Par-complex-dependent cell polarity can be cell-autonomously conferred to non-polar Drosophila S2 cells, unveiling temporal patterns toward the cortical localization of Par-complex aggregates that include a meshwork containing unit segments.
In Drosophila oocytes, the exclusion of the scaffold protein PAR3 from the posterior cortex depends on PAR1 and endocytosis, while its anterior localisation requires microtubules and recycling endosomes.
The basic helix-loop-helix transcription factor, HES3, acts downstream of the PAX3-FOXO1 fusion oncogene to impair muscle differentiation and promote tumorigenesis in rhabdomyosarcoma, a childhood muscle cancer.
A single-molecule biophysical approach reveals that the C-terminal domain of ParB blocks ParB network formation by heterodimerization with the full-length protein, which remains bound to the DNA.
Genetic and biochemical approaches identify a new component of the cellular signaling machinery driving migration of limb muscle precursor cells during mouse embryogenesis and reveal the underlying molecular mechanism.
The kinesin-14 motor Kar3 moves along microtubules using a previously undescribed mechanism that critically requires the presence of a non-catalytic head.
Par3 is polarized in the plane of the vertebrate neural plate, binds and recruits Prickle3 to the apical membrane and promotes the formation of core planar cell polarity complexes.
Risk of punishment during reward seeking behavior is associated with a functional "disconnection" of the PFC-VTA circuit due to a transient loss of VTA-driven theta oscillation.
