کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10803031 | 1055764 | 2008 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Increase in Fru-2,6-P2 levels results in altered cell division in Schizosaccharomyces pombe
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کلمات کلیدی
PI3KTP53-induced glycolysis and apoptosis regulatorTIGARDAPI4′,6-diamidino-2-phenylindole - 4 '، 6-دیامیدینو-2-فنیلینول6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase - 6-فسفورفتو-2-کیناز / فروکتوز-2،6-بیسفسفاتازFru-2,6-P2 - FRU-2،6-P2MAPK - MAPKROS - ROSProliferation - ترویجFructose 2,6-bisphosphate - فروکتوز 2،6-بیسفسفاتPhosphatidylinositol 3-kinase - فسفاتیدیلینواستیل 3-کینازFission yeast - مخمر شکافتنhemagglutinin - هماگلوتینینmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenCell cycle control - کنترل چرخه سلولیGlycolysis - گلیکولیز یا قندکافتReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Increase in Fru-2,6-P2 levels results in altered cell division in Schizosaccharomyces pombe Increase in Fru-2,6-P2 levels results in altered cell division in Schizosaccharomyces pombe](/preview/png/10803031.png)
چکیده انگلیسی
Mitogenic response to growth factors is concomitant with the modulation they exert on the levels of Fructose 2,6-bisphosphate (Fru-2,6-P2), an essential activator of the glycolytic flux. In mammalian cells, decreased Fru-2,6-P2 concentration causes cell cycle delay, whereas high levels of Fru-2,6-P2 sensitize cells to apoptosis. In order to analyze the cell cycle consequences due to changes in Fru-2,6-P2 levels, the bisphosphatase-dead mutant (H258A) of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase enzyme was over-expressed in Schizosaccharomyces pombe cells and the variation in cell phenotype was studied. The results obtained demonstrate that the increase in Fru-2,6-P2 levels results in a defective division of S. pombe, as revealed by an altered multisepted phenotype. The H258A-expressing cells showed impairment of cytokinesis, but normal nuclear division. In order to identify cellular mediators responsible for this effect, we transformed different S. pombe strains and observed that the cytokinetic defect was absent in cells defective for Wee1 kinase function. Therefore, in S. pombe, Wee1 integrates the metabolic signal emerging from changes in Fru-2,6-P2 content, thus coupling metabolism with cell proliferation. As the key regulators of the cell cycle checkpoints are conserved throughout evolution, these results may help to understand the experimental evidences obtained by manipulation of Fru-2,6-P2 levels in mammalian cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1783, Issue 1, January 2008, Pages 144-152
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1783, Issue 1, January 2008, Pages 144-152
نویسندگان
Silvia Fernández de Mattos, Vicenç Alemany, Rosa Aligué, Albert Tauler,