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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.
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.
This study identifies an altered chromatin conformation associated to a cardiac disorder observed in 7 independent families. A deletion of 2 diverging CTCF binding sites on 4q25 induces TAD fusion and leads to PITX2 expression dysregulation.
DNA methylation data of whole blood from Han Chinese individuals are used to map mQTLs, finding that cis- and trans-mQTLs show distinct patterns of East Asians (EA) ancestry-specific colocalization with complex trait variation.
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.