Understanding how loss of CO₂/H⁺ vascular reactivity affects respiratory control may facilitate development of treatments for breathing problems in this population.

Cellular and chemogenetic approaches identify a novel mode of chemotransduction involving regulation of basal breathing by CO₂/H+-dependent disinhibition.

Enteric bacteria associated with bloodstream infections are attracted to human serum through L-serine and the chemoreceptor Tsr, and in an enterohemorrhagic lesion model use chemotaxis to invade damaged vasculature.

Olfactory neurons of insects, once thought to express only a single type of olfactory receptor, exhibit widespread co-expression of receptors from multiple chemosensory gene families.

CO₂/H⁺-dependent purinergic signaling by astrocytes provides specialized control of vascular tone in a brainstem respiratory center in a manner that contributes to respiratory behavior.

Bacterial cytoplasmic chemoreceptors assemble into a sandwich of two hexagonally packed arrays.

A quantitative trait locus that includes two pheromone receptor genes affects foraging behavior; for one of the genes, the two alleles of the QTL have opposite effects because of distinct sites of expression.

The slope of the chemoattractant concentration gradient is a driving force for sperm chemotaxis, by coordinating the entrainment of information flow between sensing, signaling and motility.

Expression of a Dravet syndrome-associated mutation in inhibitory neurons disrupts activity of brainstem respiratory neurons and diminishes respiratory behavior in conjunction with seizures and premature death.

Knockdown of PHOX2B in the chemosensitive area of the retrotrapezoid nucleus of adult rats reduces CO₂ responses and the expression of the proton sensors TASK2 and GPR4.