405 Eberhart Building
Gene Environment Interactions and Epigenetics
Ph.D., Hokkaido University
My research interests are to elucidate mechanisms underlying gene environment interactions and developmental origins of adult and transgenerational health abnormalities. My group takes comparative, molecular, cellular, and bioinformatics analysis approaches and utilizes cell/tissue culture and animal models (fish and rodents). Current projects include basic science of germ cell epigenetic programming, epigenotoxicity of environmental stressors such as: pharmaceuticals, pesticides, bisphenol A, marijuana (including its metabolites), engineered nanoparticles, etc., and trangenerational inheritance of epimutations.
Environmental chemicals can induce a variety of adverse health effects via disruption of normal endocrine function in eukaryotic organisms. These chemically induced effects are not only observed as immediate organismal responses (direct toxic effects), but also as a variety of diseases in the future generations who were never exposed. The organism that develops abnormal health conditions without direct exposure to stressors, but rather because prior generations were exposed, is said to have a transgenerational phenotype. Transgenerational phenotypes have been observed in many organisms, including humans, rodents, fish, and plants. Mechanisms underlying transmission of transgenerational health effects are poorly understood; however, evidence suggests that sperm (in the majority of cases, or sometimes eggs) carry such effect in the form of epigenetic modifications, warranting a call for the comprehensive study of germ cell epigenetics and gene-environment interactions. We are striving: 1) to identify chemical exposure and phenotype-specific epigenetic and transcriptomic alterations in germline cells and somatic tissues, including circulating exosomes 2) to understand the role of the identified alterations in disease onset, and 3) to erase epimutations in individuals with transgenerational phenotypes using Crispr-Cas9 method.
Bhandari, R.K. (2016). Medaka as a model for studying environmentally induced transgenerational inheritance phenotypes. Environmental Epigenetics 2:1-9.
Skinner, M.K., Bhandari, R.K., Haque, M.M., Nilsson, E.E. (2016). Environmentally induced epigenetic transgenerational inheritance of altered SRY genomic binding during gonadal sex determination. Environmental Epigenetics 1: 1-10. doi: 10.1093/eep/evv004
Bhandari R.K., vom Saal, F.S., Tillitt, D. E. (2015). Transgenerational effects from early developmental exposures to bisphenol A or 17α-ethinylestradiol in medaka, Oryzias latipes. Scientific Reports, 5 : 9303.
Bhandari RK, Deem SL, Holliday DK, Jandegian CM, Kassotis CD, Nagel SC, Tillitt DE, Vom Saal FS, Rosenfeld CS (2015). Effects of the environmental estrogenic contaminants bisphenol A and 17α-ethinylestradiol on sexual development and adult behaviors in aquatic wildlife species. General and Comparative Endocrinology. 214:195-219.
Skinner MK, Guerrero-Bosagna C, Haque M, Nilsson E, Bhandari RK, McCarrey JR (2013) Environmentally induced transgenerational epigenetic reprogramming of primordial germ cells and the subsequent germ line. PLoS One. 8(7):e66318.
Developmental Biology (BIO 464, Spring 2017)
Molecular Approaches to Research: Transgenerational Inheritance (Bio 596, Fall 2017)
Human Embryology and Teratology (Bio 614, Fall 2017)