Ultrastructural changes in the endoplasmic reticulum during dormancy release of apple embryos (Pyrus malus L.)

Apple embryos were treated by cold (0°C) within the fruits, to break their dormancy; the controls were treated at 12°C or at 20°C. Ultrastructural features of meristematic cells in the embryonic axis were compared for each treatment. The organization of the cells of dormant embryos was described: Endoplasmic reticulum consisted in some short rough cisternae; lipid droplets regularly arranged near the plasmalemma constituted a kind of shell; mitochondria had a few cristae; and dictyosomes were rarely observed. All these features are typical of dry seeds. After cold treatments, the only evolution observed was in the endoplasmic reticulum, where highly organized stacks appeared progressively as a function of time at 0°C. An intermediate temperature (12°C) induced similar formations in the reticulum but they were rarely observed and their degree of organization was lower than that obtained at 0°C. At 20°C, endoplasmic reticulum resembled that of the dormant embryo cells. The relation between the appearance of these structures in the reticulum and the disappearance of dormancy induced by cold is discussed.Abbreviations ER endoplasmic reticulum - RER rough endoplasmic reticulum     

Hemoglobins of the tadpole of the bullfrog, Rana catesbeiana. Amino acid sequence of the alpha chain of a major component

The complete amino acid sequence has been determined for the alpha chain of component III of the hemoglobin of the tadpole of the bullfrog, Rana catesbeiana. The chain comprises 141 residues of which 80 (57%) are identical to those in the corresponding positions of the human chain. Almost the same extent of similarity exists in the comparison with the sequenced part of the alpha chain of the adult bullfrog. The major features of this chain are: 1) each residue which is common to all other alpha chains of known sequence is also found in this alpha chain; 2) an acetylated NH2 terminus prevents formation of one of the salt bridges found in human hemoglobin which is responsible for part of the alkaline Bohr effect in mammalian hemoglobins; and 3) a prolyl residue at alpha 99 (G6) must distort the G helix.     

Solvent perturbation of the fluorescence of fluorescein bound to specific antibody. Fluorescence quenching of the bound fluorophore by iodide

Differential accessibility of liganded, high affinity rabbit anti-fluorescyl IgG antibody combining sites to the aqueous milieu has been investigated by solvent perturbation of the extrinsic fluorescence of bound fluorophore. Iodide, a dynamic quencher of fluorescein, was selected for use in these studies after examination of a number of water-soluble fluorescence quenchers. Quenching of antibody-bound fluorophore by iodide was measured with a number of liganded anti-fluorescyl IgG preparations, demonstrating partial solvent exposure of the fluorophore as well as heterogeneity of the high affinity antibody populations. Fluorescence quenching, lifetime, and absorption spectroscopy provided evidence that the antibody-bound fluorophore quenched by iodide interacted with it directly and that anomalous binding of the anion to the surface of the protein, resulting in ground state perturbations of the immunoglobulin, could not explain the observed results.     

Characterization of surface alloantigens of murine neutrophils

Serological analysis of highly purified (>97%) mouse peritoneal exudate neutrophils using a protein-A rosetting technique, showed that these cells possessed the surface phenotype: Ig^–, Thy-1^–, Ly-1^–, Ly-2^–, Ly-3^–, Ly-4⁺, Ly-5⁺, Ly-6⁺, Ly-7^–, Ia^–, FcR⁺ and C3R⁺.     

On the fine structure of the regressing ecdysial glands of Carcinus maenas L. (Crustacea decapoda) parasitized by Sacculina carcini thompson

