Regulation of stem elongation in chinese cabbage by inflorescence removal and application of growth regulators

The effect of inflorescence removal on stem elongation in Chinese cabbage cv. Spring A was studied. Removal of the inflorescence before its visibility, or upon its appearance but before the beginning of bolting (stages 1–3), markedly reduced the stem length. Removal after the beginning of bolting (stage 5) had no effect on stem length.Application of GA₃ to the treated plants partially or fully restored the elongation of the flowering stem, whereas paclobutrazol inhibited the elongation of the treated, as well as the control stems. Indole-3-acetic acid (IAA) or kinetin was ineffective in restoring stem elongation of the plants from which the inflorescence had been removed. Inflorescences at stages 1–2 were found to secrete about 10 times more gibberellic acid (GA)-like activity compared with control apices or inflorescences at stage 5.It is suggested that the developing inflorescence is the major source of GAs which control stem elongation. However, shortly after the appearance of the inflorescence at the onset of bolting, stem elongation is no longer dependent on GAs derived from the apical inflorescence but require GAs from other sources.Contribution from the Agricultural Research Organization, The Volcani Center Bet Dagan, Israel No. 2218-E, 1987 series.     

Emergency and Disaster Planning at Ohio Animal Shelters

Results of a cross-sectional study to determine the level of emergency and disaster response planning at Ohio nonhuman animal shelters and the role Ohio agencies have in emergency and disaster response planning in their communities indicated a lack of preparedness coupled with underutilization of the agencies as a resource. A total of 115 agencies (68%) responded to a standardized survey mailed to 170 Ohio agencies. Most (68%) agencies agreed that emergency and disaster response planning was important to their organization, although only 13% of agencies had completed a written emergency and disaster response plan. The majority (80%) of agencies indicated they would provide critical resources in an emergency or disaster in their community. Only 38 (33%) of the responding agencies were aware of the PETS Act of 2006. Although many agencies indicated the importance of an emergency and disaster plan, there may be insufficient resources, including time and proper training, available to ensure plans are developed. Improved coordination among veterinarians, local veterinary medical associations, emergency preparedness agencies, and animal shelters would enhance the relief efforts in a crisis.     

Host autophagic degradation and associated symbiont loss in response to heat stress in the symbiotic anemone,Aiptasia pallida

Coral bleaching involves the loss of essential photosynthetic dinoflagellates (Symbiodinium sp.) from host gastrodermal cells in response to temperature or light stress. Although numerous potential cellular bleaching mechanisms have been proposed, there remains much uncertainty regarding which cellular events occur during early breakdown of the host–dinoflagellate symbiosis. In this study, transmission electron microscopy was used to conduct a detailed examination of symbiotic tissues of the tropical anemone Aiptasia pallida during early stages of host stress. Bleaching was induced by exposing specimens to a stress treatment of 32.5±0.5°C at 140±7 μ mol photons m^?2 s^?1 light intensity for 12 h, followed by 12 h at 24±1°C in darkness, repeated over a 48 h period. Ultrastructural examinations revealed numerous dense autophagic structures and associated cellular degradation in tentacle tissues after ~12 h of the stress treatment. Anemones treated with rapamycin, a known autophagy inducer, exhibited the same ultrastructural characteristics as heat‐stressed tissues, confirming that the structures observed during heat stress treatment were autophagic. In addition, symbionts appeared to be expelled from host cells via an apocrine‐like detachment mechanism from the apical ends of autophagic gastrodermal cells. This study provides the first ultrastructural evidence of host autophagic degradation during thermal stress in a cnidarian system and also supports earlier suggestions that autophagy is an active cellular mechanism during early stages of bleaching.     

IMPACT World+: a globally regionalized life cycle impact assessment method

The International Journal of Life Cycle Assessment - This paper addresses the need for a globally regionalized method for life cycle impact assessment (LCIA), integrating multiple state-of-the-art...     

