Influence of the carboxyl terminus of luteinizing hormone-releasing hormone and bradykinin on hydrolysis by brain endo-oligopeptidases

A homogeneous preparation of endo-oligopeptidase A from rabbit brain cleaves luteinizing hormone-releasing hormone (less than Glu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2) at the Tyr-Gly bond only after the removal of Gly-NH2 from the COOH-terminal position of the molecule. The influence of the carboxyl terminus on hydrolysis by brain endo-oligopeptidases was studied using bradykinin as a model substrate. The substitution of the carboxyl group of bradykinin by the amide reduces by 2.5-fold the rate of Phe-Ser bond hydrolysis by endo-oligopeptidase A but has no effect on the rate of hydrolysis of the Pro-Phe bond by endo-oligopeptidase B. On the other hand, the deletion of Phe-Arg from the COOH-terminal portion of bradykinin makes the peptide resistant to hydrolysis by endo-oligopeptidase A whereas it increases by 5-fold the rate of hydrolysis of the Pro-Gly bond by endo-oligopeptidase B.     

Protein content and enzyme levels of cultured chick embryo cells treated with camptothecin and actinomycin D.

The alkaloid camptothecin uncouples the growth and adivision of chick embryo cells. At a moderate dose (0.5 microgram/ml) it inhibits the incorporation of thymidine but not of uridine and leucine and the cell protein content increases and reaches twice that of control after 4 days of treatment. Twelve hours after addition of the drug, the activities per cell of the mitochondrial enzymes poly A hydrolase (EC 3.1. 4.21), cytochrome c oxidase (EC 1.9.3.1), and succinate dehydrogenase (EC 1.3.99.1) are greater than that of the control and keep increasing for at least 96 H. The increase in the activities of the mitochondrial enzymes precede that of NADPH-cytochrome c reductase (EC 1.6.2.4) and cytidine triphosphatase (EC 3.6.1.15), which are microsomal and plasma membranes enzymes respectively. Actinomycin D (0.01 microgram/ml) also inhibits the multiplication of the chick cells and the synthesis of DNA. The protein content of the actinomycin D treated cells decreases to 70% of the control by day 2. Nevertheless, the activities of the mitochondrial enzymes increase over that of the control but to a smaller extent that with camptothecin. The activities of the enzymes of the other organelles are not stimulated. Camptothecin at a higher dose (5.0 microgram/ml) induces effects similar to those of actinomycin D.     

Reproductive biology and pollinators in two enantiostylous Qualea species (Vochysiaceae) in the Brazilian Cerrado

• Enantiostyly is a floral polymorphism in which two floral forms in the same species differ in deflection of the stigma to right or left position. In monomorphic enantiostylous plants, flowers of the two morphs occur within the same individual, usually in the same proportion. In self‐compatible species the function of monomorphic enantiostyly is proposed to increase outcrossing rates and offer a reproductive advantage under pollination limitation. Enantiostylous species are usually self‐compatible and show heteranthery, with poricide anthers and pollen as pollinator reward; however, there are families, such as Vochysiaceae, that have different characteristics.
• We analysed the reproductive system and pollination biology of Qualea parviflora and Q. multiflora, two enantiostylous species from the Brazilian Cerrado that have specific morphological and physiological traits. For this, we characterized flower traits, performed hand pollinations and studied floral visitors.
• We found no differences between morphs in the proportion of flowers, nectar produced or its concentration, pollen quantity and fruit set. Both species were self‐incompatible and quite generalist regarding floral visitors.
• Enantiostyly in self‐incompatible plants seems to confer a reproductive advantage by reducing self‐interference resulting from stigma clogging. This novel result helps to expand our knowledge on this complex floral polymorphism and opens new avenues for future research on this topic.

     

Human exploitation shapes productivity–biomass relationships on coral reefs

Coral reef fisheries support the livelihoods of millions of people in tropical countries, despite large‐scale depletion of fish biomass. While human adaptability can help to explain the resistance of fisheries to biomass depletion, compensatory ecological mechanisms may also be involved. If this is the case, high productivity should coexist with low biomass under relatively high exploitation. Here we integrate large spatial scale empirical data analysis and a theory‐driven modelling approach to unveil the effects of human exploitation on reef fish productivity–biomass relationships. We show that differences in how productivity and biomass respond to overexploitation can decouple their relationship. As size‐selective exploitation depletes fish biomass, it triggers increased production per unit biomass, averting immediate productivity collapse in both the modelling and the empirical systems. This ‘buffering productivity’ exposes the danger of assuming resource production–biomass equivalence, but may help to explain why some biomass‐depleted fish assemblages still provide ecosystem goods under continued global fishing exploitation.     

Physiological Aspects of Melon (Cucumis melo L.) as a Function of Salinity

Journal of Plant Growth Regulation - This study evaluated the effect of saline water irrigation (4.5 dS m−1) on growth, gas exchange and mineral nutrient content in eight melon accessions and...     

Tropical Bacillus Strains Inoculation Enhances Maize Root Surface Area,Dry Weight,Nutrient Uptake and Grain Yield

Journal of Plant Growth Regulation - The rising demand for agricultural commodities in developing countries has put increasing pressure on land resources for higher yields, with associated growth...     

Incomplete mitophagy in the mevalonate kinase-deficient Saccharomyces cerevisiae and its relation to the MKD-related autoinflammatory disease in humans

Mevalonate kinase deficiency (MKD) is an autosomal recessive disorder in humans that causes systemic autoinflammatory problems to children. Previously, we used a yeast model to show that MKD results in mitochondrial malfunctioning that may finally induce mitophagy. Here, we proved that MKD indeed induced general autophagy as well as mitophagy in yeast, but these mechanisms did not go to completion. Therefore, the limitation of mevalonate kinase activity produces dysfunctional mitochondria that might not be recycled, causing metabolic dysfunctions in the cells. Understanding this mechanism may provide a piece in solving the nonspecific autoinflammatory response puzzle observed in MKD patients.