Endopeptidase Activity of Phage λ-Endolysin

JACOB and Fuerst^1,2 demonstrated the presence of a bacteriolytic enzyme (λ-endolysin) in the induced cultures of lysogenic Escherichia coli K12 (λ). The enzyme was later identified as the product of gene R; of phage λ³ which is involved in bacterial lysis at the end of a latent period. The enzyme is apt to form spheroplast-like structures in E. coli² and one would therefore expect its substrate to be murein.     

Induced Bivalent Interlocking and the Course of Meiotic Chromosome Synapsis

WHEN chromosomes pair at meiosis the bivalents so formed do not normally interlock. Heat-treatments can, however, induce bivalent interlocking in the locust Locusta migratoria. Only the longest bivalents interlock and usually only two are found per cell; two “rod” bivalents, with single chiasmata, two “ring” bivalents, each with two or three chiasmata, or one “rod” and one “ring” bivalent (Fig. 1a, b and c). The nature of this interlocking and the metaphase orientational and congressional properties of interlocked bivalents are analysed in detail elsewhere¹.     

Regulation of the Pool Size of Valine in Escherichia coli K-12

Three mutations (ilvH611, ilvH612, and ilvH613) are described which make Escherichia coli K-12 resistant to valine inhibition and are located near leu. The expression of the ilv genes appears to be normal in these mutants since the isoleucine-valine biosynthetic enzymes are not derepressed relative to the wild type. The intracellular concentration of valine is, however, higher in the mutants than in the isogenic ilvH(+) strain. These mutants also excrete valine, probably because of the high intracellular concentration of this amino acid. The pool size of valine is regulated independently from that of isoleucine and leucine. The increased intracellular concentration of valine is due to a decreased feedback inhibition that valine exerts on its own biosynthetic pathway. In fact, acetolactate synthase activity assayed in extracts of ilvH612 and ilvH613 mutants is more resistant to valine inhibition than the activity assayed in the ilvH(+) isogenic strain. Two forms of acetolactate synthase activity can be separated from these extracts by adsorption and elution on hydroxylapatite. One of them is as sensitive to valine inhibition as that of the wild type, the other is more resistant to valine inhibition.     

Noradrenaline Metabolism in Neocortex and Hippocampus Following Transient Forebrain Ischemia in Rats: Relation to Development of Selective Neuronal Necrosis

Noradrenaline (NA) metabolism in the neocortex and hippocampus was examined in rats at 1, 24, and 48 h following 15 min of reversible forebrain ischemia. As assessed by the ratio of accumulated 3,4-dihydroxyphenylalanine (DOPA) to the tissue NA level after inhibition of DOPA decarboxylase, the NA turnover rates were markedly increased (120-148% above the control) at 1 h postischemia in both the neocortex and hippocampal formation (CA1 and CA3 plus dentate gyrus). The DOPA:NA ratio went back to control levels after longer postischemic survival times. The ratio between levels of the deaminated NA metabolite, 3,4-dihydroxyphenylethyleneglycol (DOPEG), and NA, which gives another measure of NA turnover rate, showed similar changes. In the neocortex and the CA3 plus dentate gyrus, the DOPEG:NA ratio was markedly increased (89-118%) 1 h after the ischemia, but this change had disappeared at 24 and 48 h. Thus, both the DOPA accumulation experiments and the NA and DOPEG measurements indicate that following transient forebrain ischemia, there is an increased NA turnover in the hippocampus and cortex only in the early recirculation period and not after longer postischemic survival times. The degree of neuronal necrosis in the CA1 region was examined light microscopically on celestine blue-acid fuchsin-stained sections at 24, 48, and 96 h following the ischemic insult. The neuronal damage in CA1 was sparse after 24 h of recovery, had increased markedly after 48 h, and was very pronounced at 96 h.(ABSTRACT TRUNCATED AT 250 WORDS)     

The differential genetic and environmental canalization of fitness components in Drosophila melanogaster

