Hsiang-Chen Chou, Kuhulika Bhalla ... Bruce Stillman
The initiation of human genome replication requires the six-subunit origin recognition complex (ORC) and CDC6, with ORC playing additional roles during mitosis and in organization of the cell nucleus.
Brandon R Lowe, Rajesh K Yadav ... Janet F Partridge
H3-G34R, V, and W oncohistonesin fission yeast cause differential K36 modification, DNA damage sensitivity and genome stability outcomes, highlighting the need for a thorough evaluation of distinct mutations.
Augusto Berrocal, Nicholas C Lammers ... Michael B Eisen
Live quantitative monitoring of transcriptional bursting reveals that enhancers responding to different regulators use the same kinetic strategy to produce a complex composite pattern of developmental expression.
Holly E Kinser, Matthew C Mosley ... Zachary Pincus
Expression of almost half of a library of fluorescent reporters distinguish long- from short-lived individual Caenorhabditis elegans, suggesting that organism-wide differences in gene expression drive future lifespan.
Evelyn L Eastwood, Kayla A Jara ... Gregory J Hannon
Heterochromatin formation at transposon loci depends on dimerisation of the effector complex that elicits co-transcriptional silencing and this requirement is fulfilled by co-option of the conserved dimerisation hub protein, Cut-up/LC8.
Karl N Miller, Nirmalya Dasgupta ... Maria Grazia Vizioli
Cytoplasmic chromatin fragment formation pathways in senescent cells are a potential therapeutic target for modulation of inflammation in aging, which contributes to age-associated diseases.
eLife is pleased to present a Special Issue to highlight recent advances in the mechanistic understanding of aging and interventions that extend longevity.
Dingbang Ma, Dariusz Przybylski ... Michael Rosbash
Drosophila clock neurons manifest remarkable heterogeneity, which might be generally true and help explain why Drosophila has a sophisticated behavioral repertoire despite a tiny brain of about 100,000 neurons.
The mechanism underlying Shprintzen–Goldberg syndrome is solved and reveals that missense mutations in the transcriptional repressor SKI abolish ligand-induced SKI degradation, which results in attenuation of TGF-β transcriptional responses.