Browse our latest Chromosomes and Gene Expression articles

Molecular timekeeping in Neurospora crassa is robust even under severe limitation of carbon sources and the efficient adaptation to changing nutrient availability is dependent on the positive component of the circadian clock.

High throughput sequencing of Arabidopsis mutants lacking the U6 snRNA methyltransferase FIONA1/METTL16 uncovers the role of U6 methylation in splicing signal preferences.

LncRNA Neat1, with paraspeckle proteins, controls translational induction of (lymph)angiogenic and cardioprotective factors by the IRES-dependent mechanism in mouse cardiomyocytes submitted to hypoxia.

The localization of Rad53 cell cycle checkpoint kinase to many gene promoters and the dynamic changes in response to replication stress suggests that the kinase may coordinate genome stability and gene expression.

In vitro assays using Xenopus egg extracts provide evidence that mitosis-specific loading of condensin I is accelerated by phosphorylation of the N-terminal tail of its kleisin subunit.

Genetic analysis of senataxin and RNase H2-deficient mice reveals that genome stability during class switch recombination and antibody generation can be uncoupled, suggesting a role for R loop metabolism dysfunction in lymphomagenesis in patients without immune deficiency.

Lineage resolved single-cell RNA-seq of mammary carcinoma models uncovers a metabolic vulnerability of taxane-resistant clones.

Bidirectional promoter activity, which is inherent to the promoters of selection cassettes used for genome editing, causes divergent transcription that can disrupt expression of genes neighboring cassette insertion sites, causing potent off-target effects.

N6-methyladenosine (m6A) reader Pho92 is directed by Paf1C to meiotic mRNAs in an m6A-dependent and independent manner and promotes CCR4-NOT-mediated mRNA decay of m6A modified transcripts contingent on translation.

In a departure from previous findings, new results suggest that free-floating pieces of DNA which carry additional copies of cancer-driving genes do not tend to cluster or have increased transcription.