Canalization describes the process by which phenotypic variation is reduced by developmental mechanisms. A trait can be canalized against environmental or genetic perturbations. Stabilizing selelction should favor improved canalization, and the degree of a trait's canalization should be positively correlated with its impact on fitness. Here we report, for Drosophila melanogaster, measurements of environmental canalization for five fitness components. We compare them with measurements of genetic canalization, and we discuss the impact of inbreeding on both. In three experiments we measured the variation of fitness components within lines nested within temperature, treatment, and experiment. Lines differed in the position of a P element insert or in genetic background. Within lines flies were genetically nearly identical. We designated trait variation within lines as environmental canalization. The canalization of the traits increased with their impact on fitness, and the pattern was similar to that found for the canalization of fitness components against genetic differences, measured as the variation among lines nested within temperature, treatment, and experiment. This suggests that developmental mechanisms buffer the phenotype against both genetic and environmental disturbance. The results also suggest, less strongly, that inbreeding weakens canalization.     

FITNESS SENSITIVITY AND THE CANALIZATION OF LIFE-HISTORY TRAITS

Canalization is an abstract term that describes unknown developmental mechanisms that reduce phenotypic variation. A trait can be canalized against environmental perturbations (e.g., changes in temperature or nutrient quality), or genetic perturbations (e.g., mutations or recombination); this paper is about genetic canalization. Stabilizing selection should improve the canalization of traits, and the degree of canalization should be positively correlated with the traits' impact on fitness. Experiments testing this idea should measure the canalization of a series of traits whose impact on fitness is known or can be inferred, exclude differences among traits in the number of loci and alleles segregating as an explanation for the pattern of variability found, and distinguish between canalization against genetic and environmental variation. These conditions were met by three experiments within which the variation of fitness components among Drosophila melanogaster lines was measured and among which the genetic contribution to the variation among lines was clearly different. The canalization of the traits increased with their impact on fitness and did not depend on the degree of genetic differences among lines. That the flies used had been transformed by a P-element insert suggests that canalization was also effective against novel genetic variation. The results reported here cannot be explained by the classical hypothesis of reduction in the number of loci segregating for traits with greater impact on fitness and confirm that traits with greater impact on fitness are more strongly canalized. This pattern of canalization reveals an underappreciated role for development in microevolution. There is differential genetic canalization of fitness components in D. melanogaster.     

<Emphasis Type="Italic">Alona alsafadii</Emphasis> n. sp. from Yemen,a primitive,groundwater-dwelling member of the <Emphasis Type="Italic">A. karua</Emphasis>-group

The effect of algae on the production of musty-smelling compounds by actinomycetes was studied. Streptomyces spp., causing intensive musty odor, were isolated from hypertrophic Lake Kasumigaura and cultured in association with algae from the same lake. Isolate E and I effectively utilized the cyanobacteria, Microcystis aeruginosa and Anabaena spiroides, and the diatom, Synedra acus, as a carbon source and produced a musty-smelling 2-methylisoborneol in the shaken sediment cultures. High populations of algae and actinomycetes, and aerobic condition in the sediment seem responsible for the occurrence of musty odor in Lake Kasumigaura.     

Depression of Neuronal Protein Synthesis Initiation by Protein Tyrosine Kinase Inhibitors

Abstract— Growth factors stimulate cellular protein synthesis, but the intracellular signaling mechanisms that regulate initiation of mRNA translation in neurons have not been clarified. A rate-limiting step in the initiation of protein synthesis is the formation of the ternary complex among GTP, eukaryotic initiation factor 2 (elF-2), and the initiator tRNA. Here we report that genistein, a specific tyrosine kinase inhibitor, decreases tyrosine kinase activity and the content of phosphotyrosine proteins in cultured primary cortical neurons. Genistein inhibits protein synthesis by >80% in a dose-dependent manner (10–80 μg/ml) and concurrently decreases ternary complex formation by 60%. At the doses investigated, genistein depresses tyrosine kinase activity and concomitantly stimulates PKC activity. We propose that a protein tyrosine kinase participates in the initiation of protein synthesis in neurons, by affecting the activity of elF-2 directly or through a protein kinase cascade.