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Epigenetics is the study of molecular processes that influence the flow of information between a constant DNA sequence and variable gene expression patterns. This includes investigation of nuclear organization, DNA methylation, histone modification and RNA transcription. Epigenetic processes can result in intergenerational (heritable) effects as well as clonal propagation of cell identity without any mutational change in DNA sequence.
Researchers find that brief and reversible inhibition of a gene-silencing mechanism leads to irreversible tumour formation in fruit flies, challenging the idea that cancer is caused only by permanent changes to DNA.
A triplet repeat expansion in Arabidopsis induces gene silencing that results in a severe growth defect. We show that an interplay between a SUMO protease and histone readers of active and inactive marks is required for this gene silencing, which highlights the importance of post-translational modifiers in chromatin remodelling.
Even though glucocorticoids are potent anti-inflammatory agents, they can cause muscle wasting. Here, the authors show that targeting the glucocorticoid receptor coactivator LSD1 limits muscle loss without reducing the drugs’ efficiency on the immune system.
Here the authors develop a method to quantify all combinations of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine at individual CpG dyads, including in single cells, to identify the relationship between the local 5mC density, histone marks and maintenance methylation fidelity.
A transient perturbation of transcriptional silencing mediated by Polycomb proteins is sufficient to induce an epigenetic cancer cell fate in Drosophila in the absence of driver mutations.
Cells carrying EZH2 mutations found in lymphoma show a specific transcriptional response to PRC2 inhibition. A longitudinal study reveals unexpected genetic heterogeneity in follicular lymphomas, with implications for therapeutic strategies.
Researchers find that brief and reversible inhibition of a gene-silencing mechanism leads to irreversible tumour formation in fruit flies, challenging the idea that cancer is caused only by permanent changes to DNA.
A triplet repeat expansion in Arabidopsis induces gene silencing that results in a severe growth defect. We show that an interplay between a SUMO protease and histone readers of active and inactive marks is required for this gene silencing, which highlights the importance of post-translational modifiers in chromatin remodelling.
In this Tools of the Trade article, Dongsheng Bai and Chenxu Zhu describe SIMPLE-seq, a scalable single-cell sequencing method that simultaneously decodes the cytosine modifications 5mC and 5hmC.