Gene expression analyses in maize inbreds and hybrids with varying levels of heterosis

Background  

Heterosis is the superior performance of F₁ hybrid progeny relative to the parental phenotypes. Maize exhibits heterosis for a wide range of traits, however the magnitude of heterosis is highly variable depending on the choice of parents and the trait(s) measured. We have used expression profiling to determine whether the level, or types, of non-additive gene expression vary in maize hybrids with different levels of genetic diversity or heterosis.     

Endothelial activation during interleukin 2 immunotherapy. A possible mechanism for the vascular leak syndrome

A major sequela of immunotherapy with interleukin 2 (IL-2) is development of a vascular leak syndrome. The pathogenesis of this toxic effect is not known. We have examined pre- and post-treatment skin biopsies from 14 patients undergoing systemic administration of IL-2 for evidence of endothelial cell activation. Specifically, we have used the immunoperoxidase technique to detect the expression of three different activation antigens: endothelial-leukocyte adhesion molecule 1, detected with monoclonal antibody H4/18; intercellular adhesion molecule 1, detected with antibody RR1/1; and histocompatibility leukocyte antigen-DQ, detected with antibody Leu 10. Each of these antigens may be induced on cultured endothelial cells by various cytokines (although not by IL-2) and is expressed during endothelial cell activation in vivo at sites of delayed hypersensitivity and other immune responses. Pretreatment biopsies from each patient showed no endothelial expression of endothelial-leukocyte adhesion molecule 1 and only weak to moderate expression of intercellular adhesion molecule 1 and histocompatibility leukocyte antigen-DQ (except for one specimen unreactive with Leu 10). After 5 days of treatment, every patient showed marked endothelial expression of all three antigens (except for the same patient who remained unreactive with Leu 10). Endothelial-leukocyte adhesion molecule-1 expression was confined to postcapillary venular endothelium whereas intercellular adhesion molecule-1 and Leu 10 also were expressed on stromal cells and mononuclear cells. Thus, we conclude that i.v. administration of IL-2 leads to endothelial cell activation. Because IL-2 fails to induce the same antigens on cultured endothelial cells, we infer that IL-2 acts in vivo by inducing the production of other cytokines (e.g., interleukin 1, tumor necrosis factor, lymphotoxin, and interferon-gamma). Finally, since endothelial cell activation at sites of cell-mediated immune responses is well known to result in vascular leakiness to macromolecules, we propose that the vascular leak syndrome accompanying IL-2 therapy may arise from widespread inappropriate endothelial cell activation.     

Embryology of the thoracic and abdominal ganglia of the large milkweed bug, Oncopeltus fasciatus (Dallas), (Hemiptera, Lygaeidae)

In this study, the condensation of the three thoracic and 11 abdominal segmental ganglia to form a prothoracic and central nerve mass during embryogenesis is described. During katatrepsis, many changes occur in the organization of these ganglia; this study suggests that some of these changes are caused by mechanical forces acting on the ventral nerve cord at this time. The ventral nerve cord begins its anterior migration and coalescence ten hours after katatrepsis and is completed 63 hours later. The central ganglion is made up of the meso- and metathoracic ganglia and seven abdominal ganglia. Intrasegmental median cord nuclei are shown to form glial elements in the median sagittal plane of the neuropile and in the longitudinal connectives. Intersegmental median cord neuroblasts migrate into the posterior gangliomeres but, apparently, degenerate soon after katatrepsis. Lateral cord cells bordering on the neuropile form a glial investment that surrounds this fiber tract region. Peripheral lateral cord cells are shown to form the cells of the outer ganglionic sheath, the perineurium.     

Dispensable sequences and packaging constraints of DNA from the Streptomyces temperate phage phi C31

Deletion mutants of the temperate Streptomyces phage phi C31 were selected by two methods: resistance to the chelating agent sodium pyrophosphate, and plating of a phi C31::pBR322 hybrid phage on Streptomyces albus G to obtain large plaque mutants. The deletions defined a 7.7 kilobase (kb) segment of the phi C31 genome which is inessential for plaque formation, in addition to a shorter segment including the repressor gene. Analysis of deletions and insertions suggested that the minimum size of the phi C31 genome allowing plaque formation is 37.5 kb (91% of the wild-type length of 41.2 kb), and the maximum is at least 42.4 kb (103%). These results indicate that it should be possible to introduce up to 10 kb of foreign DNA into a suitably developed phi C31 vector.     

Lifetimes of complexes of the antibiotic x-537a (lasalocid a) with physiological cations in methanol. Determination by NMR using a dissociative shift reagent

Using a magnetic resonance method we have determined the lifetimes of the following complexes of X-537A (HX) in methanol solution at 25° C, BaX⁺, 132 μs; SrX⁺, 34 μs; CaX⁺, 24 μs, and KX, 15 μs, each with an estimated uncertainty of 30%. For NaX and LiX the lifetimes are too short to measure by the present method, The lifetime found for BaX⁺ is considerably shorter than the result obtained by Patel and Shen using a different method. The present method depends upon the broadening of the resonance lines of certain protons in X^? due to reactions such as X^? + Ba²⁺ = BaX⁺, when the resonance of the proton in the “free” X^? has been shifted from its normal frequency by Pr(III) which acts via the exchange PrX₃ ? PrX⁺₂ + X^?. To determine the lifetimes of interest the equations for a three-state spin system were derived; under the relevant conditions the final equations take the form of the Swift-Connick equations for a two-state system, with the characteristics of one of the states dependent upon the PrX₃ concentration. This dependence is used to extract the life-times from the data in a novel and simple way.