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Histone lysine methylation: critical regulator of memory and behavior

  • Timothy J. Jarome

    Dr. Timothy J. Jarome received his PhD in Neuroscience from the University of Wisconsin at Milwaukee in 2013. As a postdoctoral fellow at the University of Alabama at Birmingham, he began to collaborate with Dr. Lubin concerning the characterization of histone methylation mechanisms in memory formation.

    und Farah D. Lubin

    Dr. Farah D. Lubin received her PhD from the Department of Biology, SUNY Binghamton University, in 2001. After postdoctoral training at Baylor College of Medicine, she obtained a position in January 2009 as an Assistant Professor in the Neurobiology Department at the University of Alabama at Birmingham. Her main research work is focused on investigating the molecular and genetic basis of learning, memory, and its disorders.

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Veröffentlicht/Copyright: 27. Mai 2013
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Abstract

Histone lysine methylation is a well-established transcriptional mechanism for the regulation of gene expression changes in eukaryotic cells and is now believed to function in neurons of the central nervous system to mediate the process of memory formation and behavior. In mature neurons, methylation of histone proteins can serve to both activate and repress gene transcription. This is in stark contrast to other epigenetic modifications, including histone acetylation and DNA methylation, which have largely been associated with one transcriptional state in the brain. In this review, we discuss the evidence for histone methylation mechanisms in the coordination of complex cognitive processes such as long-term memory formation and storage. In addition, we address the current literature highlighting the role of histone methylation in intellectual disability, addiction, schizophrenia, autism, depression, and neurodegeneration. Further, we discuss histone methylation within the context of other epigenetic modifications and the potential advantages of exploring this newly identified mechanism of cognition, emphasizing the possibility that this molecular process may provide an alternative locus for intervention in long-term psychopathologies that cannot be clearly linked to genes or environment alone.


Corresponding author: Farah D. Lubin, PhD, The Evelyn F. McKnight Brain Institute, Department of Neurobiology, University of Alabama at Birmingham, Shelby Building, 1825 University Boulevard, Birmingham, AL 35294, USA, Phone: +(205) 996-2242, Fax: +(205) 934-6571

About the authors

Timothy J. Jarome

Dr. Timothy J. Jarome received his PhD in Neuroscience from the University of Wisconsin at Milwaukee in 2013. As a postdoctoral fellow at the University of Alabama at Birmingham, he began to collaborate with Dr. Lubin concerning the characterization of histone methylation mechanisms in memory formation.

Farah D. Lubin

Dr. Farah D. Lubin received her PhD from the Department of Biology, SUNY Binghamton University, in 2001. After postdoctoral training at Baylor College of Medicine, she obtained a position in January 2009 as an Assistant Professor in the Neurobiology Department at the University of Alabama at Birmingham. Her main research work is focused on investigating the molecular and genetic basis of learning, memory, and its disorders.

This study was supported in part by the National Institutes of Health grant MH097909 to F.D.L. and the Evelyn F. McKnight Brain Institute at the University of Alabama at Birmingham. We thank Travis Chapman for his assistance in preparing the figure.

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Received: 2013-3-26
Accepted: 2013-4-26
Published Online: 2013-05-27
Published in Print: 2013-08-01

©2013 by Walter de Gruyter Berlin Boston

Heruntergeladen am 18.11.2025 von https://www.degruyterbrill.com/document/doi/10.1515/revneuro-2013-0008/pdf
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