Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.4.1.18 (branching enzyme)
 628 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arbuscular mycorrhizal (AM) fungi take up photosynthetically fixed carbon from plant roots and translocate it to their external mycelium. Previous experiments have shown that fungal lipid synthesized from carbohydrate in the root is one form of exported carbon. In this study, an analysis of the labeling in storage and structural carbohydrates after (13)C(1) glucose was provided to AM roots shows that this is not the only pathway for the flow of carbon from the intraradical to the extraradical mycelium (ERM). Labeling patterns in glycogen, chitin, and trehalose during the development of the symbiosis are consistent with a significant flux of exported glycogen. The identification, among expressed genes, of putative sequences for glycogen synthase, glycogen branching enzyme, chitin synthase, and for the first enzyme in chitin synthesis (glutamine fructose-6-phosphate aminotransferase) is reported. The results of quantifying glycogen synthase gene expression within mycorrhizal roots, germinating spores, and ERM are consistent with labeling observations using (13)C-labeled acetate and glycerol, both of which indicate that glycogen is synthesized by the fungus in germinating spores and during symbiosis. Implications of the labeling analyses and gene sequences for the regulation of carbohydrate metabolism are discussed, and a 4-fold role for glycogen in the AM symbiosis is proposed: sequestration of hexose taken from the host, long-term storage in spores, translocation from intraradical mycelium to ERM, and buffering of intracellular hexose levels throughout the life cycle.
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PMID:Carbon export from arbuscular mycorrhizal roots involves the translocation of carbohydrate as well as lipid. 1264 99

The role of biomembranes in the chronic toxicity of environmentally occurring chromium acetate hydroxide was investigated by using primary human fibroblasts. Transport of chromium acetate hydroxide across the plasma membrane of the cell, and the effects of chromium (III) ions on the plasma membrane as well as other intracellular membranes, were determined during six weeks of continuous exposure by using atomic absorption spectrometry, observation of cell morphology, membrane integrity assays (for lactate dehydrogenase leakage and lysosomal membrane disruption), and mitochondrial assays (for mitochondrial dehydrogenase activity and mitochondrial transmembrane potential analysis). The type of cell death induced by long-term exposure was determined in terms of phosphatidylserine externalisation, caspase-3 activation, and chromatin fragmentation. Chromium acetate hydroxide, at a concentration of 100 micromol/l, accumulated in exposed cells, inflicting plasma membrane damage and suppressing mitochondrial function. Antioxidant co-enzyme Q, at a concentration of 10 micromol/l, partially prevented plasma membrane damage and mitochondrial dysfunction. Exposure to chromium acetate hydroxide produced apoptosis, necrosis and an intermediate type of cell death in primary human fibroblasts. These results show that the plasma membrane and mitochondrial membrane are important targets for chronic chromium acetate hydroxide toxicity, and that this in vitro system holds promise for studying the toxicity resulting from long-term exposure to metal ions.
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PMID:The role of biomembranes in chromium (III)-induced toxicity in vitro. 1618 Sep 79

The aim of this work was to discover why pea (Pisum sativum L.) embryos recessive at the r locus (rr) have a higher lipid content than embryos dominant at this locus (RR). The r locus is a gene encoding starch-branching enzyme, rr embryos have a much lower activity of this enzyme than RR embryos, and hence a reduced rate of starch synthesis. The higher lipid content of rr embryos must be a consequence of this. We suggest that neither differences in the availability of substrate for lipid synthesis as a consequence of different rates of starch synthesis, nor differences in the capacity of the pathway for malonyl-CoA synthesis, account for the different lipid contents of RR and rr embryos. Lipid contents of the two sorts of embryo first diverge at a much later stage in development than divergence in starch content. Amounts of pyruvate and acetate, and activities of enzymes that convert triose phosphate to malonyl CoA are the same in the two sorts of embryo. Most of the lipid in developing embryos is polar, structural lipid, and polar lipid accounts for a large proportion of the difference in lipid content between the two sorts of embryo. This difference in structural-lipid content reflects considerable structural differences between the two sorts of embryo and is presumably the consequence of differences in rates of lipid turnover.
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PMID:Nature of the effect of the r locus on the lipid content of embryos of peas (Pisum sativum L.). 2420 23