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Unbiased ChIP-seq screens and genetic knockouts of large Kruppel associated box zinc finger protein (KRAB-ZFP) clusters reveal that evolutionarily young KRAB-ZFPs play a redundant role in retrotransposon restriction in mice.

mSTARR-seq identifies regions of the genome where DNA methylation causally impacts gene expression, providing a map of which epigenetic marks may influence trait variation.

Epigenetic scores for blood protein levels identify those at risk of multiple age-related morbidities, up to 14 years prior to onset.

Adjuvants, MPLA and CpG especially, modulate the peptide repertoires presented on the surface of APCs, preferring the presentation of low-affinity exogenous peptides rather than high-affinity peptides.

Turning in an insect is the combined result of body-side-specific modifications in processing of local sensory feedback, and modification of local central pattern generator activity.

A robust mouse multi-tissue age predictor is presented that can be used to assess the DNA methylation age of mouse tissues and test the effects of longevity interventions.

Transgenic mice with Rett-causing mutations in MeCP2 reveal that a basic cluster in the C-terminus of the protein binds DNA and that both the methyl-CpG binding domain and the transcriptional repression domain are necessary to elicit toxicity in MECP2 duplication syndrome.

Imprinted gene expression is set up during a critical window of early embryonic development, by the translation of parental imprints by oocyte-supplied Smchd1 into allele-specific gene silencing.

Different types of epigenetic DNA modifications affect the likelihood of cytosine mutations in cancer.

Self-reactive B cells downregulate the IgM but not the IgD B cell receptor, and this serves as a critical tolerance mechanism because IgD is less sensitive to bona fide endogenous antigens than IgM.