Anti-ARPC3 monoclonal antibody, clone 3F22

Mammalian oocyte meiotic maturation involves oocyte polarization and a unique asymmetric division, but until now, the underlying mechanisms have been poorly understood. Arp2/3 complex has been shown to regulate actin nucleation and is widely involved in a diverse range of processes such as cell locomotion, phagocytosis and the establishment of cell polarity. Whether Arp2/3 complex participates in oocyte polarization and asymmetric division is unknown. The present study investigated the expression and functions of Arp2/3 complex during mouse oocyte meiotic maturation. Immunofluorescent staining showed that the Arp2/3 complex was restricted to the cortex, with a thickened cap above the meiotic apparatus, and that this localization pattern was depended on actin. Disruption of Arp2/3 complex by a newly-found specific inhibitor CK666, as well as by Arpc2 and Arpc3 RNAi, resulted in a range of effects. These included the failure of asymmetric division, spindle migration, and the formation and completion of oocyte cytokinesis. The formation of the actin cap and cortical granule-free domain (CGFD) was also disrupted, which further confirmed the disruption of spindle migration. Our data suggest that the Arp2/3 complex probably regulates oocyte polarization through its effect on spindle migration, asymmetric division and cytokinesis during mouse oocyte meiotic maturation.

Genetic contribution has been consistently implicated in several neurological disorders, however only a fraction of candidate genes can be directly linked to these disorders. Many known risk factors for psychiatric diseases are related to the enzymatic regulatory machinery of the actin based cytoskeleton of neuronal cells. Synaptic plasticity which is fundamental for neuronal function heavily relies on actin-polymerization. To gain insight into the neuronal architecture during actin-related pathologic conditions, using quantitative electron-microscopy, the authors investigated a conditional knock-out mice breed, in which they studied the result of the postnatal loss of ArpC3 subunit of the Arp2/3 complex an evolutionary conserved final output of actin signalling pathways that orchestrates de novo actin polymerization. They found, that in the hippocampus which is a particularly favourable model for synaptic plasticity and believed to play a key role in learning and memory and neocortex, synaptic architecture is significantly altered compared to the wild-type. Their results suggest that dysregulation of the actin cytoskeleton results in pathologic neuronal architecture which may contribute to the ethiology of complex neurological disorders.