Deletion of the Hoc and Soc capsid proteins affects the surface and cellular uptake properties of bacteriophage T4 derived nanoparticles.

Recently the use of engineered viral scaffolds in biotechnology and medical applications has been increasing dramatically. T4 phage capsid derived nanoparticles (NPs) have potential advantages as sensors and in biotechnology. These applications require that the physical properties and cellular uptake of these NPs be understood. In this study we used a T4 deletion mutant to investigate the effects of removing both the Hoc and Soc proteins from the capsid surface on T4 tailless NPs. The surface charge, zeta potential, size, and cellular uptake efficiencies for both the T4 NP and T4ΔHocΔSoc NP mutant were measured and compared using dynamic light scattering and flow cytometry and significant differences were detected.

The neuronal Arf GAP centaurin alpha1 modulates dendritic differentiation.

Centaurin alpha1 is an Arf GTPase-activating protein (GAP) that is highly expressed in the nervous system. In the current study, we show that endogenous centaurin alpha1 protein is localized in the synaptosome fraction, with peak expression in early postnatal development. In cultured dissociated hippocampal neurons, centaurin alpha1 localizes to dendrites, dendritic spines and the postsynaptic region. siRNA-mediated knockdown of centaurin alpha1 levels or overexpression of a GAP-inactive mutant of centaurin alpha1 leads to inhibition of dendritic branching, dendritic filopodia and spine-like protrusions in dissociated hippocampal neurons. Overexpression of wild-type centaurin alpha1 in cultured hippocampal neurons in early development enhances dendritic branching, and increases dendritic filopodia and lamellipodia. Both filopodia and lamellipodia have been implicated in dendritic branching and spine formation. Following synaptogenesis in cultured neurons, wild-type centaurin alpha1 expression increases dendritic filopodia and spine-like protrusions. Expression of a GAP-inactive mutant diminishes spine density in CA1 pyramidal neurons within cultured organotypic hippocampal slice cultures. These data support the conclusion that centaurin alpha1 functions through GAP-dependent Arf regulation of dendritic branching and spines that underlie normal dendritic differentiation and development.