No abstract

A genomic clone encoding the Purkinje cell-specific L7 protein has been isolated and utilized to drive the expression of beta-galactosidase in mice. Three independent transgenic lines, germ line transformed with an L7-beta-galactosidase fusion gene, exhibit beta-galactosidase expression in both cerebellar Purkinje cells and retinal bipolar neurons. This distribution is the same as that previously determined for the L7 protein by immunohistochemistry. The transgenic murine lines can be used to obtain populations of marked Purkinje and bipolar neurons. Similar L7 promoter constructs can be used to express other foreign genes specifically in these two classes of neurons.

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Parthenogenetic mouse embryos pose an interesting problem in the study of early mammalian development. Haploid or diploid parthenogenones, resulting from spontaneous or experimental activation of unfertilized eggs, will undergo apparently normal preimplantation development but die in the early post-implantation stages. However, in aggregation chimaeras with fertilized embryos, parthenogenetic embryos have the ability to differentiate into many tissue types, including gametes which can give rise to normal offspring. Furthermore, it has been reported that viable young were obtained from the transfer of inner cell-mass nuclei of parthenogenetic blastocysts to enucleated fertilized eggs. These observations suggest that sperm have some additional role, apart from restoring a complete genome, that is necessary for normal development. To investigate whether sperm-related modifications to the egg cytoplasm are important, we have used an efficient nuclear transfer technique in which a complete karyoplast, comprised of pronuclei, surrounding cytoplasm and a portion of the egg plasma membrane, is transferred utilizing Sendai virus membrane fusion. Embryos produced by the transfer of pronuclei from diploid parthenogenetic eggs to enucleated fertilized eggs died very soon after implantation, whereas viable young were obtained from the transfer of fertilized egg pronuclei into enucleated parthenogenetic eggs. This shows that the death of parthenogenones is not due to a lack of cytoplasmic factors from the sperm.

Mouse strains with null mutations in the gamma interferon gene (Ifng) or the gamma interferon receptor gene (Ifngr) have been engineered. The use of these strains as animal models of viral and bacterial infections has enhanced our understanding of the role of gamma interferon (IFN-γ) in the host immune response. However, direct comparisons between Ifng−/− (GKO) and Ifngr−/− (RGKO) mice have been problematic because previously available strains of these mice have had different genetic backgrounds (i.e., C57BL/6 and BALB/c for GKO mice and 129/Sv//Ev for RGKO mice). To enable direct comparison of herpes simplex virus type 1 (HSV-1) infections in GKO and RGKO mice, we introduced the IFN-γ null mutation into the 129/Sv//Ev background. We report that, after HSV-1 inoculation, mortality was significantly greater in RGKO mice than in GKO mice (38 versus 23%,P = 0.0001). Similarly, the mortality from vaccinia virus challenge was significantly greater in RGKO mice than in GKO mice. With differences in genetic background excluded as a confounding issue, these results are consistent with the existence of an alternative ligand(s) for the IFN-γ receptor that is also capable of mediating protection against viral challenge.