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The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
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Chromatin is the massive complex of DNA and proteins packaged inside the nucleus. The complexity of chromatin folding and how it is packaged inside the nucleus greatly influences  access to genetic information. Generally, the nucleus' periphery is considered transcriptionally repressive, while the cell's interior is considered a transcriptionally active area. 
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The extent of chromatin compaction can be studied by staining chromatin using specific DNA binding dyes. Under the microscope, the dense-compacted regions that take up more dye are called heterochromatin. Heterochromatin is further classified into two forms – constitutive heterochromatin and facultative heterochromatin.
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A Neuronal Activity-Dependent Dual Function Chromatin-Modifying Complex Regulates Arc Expression

Nicodemus E Oey1, How Wing Leung1, Rajaram Ezhilarasan1

  • 1Program in Neuroscience and Behavioral Disorders, Duke-NUS Graduate Medical School , Singapore, 169857, Singapore.

Eneuro
|October 15, 2015
PubMed
Summary
This summary is machine-generated.

Researchers discovered a PHF8-TIP60 complex that regulates neuronal plasticity by modifying chromatin. This epigenetic mechanism is crucial for activity-induced gene expression, offering therapeutic potential for memory disorders.

Keywords:
chromatin modificationepigeneticshistone acetylationimmediate early geneneuronal activitytranscription

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Area of Science:

  • Neuroscience
  • Epigenetics
  • Molecular Biology

Background:

  • Chromatin modification, including histone methylation and acetylation, is vital for neuroplasticity.
  • The specific molecular machinery mediating these epigenetic changes in neurons remained largely unknown.
  • The Arc gene is a key mediator of synaptic plasticity and its expression is activity-dependent.

Purpose of the Study:

  • To identify the machinery responsible for activity-induced chromatin modification in neurons.
  • To investigate the role of the histone demethylase PHF8 and acetyltransferase TIP60 in regulating Arc gene expression.
  • To elucidate the epigenetic mechanism linking synaptic activity to gene transcription.

Main Methods:

  • Chromatin immunoprecipitation to assess recruitment to the Arc promoter.
  • Analysis of histone modifications (H3K9me2 and H3K9acS10P) upon synaptic stimulation.
  • Gain-of-function and interference experiments in primary rat hippocampal neurons.
  • Global proteomics to identify complex interactors.
  • Super-resolution microscopy to visualize molecular interactions.

Main Results:

  • A PHF8-TIP60 complex was identified as a key regulator of activity-induced Arc gene expression.
  • The complex rapidly recruits to the Arc promoter upon synaptic activity, counteracting H3K9me2 and promoting H3K9acS10P.
  • Gain-of-function enhanced Arc expression, while interference abrogated it.
  • Proteomics revealed interactors involved in mRNA processing, including PSF.
  • PHF8, TIP60, and PSF interact at the single-molecule level.

Conclusions:

  • The PHF8-TIP60 complex acts as a crucial epigenetic regulator of neuronal activity-dependent gene transcription.
  • This complex facilitates the permissive chromatin state required for Arc gene activation.
  • The findings highlight a mechanism with implications for understanding and treating disorders of learning and memory.