The human lipoprotein lipase gene was cloned and characterized. It is composed of 10 exons spanning -30 kilobases. The first exon encodes the 5'-untranslated region, the signal peptide plus the first two amino acids of the mature protein. The next eight exons encode the remaining 446 amino acids, and the tenth exon encodes the long 3'-untranslated region of 1948 nucleotides. The lipoprotein lipase transcription start site and the sequence of the 5'-flanking region were also determined. We compared the organization of genes for lipoprotein lipase, hepatic lipase, pancreatic lipase, and Drosophila yolk protein 1, which are members of a family of related genes. A model for the evolution of the lipase gene family is presented that involves multiple rounds of gene duplication plus exon-shuffling and intron-loss events.

A dog whole-genome radiation hybrid (WGRH) panel including 126 clones was constructed by fusing dog fibroblasts irradiated at 5000 rads with thymidine kinase-deficient hamster cells. The average retention frequency of the panel designated as RHDF5000 is 21%, and its resolution power is estimated at 600 kb. The data provided by typing 400 markers were used to estimate linkage power changes subsequent to panel reduction. These changes were analyzed by recomputing typing data from five reduced panels. From these simulations, the parameters allowing investigation of the evolution of the linkage power in the course of panel reduction were determined. Guidelines for constructing a WGRH panel are proposed.

The complete nucleotide sequence of Saccharomyces cerevisiae chromosome X (745 442 bp) reveals a total of 379 open reading frames (ORFs), the coding region covering approximately 75% of the entire sequence. One hundred and eighteen ORFs (31%) correspond to genes previously identified in S. cerevisiae. All other ORFs represent novel putative yeast genes, whose function will have to be determined experimentally. However, 57 of the latter subset (another 15% of the total) encode proteins that show significant analogy to proteins of known function from yeast or other organisms. The remaining ORFs, exhibiting no significant similarity to any known sequence, amount to 54% of the total. General features of chromosome X are also reported, with emphasis on the nucleotide frequency distribution in the environment of the ATG and stop codons, the possible coding capacity of at least some of the small ORFs (<100 codons) and the significance of 46 non‐canonical or unpaired nucleotides in the stems of some of the 24 tRNA genes recognized on this chromosome.

The antigenicity of Murine Sarcoma Virus ( M S V ) transformed mouse, rat and hamster cells has been studied by several techniques designed to detect surface antigens. Antigens were readily demonstrated on neoplastic mouse and rat cells. There was complete cross-reactivity between cells induced by the Harvey ( M S V-H) or Moloney ( M S V -M ) strains of MSV and by Moloney Leukemia Virus ( M L V ) . No evidence of a distinct or separate '' MSV-non-MLV" antigen could be obtained by cross absorptions of'MSV/MLV antisera and cells, or by tests designed to break M L V tolerance. Such results favor the view that MSV and M L V are closely related entities. With the 8303 line of MSV-M transformed hamster cells serological tests revealed little if any reactivity with strongly positive mouse anti-MSVIML V antisera. In 465CHUAT Er AL.would distinguish it from the leukemia viruses, either by kinetics of inactivation (Mahy et al., 1966;Moloney, 1966a, b), size (Mahy, 1966; Hartley and Rowe, 1966), electron microscopic appearance (Mitchiner, 1967;Dalton, 1966;Leclerc et a/., 1967), or immunology (Moloney, 1966a, b ; Hartley and Rowe, 1966;Law et al., 1968; Fefer et a/., 1967a, b). Immunologic studies have shown that anti-MLV sera will neutralize focus and tumor formation by MSV (Moloney, 1966a, b ; Hartley and Rowe, 1966), anti-MSV sera will stain surface antigens on MLV-induced lymphoma cells (Fefer et a/., 1967a, b), and mice immunized against MLV or MSV will show specific resistance to the growth of MLV lymphomas or MSV sarcomas (Fefer et al., 1967a;Law et al., 1968). The purpose of the present work was to characterize the specificity of surface antigens on MSV tumor cells with the aid of various immunological techniques. Attention was focused on cross-reactions between antigens induced by MSV-M and MSV-H and between MSV and MLV, and on attempts to detect virus-determined antigen(s) on MSV hamster cells. MATERIAL AND METHODS AnimalsFrom the colonies of the Institute for Tumor Biology and the National Institute for Medical Research, the following lines of inbred mice and their F, hybrids were used: A/%, C57BL, C3H, C57 Leaden, BALB/c, CBA and dba/2. Tumor linesLines of MLV-induced lymphomas and MSVinduced sarcomas were utilized. The former were maintained in mice in either solid or ascitic form. The latter, of mouse, rat and hamster origin, were induced by MSV-M or MSV-H and were maintained in in vivo and/or in vitro passage. The transplant lines were well-established autonomous neoplasms that grew progressively in host animals. The culture lines originated from either in vitro-transformed cells or tumors. A complete summary of all tumor lines is given in Table I. MH-199 medium with 10% fetal calf serum (FCS) was used for mouse and rat MSV lines and the hamster thyroid SV40 lines. It consists of equal proportions of Parker's 199 and Eagle's Minimal Essential Medium (MEM) with additional vitamins and amino acids. All of the other cells were grown on MEM with 10% FCS, except the human MAS line which was grown in Parker's 19...

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