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      The Emerging Role of Chromatin Remodeling Factors in Female Pubertal Development

      , , *

      Neuroendocrinology

      S. Karger AG

      Epigenetics, Puberty, Kiss1, GnRH

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          Abstract

          To attain sexual competence, all mammalian species go through puberty, a maturational period during which body growth and development of secondary sexual characteristics occur. Puberty begins when the diurnal pulsatile gonadotropin-releasing hormone (GnRH) release from the hypothalamus increases for a prolonged period of time, driving the adenohypophysis to increase the pulsatile release of luteinizing hormone with diurnal periodicity. Increased pubertal GnRH secretion does not appear to be driven by inherent changes in GnRH neuronal activity; rather, it is induced by changes in transsynaptic and glial inputs to GnRH neurons. We now know that these changes involve a reduction in inhibitory transsynaptic inputs combined with increased transsynaptic and glial excitatory inputs to the GnRH neuronal network. Although the pubertal process is known to have a strong genetic component, during the last several years, epigenetics has been implicated as a significant regulatory mechanism through which GnRH release is first repressed before puberty and is involved later on during the increase in GnRH secretion that brings about the pubertal process. According to this concept, a central target of epigenetic regulation is the transcriptional machinery of neurons implicated in stimulating GnRH release. Here, we will briefly review the hormonal changes associated with the advent of female puberty and the role that excitatory transsynaptic inputs have in this process. In addition, we will examine the 3 major groups of epigenetic modifying enzymes expressed in the neuroendocrine hypothalamus, which was recently shown to be involved in pubertal development and progression.

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          Most cited references 81

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          Mechanisms of polycomb gene silencing: knowns and unknowns.

          Polycomb proteins form chromatin-modifying complexes that implement transcriptional silencing in higher eukaryotes. Hundreds of genes are silenced by Polycomb proteins, including dozens of genes that encode crucial developmental regulators in organisms ranging from plants to humans. Two main families of complexes, called Polycomb repressive complex 1 (PRC1) and PRC2, are targeted to repressed regions. Recent studies have advanced our understanding of these complexes, including their potential mechanisms of gene silencing, the roles of chromatin modifications, their means of delivery to target genes and the functional distinctions among variant complexes. Emerging concepts include the existence of a Polycomb barrier to transcription elongation and the involvement of non-coding RNAs in the targeting of Polycomb complexes. These findings have an impact on the epigenetic programming of gene expression in many biological systems.
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            The COMPASS family of histone H3K4 methylases: mechanisms of regulation in development and disease pathogenesis.

            The Saccharomyces cerevisiae Set1/COMPASS was the first histone H3 lysine 4 (H3K4) methylase identified over 10 years ago. Since then, it has been demonstrated that Set1/COMPASS and its enzymatic product, H3K4 methylation, is highly conserved across the evolutionary tree. Although there is only one COMPASS in yeast, Drosophila possesses three and humans bear six COMPASS family members, each capable of methylating H3K4 with nonredundant functions. In yeast, the histone H2B monoubiquitinase Rad6/Bre1 is required for proper H3K4 and H3K79 trimethylations. The machineries involved in this process are also highly conserved from yeast to human. In this review, the process of histone H2B monoubiquitination-dependent and -independent histone H3K4 methylation as a mark of active transcription, enhancer signatures, and developmentally poised genes is discussed. The misregulation of histone H2B monoubiquitination and H3K4 methylation result in the pathogenesis of human diseases, including cancer. Recent findings in this regard are also examined.
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              Polycomb silencing mechanisms and the management of genomic programmes.

              Polycomb group complexes, which are known to regulate homeotic genes, have now been found to control hundreds of other genes in mammals and insects. First believed to progressively assemble and package chromatin, they are now thought to be localized, but induce a methylation mark on histone H3 over a broad chromatin domain. Recent progress has changed our view of how these complexes are recruited, and how they affect chromatin and repress gene activity. Polycomb complexes function as global enforcers of epigenetically repressed states, balanced by an antagonistic state that is mediated by Trithorax. These epigenetic states must be reprogrammed when cells become committed to differentiation.
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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                978-3-318-06640-1
                978-3-318-06641-8
                0028-3835
                1423-0194
                2019
                September 2019
                07 February 2019
                : 109
                : 3
                : 208-217
                Affiliations
                Division of Genetics, Oregon National Primate Research Center, Oregon Health and Science University (OHSU), Beaverton, Oregon, USA
                Author notes
                *Alejandro Lomniczi, Division of Genetics, Oregon National Primate Research Center, Oregon Health and Science University (OHSU), Beaverton, OR 97006 (USA), E-Mail lomniczi@ohsu.edu
                Article
                497745 PMC6794153 Neuroendocrinology 2019;109:208–217
                10.1159/000497745
                PMC6794153
                30731454
                © 2019 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 3, Pages: 10
                Categories
                At the Cutting Edge

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