Activated macrophages initiate a robust DNA damage response that depends on type I IFN and regulates their genetic program and inflammasome activation, establishing a mechanistic link between DNA damage responses and innate immunity.

A response regulator acquired via lateral gene transfer has rewired an ancestral genetic circuitry and regulates alternative pathogenic lifestyles.

Histone H3T11 phosphorylation regulates chronological lifespan by linking nutritional stress-response signals to chromatin.

The hypoxia-inducible factor HIF drives transcription of the gene cyp-36A1, which encodes a cytochrome P450 enzyme that acts via a putative intercellular signal to regulate the nuclear receptor NHR-46 and consequently stress resistance and behavior.

Transcriptome analysis reveals an alternative splicing program induced in the arterial endothelium under low-flow inflammatory conditions by platelet and macrophage recruitment and dependent upon the RNA-binding splice factor Rbfox2.

Caprin-2 is up-regulated in the rat hypothalamus by osmotic stress and controls vital homeostatic osmoregulatory mechanisms by altering the length of the poly(A) tail on arginine vasopressin mRNAs.

Mice with a mutation that disrupts the release of growth hormone show greatly increased lifespan, which can be further increased by caloric restriction.

Dynamic regulation of the heat shock response depends on a negative feedback loop in which Hsf1 activates expression of Hsp70 and Hsp70 specifically and directly represses Hsf1 transactivation.

Genetic and biochemical analyses reveal that PERK is important for the survival of activated satellite stem cells during regeneration of injured skeletal muscle.

An identical DNA base pair change has occurred in divergent sticklebacks to alter the expression of a major developmental gene controlling armor plates, thus providing a molecular link between particular enhancer changes, cell signaling, and repeated skeletal evolution in natural populations.