Summary The ecdysial glands (Y organs) of the crab Carcinus maenas regress in the presence of an external parasite, Sacculina carcini. This regression is more or less severe and may lead to complete autolysis. Three gradual stages in this involutionary process are described. In stage I, the gland cells are nearly normal. Nuclei and cytoplasmic organelles remain unchanged, but large vacuoles begin to appear. Stage II corresponds to more or less drastic nuclear pyknosis and cytoplasmic alterations. Myelin figures are large and numerous. Lysosomes and autophagic vacuoles with phosphatase activity are abundant. However, the general cellular architecture remains preserved. Stage III corresponds to irreversible cytolysis; nuclear envelopes and plasma membranes have disappeared. What remains is an accumulation of cellular debris becoming engulfed by circulating hemocytes. Not all of the gland cells of any given Y organ show the same degree of regression; degeneration is asynchronous.Structures seemingly corresponding to absorptive roots of the parasite are seen. Their lumen is coated with microvilli. The putative direct and indirect influences of the rhizocephalan parasite on its host are discussed. Our results on regressing Y organs of parasitized crabs are compared with those on regressing ecdysial glands of insects.Dedicated to the memory of Sir Francis Knowles, the first investigator to examine the ultrastructure of the Y organ of Carcinus maenas We wish to express our thanks to Professor Berta Scharrer for her critical advice     

Amino acid sequence of neurotoxin I from Centruroides sculpturatus Ewing

The further characterization of toxin I from venom of the scorpion Centruroides sculpturatus Ewing (region, Southwestern United States) is reported. Toxin I is a single polypeptide chain of 64 amino acid residues crosslinked by four disulfide bridges. The complete amino acid sequence of toxin I was deduced from the sequence of its tryptic peptides and overlaps provided by its chymotryptic peptides. Toxin I has an amino terminal lysyl residue and a carboxyl terminal threonyl residue.The amino acid sequences of toxin I and neurotoxic variants 1, 2, and 3, likewise isolated from C. sculpturatus venom, differ at 26 positions.The sequences of toxin I from C. sculpturatus and toxins I and II from the North African scorpion, Androctonus australis Hector, are also compared.     

Molecular Epidemiology of Carbapenem Non-Susceptible Acinetobacter baumannii in France

Carbapenem-resistant Acinetobacter baumannii have emerged globally. The objective of this study was to investigate the epidemiology, clonal diversity and resistance mechanisms of imipenem non-susceptible A. baumannii isolates in France. Between December 2010 and August 2011, 132 notifications were collected, including 37 outbreaks corresponding to 242 cases (2 to 55 per cluster). Multilocus sequence typing, pulsed-field gel electrophoresis (PFGE) and characterisation of carbapenemase-encoding genes were performed on 110 non-repetitive isolates. Gene bla _OXA-23 was the most frequently detected (82%), followed by bla _OXA-24 (11%) and bla _OXA-58 (7%). Eleven sequence types (ST) were distinguished, among which sequence types ST1, ST2 (64%), ST20, ST25, ST85 and ST107. Isolates from epidemiological clusters had the same ST and resistance genes, indicating probable transmission within centres. In contrast, PFGE types of isolates differed among centres, arguing against transmission among centers. This study provides the first epidemiological snapshot of the population of A. baumannii with reduced susceptibility to carbapenems from France, and further underlines the predominance of international clones.     

Expression of the TEL-Syk Fusion Protein in Hematopoietic Stem Cells Leads to Rapidly Fatal Myelofibrosis in Mice

The TEL-Syk fusion protein was isolated from a patient with myelodysplasia with megakaryocyte blasts. Expression of TEL-Syk transforms interleukin-3 (IL-3)-dependent Ba/F3 cells in vitro by deregulating STAT5-mediated signal transduction pathways. In vivo, TEL-Syk expression in pre-B cells blocks B cell differentiation, leading to lymphoid leukemia. Here, we demonstrate that TEL-Syk introduced into fetal liver hematopoietic cells, which are then adoptively transferred into lethally irradiated recipients, leads to an aggressive myelodysplasia with myelofibrosis that is lethal in mice by 60–75 days. Expression of TEL-Syk induces a short-lived myeloexpansion that is rapidly followed by bone marrow failure and extreme splenic/hepatic fibrosis accompanied by extensive apoptosis. The disease is dependent on Syk kinase activity. Analysis of serum from TEL-Syk mice reveals an inflammatory cytokine signature reminiscent of that found in the sera from patients and mouse models of myeloproliferative neoplasms. TEL-Syk expressing cells showed constitutive STAT5 phosphorylation, which was resistant to JAK inhibition, consistent with deregulated cytokine signaling. These data indicate that expression of TEL-Syk in fetal liver hematopoietic cells results in JAK-independent STAT5 phosphorylation ultimately leading to a uniquely aggressive and lethal form of myelofibrosis.