Calcium response profiling of large populations of enteric neurons reveals hard-wired neural circuits that reflect the motility program portfolio of the intestinal region they occupy.

Channel activity is a novel regulatory mechanism for channel mobility in the plasma membrane.

A small surface protein regulates gliding motility and host cell invasion by the sporozoite stage of the malaria parasite.

Toxoplasma gondii formins have several non-overlapping roles including generating an apico-basal flux of F-actin that is controlled by phosphorylation and methylation and is essential for motility.

Hydrodynamic and steric interactions slow vesicle mobility and are predicted to ultimately limit vesicle supply to the active zone during sustained high-frequency signalling at a central synapse.

Combining parasite genetic and human mobility data can provide detailed information on local and cross-border connectivity, allowing programs to strengthen local and regional coordination for successful elimination of malaria.

Human mobility drives malaria importation within countries and threatens elimination interventions, but can be measured using new approaches that combine parasite genetics, mobile phone data, travel surveys and models.

The transport of proteins along flagellar microtubules generates the force that enables flagella to propel cells across surfaces.

Malaria parasites enter the host via the skin, where they are inoculated by an infected mosquito as it probes for blood: the inoculation site is a bottleneck for the parasite and the only time when the parasite is extracellular for more than a few minutes, thus possibly presenting the best opportunity for antibody-mediated inhibition of infection.

The motor protein kinesin utilizes its fuel molecule by active and concerted motions of its subdomains, while it rapidly interacts with the microtubule track by forming a wet and dynamic interface.