The goblet cavity matrix in the larval midgut of Hyalophora cecropia

The larval midgut of the silkmoth Hyalophora cecropia was examined using scanning electron microscopy. Goblet cells were observed to contain within their cavities a matrix plug. This matrix material was extruded onto the lumen side of the epithelium when the tissue was stretched. The rôle of this matrix material in maintenance of the capacity of the midgut to transport ions in vivo and in vitro is discussed.     

The mechanism of action of ethanolamine ammonia-lyase, an adenosylcobalamin-dependent enzyme. Reaction of the enzyme.cofactor complex with 2-aminoacetaldehyde

Ethanolamine ammonia-lyase (EC 4.3.1.7) catalyzes the adenosylcobalamin-dependent deamination of ethanolamine and 2-aminopropanol. Incubation of the enzyme.cofactor complex with 2-aminoacetaldehyde leads to rapid cleavage of the carbon--cobalt bond accompanied by the destruction of the corrinoid portion of the cofactor. During this reaction the adenosyl portion of the cofactor is oxidized to 4',5'-anhydroadenosine, and the aminoacetaldehyde is converted to acetic acid, which remains associated with the enzyme as a noncovalent complex which survives gel filtration. There is no evidence for the alkylation of the corrin metal by the substrate analog. The enzyme.AdoCbl complex is thus able to eliminate an amino group from a substrate analog without the formation of a new alkyl cobalamin in which the analog is a ligand. These observations do not support the participation of what might be termed "substratylcobalamin" as an intermediate in the ammonia migration occurring in reactions catalyzed by ethanolamine ammonia-lyase.     

Ras proteins activate calcium channels in neuronal cells.

Ras (p21) proteins are involved in the control of cell growth and differentiation, but the mechanism by which they exert these effects is not yet known. Here we present evidence that c-Ha-ras (p21(Gly-12)) and its oncogenic mutant T24-ras (p21(Val-12)) selectively induce omega-conotoxin and dihydropyridine-sensitive Ca2+ currents within a few hours after introduction into the cytoplasm of neuroblastoma x glioma hybrid cells. Whereas control cells exhibited a mean Ca2+ current of 250 pA, it amounted to 730 pA in cells pretreated with ras protein. In cells loaded with p21(Gly-12), the effect occurred after 2 hours and was terminated after 8 hours. In contrast, introduction of p21(Val-12) resulted in a prolonged delay (6 hours) of the effect which lasted for more than 24 hours. When ras proteins were preactivated with the non-hydrolysable GTP analog GppNHp, the time courses of both p21(Gly-12) and p21(Val-12) effects were fast and sustained, suggesting that in intact cells (i) the GDP/GTP exchange is faster for p21(Gly-12) compared to p21(Val-12) and (ii) inactivation of p21(Gly-12) is mediated by GAP-induced GTPase activity. T-type Ca2+ currents and K+ currents were unaffected by ras proteins.     

Clustering of mutations inactivating a Chi recombinational hotspot

Chi sites promote Rec-mediated recombination in bacteriophage λ. Nine independent, nitrous acid-induced mutations were obtained within one of these sites, χ⁺C. Eight of the mutations completely inactivated the Chi site, while one mutation left partial activity. Nucleotide sequence analysis showed that the mutations were located at four different sites one to four base-pairs from the site of the χ⁺C mutation that created the active Chi locus. This interval is within a region of homology common to the χ⁺C locus and another sequenced Chi locus, χ⁺B. These results support the view that Chi is a unique nucleotide sequence and suggest the extent of the Chi sequence.     

Liver tissue graft rejection in murine major histocompatibility complex mutants

Liver tissue grafts between seven H-2 mutants and their parental strains have been studied. Each of these mutants was originally identified by reciprocal mutant—parental strain skin graft rejection. However, liver grafts among mutants and parental standard strains are not uniformly rejected. Liver graft rejection also fails to correlate with mutant—parental stimulation in CML and MLC. In addition, the immune reaction pattern of female mutant animals against grafts of male liver differs from the reaction pattern found in parental standard strains. Several explanations for the differences between immune response to liver and skin grafts are proposed, including different T cell subsets involved in recognition, availability of antigenic sites to immunocompetent cells, and structural differences between mutant and parental H-2 antigens. Abbreviations used in this paper: bml, 2, 3, 4,14; dml; fm2=mutants of strains C57BL/6, B10.D2 and B10.M respectively; B6=C57BL/6     

Prevention of macrophage tumoricidal activity by agents known to increase cellular cyclic AMP.

The concept of T-T cell interaction which was first suggested during cell-mediated immune response to alloantigens was evaluated in a syngeneic tumor system. The combination of lymph node and thymus cells from BALB/c mice immune against syngeneic tumor cells, mKSA, was shown to exhibit collaboration with respect to in vitro generation of effector cells capable of preventing growth of corresponding tumor cells in the tumor cell neutralization assay. While each cell population of either anatomical site did not prevent tumor growth when tested alone, combinations of both did. The antigen specificity of effector cells generated by synergizing cultures was similar to that of effectors derived from cultures containing optimal numbers of responding lymph node cells. The lymph node and thymus cell populations participating in synergy were found to be thymus dependent. These results suggest that we may be dealing with the same or similar T₁- and T₂-cell populations described before as displaying synergy in response to alloantigens in the graft versus host, mixed lymphocyte, and cell-mediated cytotoxicity reactions.     

Nephrogenic diabetes insipidus in an Australian aboriginal kindred.

Four Australian aboriginal children were found to have nephrogenic diabetes insipidus. They are the sons of 3 sisters who were shown to have a urinary concentrating defect uncorrected by vasopressin. An extensive genealogy did not reveal any caucasian genetic influence suggesting that a new genetic mutation was responsible.