefully choreographed changes in gene expression promote neural stem cell differentiation into the enormously complex array of cell types that pattern the stable synaptic connections that will persist for a lifetime. A teratogen that alters the epigenetic program of even a few neuro-progenitor stem cells during fetal growth is likely to disproportionately influence subsequent brain development and has the potential to impart severe neurological birth defects. My laboratory is currently exploring the impact of in utero exposure to alcohol on DNA methylation and histone post-translational modification using a stem cell model.

Extra-embryonic Endoderm Stem Cells
XEN - Cells