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X Chromosome Factors that Contribute to Sex Differences in Disease

C.E. Credits: P.A.C.E. CE Florida CE
Speaker
  • Distinguished Research Professor, Department of Integrative Biology & Physiology University of California, Los Angeles
    Biography

      Arthur P. Arnold (AB, Grinnell College; PhD, The Rockefeller University) studies mechanisms causing sex differences in physiology and disease.  His research has included the discovery of large structural sexual dimorphisms in the CNS, development of several animal models for studying sex differences, and studies of mechanisms by which sex-biasing factors operate, including sex chromosome effects. Dr. Arnold is Distinguished Research Professor in the Department of Integrative Biology & Physiology at UCLA, and a fellow of the AAAS and the John Simon Guggenheim Memorial Foundation. Previous positions include departmental Chair, Associate Director of the UCLA Brain Research Institute, Chair of the UCLA interdepartmental PhD and undergraduate programs for neuroscience, founding President of the Society of Behavioral Neuroendocrinology, and founding Editor-in-Chief of Biology of Sex Differences.


    Abstract

    Many diseases show sex differences in incidence or progression, suggesting that one sex has inherent biological factors that protect from or exacerbate disease. Historically the root causes of all sex differences in tissue phenotypes were thought to be the gonadal hormones. The advent of specialized mouse models has uncovered non-hormonal origins of sex bias in disease, caused by inherent inequality of XX vs. XY sex chromosomes. For example, the Four Core Genotypes and XY* models allow the investigator to compare mice with different sex chromosomes, but with the same type of gonad. Use of these mouse lines in several models of disease has now progressed far enough that specific X or Y genes have been identified that give rise to molecular cascades causing sex differences in disease. The number of X chromosomes, one vs. two, causes sex differences in models of metabolism and adiposity, of autoimmune disease, of Alzheimer’s disease, and bladder cancer. The underlying genes that cause the X chromosome effects are X-linked Kdm5c and Kdm6a, two lysine demethylases acting on H3K4 to activate or reduce gene expression elsewhere in the genome. The genes escape X inactivation and are expressed from all X chromosomes, so that XX cells express a higher dose than XY cells. This inherent inequality influences diverse tissues and diseases. Just as the discovery of gonadal hormonal sex-biasing factors, such as testosterone and estradiol, catalyzed waves of discovery of downstream mechanisms leading to sexual dimorphism in many tissues, we now expect the discovery of new sex chromosomal sex-biasing factors to lead to new research on novel pathways causing sex differences in diverse tissues related to numerous diseases. Supported by NIH grants OD026560, HD100298, HD076125, DK083561, HL1311820

    Learning Objectives:

    1. Understand mouse models that test inherent sex differences in X and Y gene dose that cause sex differences in disease.

    2. Appreciate new evidence about specific X genes that are the origins of sex bias in the genome.


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