Previous results identified a domain in the major capsid scaffold protein, ICP35, required for interaction with pU,6 and its incorporation into capsids formed in vitro (G. P. Singer et al.,
J. Virol. 74:6838-6848, 2005). In the current studies, PU(L)6 and scaffold proteins were found to coimmunoprecipitate from lysates of both HSV-infected cells and mammalian cells expressing scaffold proteins and PU(L)6. The coimmunoprecipitation of PU(L)6 and scaffold proteins was precluded upon deletion of codons 143 to 151 within U(L)26.5, encoding ICP35. While wild-type scaffold proteins colocalized with PU(L)6 when transiently coexpressed as viewed by indirect immunofluorescence, deletion of UL26.5 codons 143 to 151 precluded this colocalization. A recombinant herpes simplex virus, vJB11, was generated that lacked U(L)26.5 codons 143 to 151. A virus derived from selleck chemical this mutant but bearing a restored U(L)26.5 was also generated. vJBI1 was unable to cleave or package viral DNA, whereas the restored virus packaged DNA normally. vJBI1 produced ample numbers of B capsids in infected cells, but these lacked normal levels of pU(L)6. The deletion in U(L)26.5 also rendered PU(L)6 resistant to detergent extraction from
vJ1311-infected cells. These data indicate that, as was observed in vitro, amino acids 143 to 151 of ICP35 are critical for (i) interaction between scaffold proteins and PU(L)6 and (ii) incorporation of the HSV portal into capsids.”
“In the rat, a number of sensory modalities converge in the perirhinal cortex (PC). Glutathione peroxidase The neural pathway from the perirhinal cortex to Dorsomorphin manufacturer the entorhinal cortex (EC) is considered one of the main routes into the entorhinal-hippocampal network. Evidence accumulated recently suggests that EC and PC, far from being passive relay stations, actively gate impulse traffic between neocortex and hippocampus. Using slice
preparation maintaining the neurocircuit connecting PC, EC, hippocampal formation and amygdala, we investigated the associative function of PC and EC with respect to sensory and motivational stimuli and the influence of the association on the neurocircuit. In horizontal slices located ventrally to the rhinal sulcus, where we stimulated area 35 and the lateral amygdala, both inputs can be independently conveyed to the dentate gyrus. In slightly more dorsal slices where we stimulated area 36 and the lateral amygdala, the coincidence of the two inputs was needed to activate the hippocampus. This need for association of the two inputs was apparently mediated by the deep layer of EC. In all instances activation of the deep layers of EC was sufficient to activate the dentate gyrus, suggesting the relevance of the deep layers in cortico-hippocampal interactions. (c) 2008 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.