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We present a genetic linkage map of mouse chromosome 8 that spans 53 cM and includes eight cloned loci. This map was derived from analysis of 100 progeny of an interspecific backcross between Mus spretus and Mus musculus domesticus. Genes that were mapped in this analysis include L7, Plat, Lpl, Ucp, Es, Mt-1, Um, and Tat. This analysis positions a new extremely proximal marker on chromosome 8, which is discussed as a potential candidate gene for the nervous locus. These linkage data will be useful for the mapping of additional loci on chromosome 8.

The lurcher ( Lc ) mutant mouse strain exhibits postnatal degeneration of cerebellar Purkinje cells. We have typed progeny from an intersubspecific, phenotypic backcross at seven loci to develop a genetic linkage map which spans approximately 35 cM surrounding and including the Lc locus on mouse chromosome 6. [ (Mus musculus castaneus × B6CBA -A w-J A-Lc ) F 1 × B6CBA -A w-J A ] N 2 progeny were scored visually for the lurcher phenotype and molecularly, through restriction fragment length polymorphism analysis, for six cloned markers. Two candidate genes, Npy and Pcp-1 , which map to mouse chromosome 6 and which are expressed in the cerebellum, are demonstrated to be distinct from Lc . Three genes are shown to be closely linked to the Lc locus, and the map order cen- Cpa-Npy-Cbl-1-Lc-Igk, Fabpl-Pcp-1 is determined. The molecular genetic linkage map presented here represents progress toward isolating a clone of the Lc gene.

The gene apparently responsible for a heritable form of murine pituitary-dependent dwarfism (Ames dwarf, df) has been positionally cloned, identifying a novel, tissue-specific, paired-like homeodomain transcription factor, termed Prophet of Pit-1 (Prop-1). The df phenotype results from an apparent failure of initial determination of the Pit-1 lineage required for production of growth hormone, prolactin or thyroid-stimulating hormone, resulting in dysmorphogenesis and failure to activate Pit-1 gene expression. These results imply that a cascade of tissue-specific regulators is responsible for the determination and differentiation of specific cell lineages in pituitary organogenesis.

The meander tail mouse harbors a recessive mutation on chromosome 4 that affects the anterior lobes of the cerebellum and the caudal vertebrae. Examination of the mea mea cerebellum reveals that the complete disorganization of all cell types seen in the anterior lobes is separated by a sharp and consistent boundary from the normal cytoarchitecture of the posterior lobes. In the absence of any biochemical information regarding the affected gene product, attempts to clone the gene must rely on the strategy of reverse genetics. As an initial step in this process we have constructed a genetic linkage map spanning 68 cM of chromosome 4 using an intersubspecific phenotypic backcross. The loci included in this analysis are Calb, Ggtb, Lv, b, Ifa, mea, D4Rp1, Glut-1, Lck, Lmyc-1 , and Eno-1 . This analysis positions the mea phenotypic locus in the interval between Ifa and Glut1 . These results also further define regions of homology between mouse chromosome 4 and human chromosomes 8, 1, and 9. This linkage map provides the means to evaluate candidate genes, and to identify tightly linked markers useful for cloning the meander tail locus.

1. 1. Cytosolic isocitrate dehydrogenase from rat and pig ovaries differs from that described in other tissues. It is more labile, has higher K m -values for substrates, higher optimal pH, and its activity is modulated by varying ratios of Ca 2+ : Mg 2+ . The ovarian enzyme exhibits acute and long term responses to in vivo administration of gonadotropins. 2. 2. A partial purification yielding a 70-fold increase in specific activity of this NADP + dependent enzyme is described. The enzyme mol wt = 58,000 ± 3000 daltons and pI = 4.9. 3. 3. The unique properties of the enzyme are discussed in relation to its probable metabolic role in ovary.

Summary Murine, polyclonal and monoclonal antibodies, raised against sporozoites of Eimeria tenella, were tested for their ability to neutralize sporozoite infectivity in vitro and in vivo. Neutralization was effected via three mechanisms. Firstly, sporozoites fixed complement, at low titres, and lysis occurred by the alternative pathway of complement activation. Secondly, in the absence of complement activity, the murine heat-inactivated, hyperimmune antiserum neutralized sporozoites at relatively low titres. At high titres, even though sporozoites were agglutinated, neither the heat-inactivated hyperimmune antiserum nor the monoclonal antibody neutralized sporozoites. Finally, in the presence of complement and specific antibodies, at titres which by themselves would not neutralize sporozoites, neutralization was effected due to lysis via the classical pathway of complement activation.