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

The location of neurons responsible for increasing the breathing rate upon detecting elevated levels of CO₂ in the blood has been pinpointed to the retrotrapezoid nucleus in the brainstem.

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.

New evidence for the impaired breathing activity is related to non-polyalanine repeat expansion mutations form of congenital central hypoventilation syndrome neuropathology.

Recordings from brainstem nuclei involved in chemosensory regulation of breathing in awake freely behaving mice show different complementary types of neuronal responses to hypercapnia in the retrotrapezoid nucleus and the rostral medullary raphe.

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

Astrocytes modulate neuronal networks during hypercapnia, introducing a novel gliotransmitter pathway where prostaglandin E2 regulates breathing.

Yeast cells adapt to harmful superoxide generated during mitochondrial oxidative phosphorylation by arresting respiration through mtDNA deletions whose emergence depend on superoxide dismutase 2 and the retrograde pathway.

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.

Structures of RNA polymerase I transcription machinery revealed a ratcheting motion within the complex in coordination with three distinct functional states, implicating a novel mechanism for promoter bubble opening in the absence of ATP hydrolysis.