BGDB: a database of bivalent genes

Bivalent DNA Vaccination with Genes Encoding Leishmania major Cysteine Proteinases Type I and II Protects Mice Against Infectious Challenge

MicroRNAs of the miR-290–295 Family Maintain Bivalency in Mouse Embryonic Stem Cells

Numerous developmentally regulated genes in mouse embryonic stem cells (ESCs) are marked by both active (H3K4me3)- and polycomb group (PcG)-mediated repressive (H3K27me3) histone modifications. This bivalent state is thought to be important for transcriptional poising, but the mechanisms that regulate bivalent genes and the bivalent state remain incompletely understood. Examining the contributi...

Bivalent chromatin marks developmental regulatory genes in the mouse embryonic germline in vivo.

Developmental regulatory genes have both activating (H3K4me3) and repressive (H3K27me3) histone modifications in embryonic stem cells (ESCs). This bivalent configuration is thought to maintain lineage commitment programs in a poised state. However, establishing physiological relevance has been complicated by the high number of cells required for chromatin immunoprecipitation (ChIP). We develope...

Regulation of Pluripotency and Self- Renewal of ESCs through Epigenetic- Threshold Modulation and mRNA Pruning

Embryonic stem cell (ESC) pluripotency requires bivalent epigenetic modifications of key developmental genes regulated by various transcription factors and chromatin-modifying enzymes. How these factors coordinate with one another to maintain the bivalent chromatin state so that ESCs can undergo rapid self-renewal while retaining pluripotency is poorly understood. We report that Utf1, a target ...

Cell-Cycle Control of Bivalent Epigenetic Domains Regulates the Exit from Pluripotency

Here we show that bivalent domains and chromosome architecture for bivalent genes are dynamically regulated during the cell cycle in human pluripotent cells. Central to this is the transient increase in H3K4-trimethylation at developmental genes during G1, thereby creating a "window of opportunity" for cell-fate specification. This mechanism is controlled by CDK2-dependent phosphorylation of th...