IRS-2 Deficiency Impairs NMDA Receptor-Dependent Long-term Potentiation

The beneficial effects of insulin and insulin-like growth factor I on cognition have been documented in humans and animal models. Conversely, obesity, hyperinsulinemia, and diabetes increase the risk for neurodegenerative disorders including Alzheimer's disease (AD). However, the mechanisms by which insulin regulates synaptic plasticity are not well understood. Here, we report that complete disruption of insulin receptor substrate 2 (Irs2) in mice impairs long-term potentiation (LTP) of synaptic transmission in the hippocampus. Basal synaptic transmission and paired-pulse facilitation were similar between the 2 groups of mice. Induction of LTP by high-frequency conditioning tetanus did not activate postsynaptic N-methyl-D-aspartate (NMDA) receptors in hippocampus slices from Irs2−/− mice, although the expression of NR2A, NR2B, and PSD95 was equivalent to wild-type controls. Activation of Fyn, AKT, and MAPK in response to tetanus stimulation was defective in Irs2−/− mice. Interestingly, IRS2 was phosphorylated during induction of LTP in control mice, revealing a potential new component of the signaling machinery which modulates synaptic plasticity. Given that IRS2 expression is diminished in Type 2 diabetics as well as in AD patients, these data may reveal an explanation for the prevalence of cognitive decline in humans with metabolic disorders by providing a mechanistic link between insulin resistance and impaired synaptic transmission

Conversion of the Mycotoxin Patulin to the Less Toxic Desoxypatulinic Acid by the Biocontrol Yeast Rhodosporidium kratochvilovae Strain LS11

Se describe en este artículo el descubrimiento de la degradación de la micotoxina patulina por una levaduraThe infection of stored apples by the fungus Penicillium expansum causes the contamination of fruits and fruit-derived products with the mycotoxin patulin, which is a major issue in food safety. Fungal attack can be prevented by beneficial microorganisms, so-called biocontrol agents. Previous time-course thin layer chromatography analyses showed that the aerobic incubation of patulin with the biocontrol yeast Rhodosporidium kratochvilovae strain LS11 leads to the disappearance of the mycotoxin spot and the parallel emergence of two new spots, one of which disappears over time. In this work, we analyzed the biodegradation of patulin effected by LS11 through HPLC. The more stable of the two compounds was purified and characterized by nuclear magnetic resonance as desoxypatulinic acid, whose formation was also quantitated in patulin degradation experiments. After R. kratochvilovae LS11 had been incubated in the presence of 13C-labeled patulin, label was traced to desoxypatulinic acid, thus proving that this compound derives from the metabolization of patulin by the yeast. Desoxypatulinic acid was much less toxic than patulin to human lymphocytes and, in contrast to patulin, did not react in vitro with the thiol-bearing tripeptide glutathione. The lower toxicity of desoxypatulinic acid is proposed to be a consequence of the hydrolysis of the lactone ring and the loss of functional groups that react with thiol groups. The formation of desoxypatulinic acid from patulin represents a novel biodegradation pathway that is also a detoxification process

Identification of wild apple germplasm (\u3ci\u3eMalus\u3c/i\u3e spp.) accessions with resistance to the postharvest decay pathogens \u3ci\u3ePenicillium expansum\u3c/i\u3e and \u3ci\u3eColletotrichum acutatum\u3c/i\u3e

Penicillium expansum and Colletotrichum acutatum cause blue mould and bitter rot of apples during storage which results in significant economic losses. Resistance to these pathogens in commercial apple cultivars has not been documented in the literature. An apple germplasm collection, from the centre of origin in Kazakhstan, is maintained in Geneva, New York. This collection represents a more diverse apple gene pool than commercial cultivars and was evaluated for resistance to the pathogens that cause blue mould and bitter rot. Resistance reactions were skewed towards susceptibility for both fungi and comprised the majority of accessions examined. However, resistance to P. expansum was confirmed in select accessions over multiple years. Maturation patterns and quality indices for soluble solids and acidity, which may also affect susceptibility, were highly variable and represent the genetic diversity of the germplasm collection. Resistance in four accessions to C. acutatum and two accessions resistant to both P. expansum and C. acutatum are reported here for the first time. Data from this study will serve as a foundation for conventional apple breeding programmes and molecular genetics investigations to provide resistance against blue mould and bitter rot in commercial apple varieties

yeast species for biocontrol of apple postharvest disease: an encouranging case of study for pratical use

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