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Joanna Augustynowicz Paweł Wróbel Bartosz J. Płachno Grzegorz Tylko Zbigniew Gajewski Dariusz Węgrzynek 《Planta》2014,239(6):1233-1242
The aim of the study was the analysis of Cr distribution in shoots of the macrophyte Callitriche cophocarpa by means of two X-ray-based techniques: micro X-ray fluorescence (μXRF) and electron probe X-ray microanalysis (EPXMA). Plants were treated with 100 μM (5.2 mg l?1) chromium solutions for 7 days. Cr was introduced independently at two speciations as Cr(III) and Cr(VI), known for their diverse physicochemical properties and different influence on living organisms. A comparative analysis of Cr(III)-treated plants by EPXMA and μXRF demonstrated high deposition of Cr in epidermal glands/hairs localized on leaves and stems of the plant shoots. Cr in Cr(III)-treated plants was recorded solely in glands/hairs, and the element was not present in any other structures. On the other hand, Cr in Cr(VI)-treated group of plants was rather found in vascular bundles. Moreover, the concentration of Cr in Cr(VI)-treated plants was significantly lower than in plants incubated in Cr(III) solution. The results obtained in this work suggest differences in chromium uptake, transport and accumulation dependent on the oxidative state of the element. 相似文献
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Batool Ossareh-Nazari Carlos A. Ni?o Mario H. Bengtson Joong-Won Lee Claudio A.P. Joazeiro Catherine Dargemont 《The Journal of cell biology》2014,204(6):909-917
Autophagy, the process by which proteins or organelles are engulfed by autophagosomes and delivered for vacuolar/lysosomal degradation, is induced to ensure survival under starvation and other stresses. A selective autophagic pathway for 60S ribosomal subunits elicited by nitrogen starvation in yeast—ribophagy—was recently described and requires the Ubp3-Bre5 deubiquitylating enzyme. This discovery implied that an E3 ligases act upstream, whether inhibiting the process or providing an initial required signal. In this paper, we show that Ltn1/Rkr1, a 60S ribosome-associated E3 implicated in translational surveillance, acts as an inhibitor of 60S ribosomal subunit ribophagy and is antagonized by Ubp3. The ribosomal protein Rpl25 is a relevant target. Its ubiquitylation is Ltn1 dependent and Ubp3 reversed, and mutation of its ubiquitylation site rendered ribophagy less dependent on Ubp3. Consistently, the expression of Ltn1—but not Ubp3—rapidly decreased after starvation, presumably to allow ribophagy to proceed. Thus, Ltn1 and Ubp3-Bre5 likely contribute to adapt ribophagy activity to both nutrient supply and protein translation. 相似文献
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Aritri Bir Oishimaya Sen Shruti Anand Vineet Kumar Khemka Priyanjalee Banerjee Roberto Cappai Arghyadip Sahoo Sasanka Chakrabarti 《Journal of neurochemistry》2014,131(6):868-877
This study has shown that purified recombinant human α‐synuclein (20 μM) causes membrane depolarization and loss of phosphorylation capacity of isolated purified rat brain mitochondria by activating permeability transition pore complex. In intact SHSY5Y (human neuroblastoma cell line) cells, lactacystin (5 μM), a proteasomal inhibitor, causes an accumulation of α‐synuclein with concomitant mitochondrial dysfunction and cell death. The effects of lactacystin on intact SHSY5Y cells are, however, prevented by knocking down α‐synuclein expression by specific siRNA. Furthermore, in wild‐type (non‐transfected) SHSY5Y cells, the effects of lactacystin on mitochondrial function and cell viability are also prevented by cyclosporin A (1 μM) which blocks the activity of the mitochondrial permeability transition pore. Likewise, in wild‐type SHSY5Y cells, typical mitochondrial poison like antimycin A (50 nM) produces loss of cell viability comparable to that of lactacystin (5 μM). These data, in combination with those from isolated brain mitochondria, strongly suggest that intracellularly accumulated α‐synuclein can interact with mitochondria in intact SHSY5Y cells causing dysfunction of the organelle which drives the cell death under our experimental conditions. The results have clear implications in the pathogenesis of sporadic Parkinson's disease.
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