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Monocular deprivation regulates DNA methylation in the visual cortex
Changes to DNA methylation are involved in learning and synaptic plasticity in the brain. However, the role of DNA methylation in experience-dependent plasticity during development is unclear.
To further understand visual experience regulation of DNA methylation, a team led by Tommaso Pizzorusso from the Institute of Neuroscience CNR in Pisa studied the role of DNA methylation in ocular dominance plasticity in the developing visual cortex of mice. They found that:
The data presented in this paper show that monocular deprivation regulates DNA methylation at specific loci in the visual cortex. This might highlight a wider role of DNA methylation as a mediator of experience-dependent refinement of cortical circuits during development.
Read the full text in Nature Neuroscience, May 2015.
DNA methylation is required for the oncogenic potential of BCR-ABR
Chronic myeloid leukemia (CML) is characterized by the presence of the BCR-ABL oncogene, a constituative active tyrosine kinase that mediates proliferation and differentiation pathways. Other molecular mechanisms contributing to CML onset have not previously been determined; however, epigenetic changes have recently been suggested to have an important role in leukemia pathogenesis.
A team led by Daniel Tenen from Harvard Medical School and the National University of Singapore sought to understand the functional relevance of aberrant DNA methylation in the development of CML. By reprogramming CML cells to an iPS-like state, followed by in vitro re-differentiation, the authors found that:
These data highlight the importance of DNA methylation in CML and indicate that DNA methylation is required for the oncogenic potential of BCR-ABR. This study opens up the potential for testing demethylating agents as a treatment strategy for CML.
Read the full paper at Nature Communications, May 2015
For more information on DNA methylation, view our DNA methylation articles, webinars and protocols.
A role for DNA methylation in epigenetic memory of pregnancy
During pregnancy, a large expansion of the mammary epithelium and developing ductal structures occurs to support milk production. Anecdotal evidence suggests that the response of mammary glands to pregnancy is stronger after the first pregnancy, indicating a long term memory of the pregnancy.
To confirm this, and elucidate the molecular mechanisms responsible, Camila dos Santos and colleagues from Cold Spring Harbor Laboratory and the University of Southern California compared genome-wide DNA methylation profiles in mammary cells of post-pubescence and post-pregnancy mice.
They found that:
The authors postulate that the epigenetic memory of a first pregnancy primes the activation of gene expression networks that promote mammary gland function in subsequent reproductive cycles.
Read the full paper at Cell Reports, May 2015
DNA methylation has a role in regulating gender-specific gene expression
Male and female genomes differ in only their X and Y chromosomes, and little is understood about how changes in the expression of autosomal genes arise.
To understand whether DNA methylation has a role in gender-specific gene expression, a team led by Howard Cedar from Cedars-Sinai Medical Center in California undertook a high-throughput analysis to characterize DNA methylation differences between males and females. Here is what they found:
This paper presents an example of how DNA methylation changes brought on during development can be maintained and regulate gene expression in the adult. The authors suggest that methylation may play a general role in regulating male and female characteristics independent of sex determination.
Read the full paper at Genes and Development, May 2015.
Transcription of lncRNAs is required for super-enhancer chromosomal interactions
The RNA exosome complex is responsible for the degradation and processing of RNAs both in the nucleus and the cytosol. In this study, a team led by Uttiya Basu from Columbia University sought to elucidate the role of the RNA exosome in chromatin-associated events.
By looking at the transcriptomes of embryonic stem cells (ESCs) and B cells in which core components of the RNA exosome were ablated, they found that:
The authors propose that super-enhancers regulate genes through interactions dependent on the transcription of RNA exosome-substrate transcripts. The data suggest that the RNA exosome may resolve deleterious secondary DNA structures, to protect lncRNA expressing enhancers and regulate super-enhancer chromosomal interactions.
Read the full paper at Cell, May 2015.
Find out more with our guide to non-coding RNAs.
A role for H3.3 in transposable element silencing
Transposable elements play a role in genetic variation, adaptation and evolution. Hosts have evolved the ability to silence transposable elements to prevent genome instability caused by transposable element activity, with H3K9 trimethylation known to silence endogenous retroviral elements (ERVs) containing long terminal repeats.
While the histone variant H3.3 has traditionally been associated with gene activation, it has also been shown to be present in constitutive and facultative heterochromatin. Simon Elsässer, Laura Banaszynski and colleagues from the MCR Laboratory of Molecular Biology in Cambridge, Karolinska Institutet, Rockefeller University and the UT Southwestern Medical Center in Texas used ChIP-seq to understand if H3.3 plays a role in silencing of ERVs.
They found that:
In this paper, the authors have provided further evidence of the important role of H3.3 in establishing silenced chromatin. They propose a model in which H3.3-containing chromatin recruits KAP1 to ERVs, which in turn recruits DAXX-ATRX for the maintenance of H3.3.
Read the full paper in Nature, May 2015.
Need more information on histone modifications? Take a look at our histone modification guide.
A new technique to assess chromatin accessibility in individual cells
Chromatin state is heterogeneous within cell populations. However, methods to characterize the epigenome, such as DNase-seq and ATAC-seq, measure an average of chromatin states, thus masking this heterogeneity.
To gain data from thousands of single cells without requiring individual processing, a team led by Jay Shendure from the University of Washington applied combinatorial cellular indexing integrated with ATAC-seq to measure chromatin accessibility of single cells.
The new method involves:
In this paper, the authors demonstrate that this method is suitable for clustering cells based on chromatin accessibility and identifying modules of coordinately regulated chromatin accessibility. The authors argue that the simplicity and scalability of this method could accelerate the characterization of complex tissues.
Read the full paper in Science, May 2015.