Alternative 9-1-1 complexes have evolved to play essential roles in mammalian meiosis and function to activate the protein kinase ATR and promote key meiotic events necessary for fertility.

A Topbp1 mutant mouse reveals a non-canonical role for the ATR-TOPBP1 signaling axis in meiosis, separating ATR signaling and meiotic sex chromosome inactivation from sex body formation.

Chromatin profiling of Drosophila testes reveals activation of the transcriptional program of the germline, widespread changes in RNA polymerase progression, and the absence of chromosomal regulation across the X chromosome.

Genetic analyses reveal that purely quantitative changes in the relative copy number of chromosomes can be sufficient to disrupt the epigenetic mechanisms that define the cells' differentiated state.

Redundant pathways prevent heterochromatin spreading and ectopic heterochromatin assembly; and plasticity of heterochromatin assembly allows cells to adapt to heterochromatin stress.

Drosophila p53 protein isoforms function during oogenesis to ensure the integrity of the transmitted genome, a function that is conserved to humans.

Genomic imprinting in the bryophyte Marchantia polymorpha by Polycomb results in maternal dominance of embryonic gene expression.

The GC content of human mRNAs is key to P-body localization and protein yield, and has a major impact on their post-transcriptional control.

Genome-wide profiling and functional analyses reveal a network of heterochromatin and small RNA factors that silences repetitive elements and prevents genotoxic stress to ensure fertility.

Increased Notch signaling enhances germ cell reprograming in C. elegans by antagonizing PRC2-mediated repression, which results in the activation of UTX-1 and other reprograming-promoting genes.