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A Drosophila fertility gene is identified that acts as a linker between HP1a and local H3K4 demethylation during HP1a-mediated gene silencing that is required for ovary development and transposon silencing..

Heterochromatin proteins like the SIR complex in budding yeast use different mechanisms for recruitment to nucleation sites and long-range spread to create a domain of transcriptional silencing.

In the cochlea, repressor element 1-silencing transcription factor (REST) regulates the expression levels of K_v7.4 and alterations of REST functions result in progressive hearing loss.

Pervasive ‘futile cycling’ by chromatin-modifying factors suggests a mechanism for creating new links in gene regulatory networks.

By linking export and licensing of a piRNA precursor transcript, channel nuclear pore complex subunits Nup54 and Nup58 are specifically required to silence transposons in the Drosophila ovary.

Silencers and enhancers targeted by a common transcription factor in photoreceptors are distinguished by the number and diversity of binding transcription factor binding sites they contain.

Zebrafish early embryos initially package their developmental genes and enhancers in 'active' chromatin that subsequently receives polycomb repressive complex 1 (PRC1)-mediated histone H2A ubiquitylation, which confers silencing/poising – prior to Aebp2-PRC2-guided H3K27me3 addition.

Dnmt3a and Dnmt3b are dispensable for epidermal homeostasis but act as potent tumor suppressors regarding skin squamous tumorigenesis.

SUMO-dependent pathway is responsible for selective repression of damaged rDNA and silencing of intact surplus units revealing an epigenetic mechanism that controls the differential expression of identical sequences in the same cell.

Silencing of gene regulatory elements by modifications of DNA-bound proteins promotes the progression of early mouse development.