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      Differential regulation of SC1/PRDM4 and PRMT5 mediated protein arginine methylation by the nerve growth factor and the epidermal growth factor in PC12 cells ☆

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          • •

            SC1/PRMT5 histone methyltransferase activity is down-regulated by NGF, but not EGF.

          • •

            NGF reduces the nuclear, but not the cytosolic SC1/PRMT5-mediated HMTase activity.

          • •

            SC1 and PRMT5 are found in the nucleus and the cytosol of primary mouse neurons.

          Abstract

          During neuronal development, the neuroepithelial stem cells (NSCs) initially undergo proliferative divisions, later switching to neurogenic ones whereby one NSC and a post-mitotic neuron are generated. We recently showed that a member of the PRDM family of transcriptional regulators, PRDM4/SC1, recruits a type II protein arginine methyltransferase, PRMT5, to maintain the “stem-like” cellular state of the embryonic mouse cortical NSCs. However, little is known about the regulation of activity of this complex under proliferation- or differentiation-inducing growth conditions.

          In the present work I investigate the regulation of SC1/PRMT5-mediated methylation activity in PC12 cells treated with EGF or NGF. I present evidence that NGF down-regulates SC1/PRMT5 methyltransferase (MTase) activity and that the reduction in SC1/PRMT5 MTase activity occurs mainly in the nucleus. I suggest that high levels of SC1/PRMT5 activity are associated with the proliferative state of the cells.

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          Transcriptional control of brown fat determination by PRDM16.

          Patrick Seale, Shingo Kajimura, Wenli Yang … (2007)
          Brown fat cells are specialized to dissipate energy and can counteract obesity; however, the transcriptional basis of their determination is largely unknown. We show here that the zinc-finger protein PRDM16 is highly enriched in brown fat cells compared to white fat cells. When expressed in white fat cell progenitors, PRDM16 activates a robust brown fat phenotype including induction of PGC-1alpha, UCP1, and type 2 deiodinase (Dio2) expression and a remarkable increase in uncoupled respiration. Transgenic expression of PRDM16 at physiological levels in white fat depots stimulates the formation of brown fat cells. Depletion of PRDM16 through shRNA expression in brown fat cells causes a near total loss of the brown characteristics. PRDM16 activates brown fat cell identity at least in part by simultaneously activating PGC-1alpha and PGC-1beta through direct protein binding. These data indicate that PRDM16 can control the determination of brown fat fate.
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            Establishment of a noradrenergic clonal line of rat adrenal pheochromocytoma cells which respond to nerve growth factor.

            L A Greene, A S Tischler (1976)
            A single cell clonal line which responds reversibly to nerve growth factor (NGF) has been established from a transplantable rat adrenal pheochromocytoma. This line, designated PC12, has a homogeneous and near-diploid chromosome number of 40. By 1 week's exposure to NGF, PC12 cells cease to multiply and begin to extend branching varicose processes similar to those produced by sympathetic neurons in primary cell culture. By several weeks of exposure to NGF, the PC12 processes reach 500-1000 mum in length. Removal of NGF is followed by degeneration of processes within 24 hr and by resumption of cell multiplication within 72 hr. PC12 cells grown with or without NGF contain dense core chromaffin-like granules up to 350 nm in diameter. The NGF-treated cells also contain small vesicles which accumulate in process varicosities and endings. PC12 cells synthesize and store the catecholamine neurotransmitters dopamine and norepinephrine. The levels (per mg of protein) of catecholamines and of the their synthetic enzymes in PC12 cells are comparable to or higher than those found in rat adrenals. NGF-treatment of PC12 cells results in no change in the levels of catecholamines or of their synthetic enzymes when expressed on a per cell basis, but does result in a 4- to 6-fold decrease in levels when expressed on a per mg of protein basis. PC12 cells do not synthesize epinephrine and cannot be induced to do so by treatment with dexamethasone. The PC12 cell line should be a useful model system for neurobiological and neurochemical studies.
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              PRMT5-mediated methylation of histone H4R3 recruits DNMT3A, coupling histone and DNA methylation in gene silencing.

              Quan Zhao, Gerhard Rank, Yuen Tan … (2009)
              Mammalian gene silencing is established through methylation of histones and DNA, although the order in which these modifications occur remains contentious. Using the human beta-globin locus as a model, we demonstrate that symmetric methylation of histone H4 arginine 3 (H4R3me2s) by the protein arginine methyltransferase PRMT5 is required for subsequent DNA methylation. H4R3me2s serves as a direct binding target for the DNA methyltransferase DNMT3A, which interacts through the ADD domain containing the PHD motif. Loss of the H4R3me2s mark through short hairpin RNA-mediated knockdown of PRMT5 leads to reduced DNMT3A binding, loss of DNA methylation and gene activation. In primary erythroid progenitors from adult bone marrow, H4R3me2s marks the inactive methylated globin genes coincident with localization of PRMT5. Our findings define DNMT3A as both a reader and a writer of repressive epigenetic marks, thereby directly linking histone and DNA methylation in gene silencing.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neurosci Lett
                Journal ID (iso-abbrev): Neurosci. Lett
                Title: Neuroscience Letters
                Publisher: Elsevier Scientific Publishers Ireland
                ISSN (Print): 0304-3940
                ISSN (Electronic): 1872-7972
                Publication date PMC-release: 29 August 2013
                Publication date (Print): 29 August 2013
                Volume: 550
                Issue: 100
                Pages: 87-92
                Affiliations
                [0005]Wolfson Institute for Biomedical Research, University College London, London, WC1E 6BT, United Kingdom
                Author notes
                [* ]Tel.: +44 0 207 679 6272; fax: +44 0797 390 5794. a.chittka@ 123456ucl.ac.uk
                Article
                Publisher ID: S0304-3940(13)00598-3
                DOI: 10.1016/j.neulet.2013.06.051
                PMC ID: 3776221
                PubMed ID: 23831350
                SO-VID: 5928be8b-2fcf-4aae-a774-44b5d09a3d6c
                Copyright © © 2013 The Author
                License:

                This document may be redistributed and reused, subject to certain conditions.

                History
                Date received : 20 March 2013
                Date revision received : 22 June 2013
                Date accepted : 24 June 2013
                Categories
                Subject: Article

                ScienceOpen disciplines: Neurosciences
                Keywords: sc1, schwann cell factor 1,prmt, protein arginine methyltransferase,prdm, positive regulatory domain protein,ngf, nerve growth factor,egf, epidermal growth factor,nsc, neural stem cells,(h)mtase, (histone) methyltransferase,prdm4,prmt5,histone arginine methylation,pc12 cells,ngf
                Data availability:
                ScienceOpen disciplines: Neurosciences
                Keywords: sc1, schwann cell factor 1, prmt, protein arginine methyltransferase, prdm, positive regulatory domain protein, ngf, nerve growth factor, egf, epidermal growth factor, nsc, neural stem cells, (h)mtase, (histone) methyltransferase, prdm4, prmt5, histone arginine methylation, pc12 cells, ngf

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