The pressure of fluid in the inner ear is controlled by opening of cellular valves in the endolymphatic sac to allow for regulated transepithelial fluid flow.

The RNA-binding protein MSI1, which is required for stem cell and cancer cell proliferation in the brain and epithelial tissues, also directly senses the concentration of long non-esterified omega-9 fatty acids.

Size regulation of the otic vesicle, the progenitor of the inner ear, is mediated by mechanical feedback involving fluid influx, hydraulic pressure, and tissue mechanics.

Mammalian Dscams require different intracellular interactions in different cell types during neural circuit formation to promote self-avoidance.

Loss of functional dystroglycan disrupts the formation and function of CCK⁺/CB₁R⁺ inhibitory synapses in hippocampal CA1, resulting in reduced seizure thresholds in mouse models of dystroglycanopathy.

Mice with aquaporin-4 channel deletion exhibit larger interstitial spaces, brain volume and water content, alongside reduced CSF space volume, which may increased resistance towards brain fluid efflux and suppress glymphatic flow.

Giant ankyrin-B enables the transduction of Sema 3A repelling cues and is important for normal axonal connectivity.

Brain-specific inactivation of cohesin-STAG2 in the mouse causes myelination defects, thus implicating hypomyelination as a contributing factor to cohesinopathy and establishing oligodendrocytes as a cell system to probe the physiological function of cohesin-mediated genome folding.