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Photo of Golding, Michael 

Michael Golding
Assistant Professor
Curriculum Vitae
Contact

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

Scholarly Interests


My lab is interested in understanding the epigenetic mechanisms that control transcription of endogenous retroviral elements within the genome. To contend with the constant threat of retroviral infection, both from exogenous as well as endogenous elements, mammalian genomes have evolved complex defense mechanisms to impede the life cycle of invading parasitic nucleic acids. Throughout evolutionary time the interplay between endogenous viral elements and the biochemical molecules that silence them have helped shape the transcriptional landscape of mammalian genomes and provided additional layers of control for expression of protein coding genes. The phenomenon known as RNA interference (RNAi) is one example of a defense mechanism that very likely evolved to control retroviral elements but which has also been adapted to modulate gene expression via regulation through microRNAs (miRNAs) and endogenous siRNAs. My research focuses on discovering the nature of the molecular signature that a cell uses to discern “self” from “non-self” (viral) and what biochemical factors and mechanisms are recruited to silence the latter. Different cell types seem to have different tolerances for retroviral activity and seemingly different mechanisms to control their expression. Within the mouse preimplantation embryo the three different stem cell types have different tolerances for retroviral activity. It has long been known that cells that give rise to the embryo silence retroviruses given the necessity of preventing insertional mutagenesis that could arise from retroviral reactivation. Surprisingly, cells that give rise to the placenta do not appear to silence retroviruses and cells of extraembryonic endoderm that give rise to the yolk sac and amnion exhibit extremely aggressive retroviral extinction. Thus with the very first differentiation event of mammalian development three different tolerances for retroviral activity and potentially three unique regulatory mechanisms exist. My lab uses a stem cell model system to examine the mechanisms governing retroviral transcription in each of these cell types.