Volatile anesthetics impair hepatic tricarboxylic acid cycle function in adult and neonatal mice, with citrate accumulation driving a neonate-specific inhibition of beta-oxidation and ketosis through their increased relative sensitivity to malonyl-CoA.

In contrast with earlier conclusions, negative selection has a major role in cancer evolution.

Transposable elements and gene amplifications can provide variation needed for novel trait refinement and adaptation to new niches, though a recalcitrant organism-environment mismatch may persist.

Genetic analyses and biochemical studies show that JMJD6 promotes MYC-mediated transformation and is required for neuroblastoma growth by complexing with pre-mRNA splicing factors.

Animal models reveal that mitochondrial complex I is dispensable for homeostatic functions of the mouse liver.

Cell-specific alternative splicing of the synaptic calcium channel gene Cacna1b is controlled by exon hypomethylation and CTCF binding and is disrupted following nerve injury.

Multi-omic analyses reveal a connection between the integrated stress response and the regulation of redox and amino acid metabolism when the TCA cycle is impaired.

TRIM32-mediated glycolytic flux generates precursors that are utilized for biomass production in non-dividing muscle, brain and tumor cells, demonstrating a universal metabolic function for TRIM32 in cell growth.

Activated Drosophila macrophages undergo transient metabolic remodeling towards Hypoxia inducible factor 1 α-driven aerobic glycolysis, a program that induces systemic metabolic changes and is crucial for resistance to infection.