Loss of Omi mitochondrial protease activity causes the neuromuscular disorder of mnd2 mutant mice

The mouse mutant mnd2 (motor neuron degeneration 2) exhibits muscle wasting, neurodegeneration, involution of the spleen and thymus, and death by 40 days of age. Degeneration of striatal neurons, with astrogliosis and microglia activation, begins at around 3 weeks of age, and other neurons are affected at later stages. Here we have identified the mnd2 mutation as the missense mutation Ser276Cys in the protease domain of the nuclear-encoded mitochondrial serine protease Omi (also known as HtrA2 or Prss25). Protease activity of Omi is greatly reduced in tissues of mnd2 mice but is restored in mice rescued by a bacterial artificial chromosome transgene containing the wild-type Omi gene. Deletion of the PDZ domain partially restores protease activity to the inactive recombinant Omi protein carrying the Ser276Cys mutation, suggesting that the mutation impairs substrate access or binding to the active site pocket. Loss of Omi protease activity increases the susceptibility of mitochondria to induction of the permeability transition, and increases the sensitivity of mouse embryonic fibroblasts to stress-induced cell death. The neurodegeneration and juvenile lethality in mnd2 mice result from this defect in mitochondrial Omi protease.     

Dissecting a circuit for olfactory behaviour in Caenorhabditis elegans

Although many properties of the nervous system are shared among animals and systems, it is not known whether different neuronal circuits use common strategies to guide behaviour. Here we characterize information processing by Caenorhabditis elegans olfactory neurons (AWC) and interneurons (AIB and AIY) that control food- and odour-evoked behaviours. Using calcium imaging and mutations that affect specific neuronal connections, we show that AWC neurons are activated by odour removal and activate the AIB interneurons through AMPA-type glutamate receptors. The level of calcium in AIB interneurons is elevated for several minutes after odour removal, a neuronal correlate to the prolonged behavioural response to odour withdrawal. The AWC neuron inhibits AIY interneurons through glutamate-gated chloride channels; odour presentation relieves this inhibition and results in activation of AIY interneurons. The opposite regulation of AIY and AIB interneurons generates a coordinated behavioural response. Information processing by this circuit resembles information flow from vertebrate photoreceptors to 'OFF' bipolar and 'ON' bipolar neurons, indicating a conserved or convergent strategy for sensory information processing.     

Zinc bioleaching from an iron concentrate using <Emphasis Type=Italic>Acidithiobacillus ferrooxidans</Emphasis> strain from Hercules Mine of Coahuila,Mexico

The iron concentrate from Hercules Mine of Coahuila, Mexico, which mainly contained pyrite and pyrrhotite, was treated by the bioleaching process using native strain Acidithiobacillus ferrooxidans (A. ferrooxidans) to determine the ability of these bacteria on the leaching of zinc. The native bacteria were isolated from the iron concentrate of the mine. The bioleaching experiments were carried out in shake flasks to analyze the effects of pH values, pulp density, and the ferrous sulfate concentration on the bioleaching process. The results obtained by microbial kinetic analyses for the evaluation of some aspects of zinc leaching show that the native bacteria A. ferrooxidans, which is enriched with a 9K Silverman medium under the optimum conditions of pH 2.0, 20 g/L pulp density, and 40 g/L FeSO₄, increases the zinc extraction considerably observed by monitoring during15 d, i.e., the zinc concentration has a decrease of about 95% in the iron concentrate.