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The subcellular localization of the prolyl hydroxylase oxygen sensor in C. elegans neurons is regulated by p38 MAP kinase signaling.

Peptidergic neurons regulate undulation and turning movements to enable Caenorhabditis elegans to gradually adjust its locomotion strategy from dispersal to local search.

Collectively migrating cells control their stiffness by Fascin-dependent control of Myosin activity, and this migratory cell stiffness regulates Myosin activity and stiffness within the cellular substrate to ultimately promote migration.

Chronic excitation of the Caenorhabditis elegans oxygen-sensing neurons alters calcium homeostasis to accelerate the decline of neural plasticity with age.

Two seemingly distinct behaviors in social C. elegans worms, namely aggregating into groups and swarming over food, are driven by the same underlying mechanisms.

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.

With the aid of a pair of sensory neurons, the nematode worm C. elegans is able to detect the Earth's magnetic field and use it to navigate towards food sources.

Nuclear export inhibition reveals concurrent epithelial and mesenchymal phenotypes that cause mechanosensitive disorder in collectively migrating epithelia.

Horizontal cell undergoes amoeboid-like migration in the developing vertebrate retina, a not previously reported migration mode in the central nervous system, that allows them to move within a densely packed tissue without predetermined paths.

Neutrophils use dorsal membrane protrusions of endothelial cells to cross the vascular wall.