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Related Concept Videos

Histone Modification02:32

Histone Modification

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The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
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Crossing over is the exchange of genetic information between homologous chromosomes during prophase I of meiosis I. Genetic recombination gives rise to allelic diversity in the newly formed daughter cells. In humans, crossing over produces genetically distinct haploid egg and sperm cells that undergo fertilization to produce unique offspring. Before cell division starts, the germ cell’s chromosome(s) undergo duplication in the S phase of the cell cycle. As the cells enter prophase I,...
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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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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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Isolation and Cultivation of Neural Progenitors Followed by Chromatin-Immunoprecipitation of Histone 3 Lysine 79 Dimethylation Mark
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Histone methylation and V(D)J recombination.

Noriko Shimazaki1, Michael R Lieber

  • 1Section of Molecular and Computational Biology, Departments of Pathology, Biochemistry and Molecular Biology, Molecular Microbiology and Immunology, USC Norris Comprehensive Cancer Ctr., Rm. 5428, 1441 Eastlake Ave., MC 9176, Los Angeles, CA, 90089-9176, USA, shimazak@usc.edu.

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Summary

Histone methylation controls V(D)J recombination, essential for lymphocyte development. Aberrant methylation may contribute to lymphoid malignancies by misdirecting the RAG complex.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Epigenetics

Background:

  • V(D)J recombination generates antigen receptor gene diversity and is crucial for lymphocyte development.
  • This process is tightly regulated by chromatin structure and specific histone modifications.
  • Recombination-active V(D)J loci exhibit hypermethylation at histone H3 lysine 4 (H3K4) and hyperacetylation of histones H3/H4.

Purpose of the Study:

  • To review the mechanisms by which histone methylation regulates V(D)J recombination.
  • To discuss the implications of aberrant histone methylation in lymphoid malignancies.

Main Methods:

  • Review of existing literature on V(D)J recombination and histone modifications.
  • Analysis of the role of the RAG complex and its interaction with chromatin.
  • Discussion of epigenetic dysregulation in cancer.

Main Results:

  • The recombination activating gene 1 (RAG1) and RAG2 complex initiates recombination by cleaving DNA at recombination signal sequences (RSS).
  • RSS sites require an open chromatin context for RAG complex recognition.
  • RAG2's plant homeodomain (PHD) finger specifically recognizes hypermethylated H3K4, enhancing RAG catalytic activity.

Conclusions:

  • Histone methylation is a key epigenetic regulator of V(D)J recombination.
  • Mistargeting of the RAG complex due to altered histone methylation patterns may play a role in lymphoid cancer development.