Structure and membrane-targeting of a Bordetella pertussis effector N-terminal domain

BteA, a 69-kDa cytotoxic protein, is a type III secretion system (T3SS) effector in the classical Bordetella, the etiological agents of pertussis and related mammalian respiratory diseases. Like other cytotoxicity-mediating effectors, BteA uses its multifunctional N-terminal domain to target phosphatidylinositol (PI)-rich microdomains in the host membrane. Despite their structural similarity, T3SS effectors exhibit a variable range of membrane interaction modes, and currently only limited structural information is available for the BteA membrane-targeting domain and the molecular mechanisms underlying its function. Employing a synergistic combination of structural methods, here we determine the structure of this functional domain and uncover key molecular determinants mediating its interaction with membranes. Residues 29–121 of BteA form an elongated four-helix bundle packed against two shorter perpendicular helices, the second of which caps the domain in a critical ‘tip motif’. A flexible region preceding the BteA helical bundle contains the characteristic β-motif required for binding its cognate chaperone BtcA. We show that BteA targets PI(4,5)P₂-containing lipoprotein nanodiscs and binds a soluble PI(4,5)P₂ analog via an extensive positively charged surface spanning its first two helices, and that this interaction is weaker for PI(3,5)P₂ and abolished for PI(4)P. We confirmed this model of membrane-targeting by observation of BteA-induced changes in the structure of PI(4,5)P₂-containing phospholipid bilayers using small-angle X-ray scattering (SAXS). We also extended these results to a larger BteA domain (residues 1–287), confirming its interaction with bilayers using calorimetry, fluorescence and SAXS methods. This novel view of the structural underpinnings of membrane targeting by BteA is an important step towards a comprehensive understanding of cytotoxicity in Bordetella, as well as interactions of a broad range of pathogens with their respective hosts.     

A role for a novel luminal endoplasmic reticulum aminopeptidase in final trimming of 26 S proteasome-generated major histocompatability complex class I antigenic peptides

Peptides presented to cytotoxic T lymphocytes by the class I major histocompatability complex are 8-11 residues long. Although proteasomal activity generates the precise C termini of antigenic epitopes, the mechanism(s) involved in generation of the precise N termini is largely unknown. To investigate the mechanism of N-terminal peptide processing, we used a cell-free system in which two recombinant ornithine decarboxylase (ODC) constructs, one expressing the native H2-K(b)-restricted ovalbumin (ova)-derived epitope SIINFEKL (ODC-ova) and the other expressing the extended epitope LESIINFEKL (ODC-LEova), were targeted to degradation by 26 S proteasomes followed by import into microsomes. We found that the cleavage specificity of the 26 S proteasome was influenced by the N-terminal flanking amino acids leading to significantly different yields of the final epitope SIINFEKL. Following incubation in the presence of purified 26 S proteasome, ODC-LEova generated largely ESIINFEKL that was efficiently converted to the final epitope SIINFEKL following translocation into microsomes. The conversion of ESIINFEKL to SIINFEKL was strictly dependent on the presence of H2-K(b) and was completely inhibited by the metalloaminopeptidase inhibitor 1,10-phenanthroline. Importantly, the converting activity was resistant to a stringent salt/EDTA wash of the microsomes and was only apparent when transport of TAP, the transporter associated with antigen processing, was facilitated. These results strongly suggest a crucial role for a luminal endoplasmic reticulum-resident metalloaminopeptidase in the N-terminal trimming of major histocompatability complex class I-associated peptides.     

Glutamine synthetase enhances the clearance of extracellular glutamate by the neural retina

Clearance of synaptic glutamate by glial cells is required for the normal function of excitatory synapses and for prevention of neurotoxicity. Although the regulatory role of glial glutamate transporters in glutamate clearance is well established, little is known about the influence of glial glutamate metabolism on this process. This study examines whether glutamine synthetase (GS), a glial-specific enzyme that amidates glutamate to glutamine, affects the uptake of glutamate. Retinal explants were incubated in the presence of [(14)C]glutamate and glutamate uptake was assessed by measurement of the amount of radioactively labeled molecules within the cells and the amount of [(14)C]glutamine released to the medium. An increase in GS expression in Müller glial cells, caused by induction of the endogenous gene, did not affect the amount of glutamate accumulated within the cells, but led to a dramatic increase in the amount of glutamine released. This increase, which was directly correlated with the level of GS expression, was dependent on the presence of external sodium ions, and could be completely abolished by methionine sulfoximine, a specific inhibitor of GS activity. Our results demonstrate that GS activity significantly influences the uptake of glutamate by the neural retina and suggest that this enzyme may represent an important target for neuroprotective strategies.