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31.
Dosage Compensation of Genes on the Left and Right Arms of the X Chromosome of DROSOPHILA PSEUDOOBSCURA and DROSOPHILA WILLISTONI 总被引:5,自引:1,他引:4
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We have investigated the occurrence of dosage compensation in D. willistoni and D. pseudoobscura, two species whose X chromosome is metacentric with one arm homologous to the X and the other homologous to the left arm of chromosome 3 of D. melanogaster. Crude extracts were assayed for isocitrate dehydrogenase (XR), glucose-6-phosphate dehydrogenase (XL?), 6-phosphogluconate dehydrogenase (XL?), and α-glycerophosphate dehydrogenase (chromosome 2) in D. willistoni, and for esterase-5 (XR), glucose-6-phosphate dehydrogenase (XL?), 6-phosphogluconate dehydrogenase (XL?) and amylase (chromosome 3) in D. pseudoobscura. Our results indicate that a mechanism for dosage compensation is operative in both arms of the X chromosome of these two species. 相似文献
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Philip W. Beesley Toni Paladino Irene Hill Claude Gravel Richard B. Hawkes James W. Gurd 《Journal of neurochemistry》1990,54(2):505-512
Glycoprotein gp50 is a neurone-specific, granule cell-enriched glycoprotein that is also a major component of isolated synaptic membranes. Here, we describe the use of a monoclonal antibody, mab SM gp50, to study the postnatal development of gp50 in the brain of normal and thyroid-deficient rats. Radioimmunoassay, enzyme-linked immunosorbent assay, and Western blotting show that gp50 is not detectable in brain until postnatal day 4 (P4) in both forebrain and cerebellum. In forebrain, the rate of increase of gp50 levels is maximal between P12 and P20. It is somewhat later in cerebellum, where peak levels are attained between P30 and P35. Immunocytochemical studies show little detectable gp50-like immunoreactivity before P16, and the staining is still weak, relative to adult tissue, at P25. The intense staining of the granule cell layer characteristic of adult cerebellum predominantly appears after P25. Development of gp50 is severely retarded in the cerebellum of thyroid-deficient rats, particularly during the second and third postnatal weeks. However, by the fourth postnatal week, gp50 levels in normal and hypothyroid animals are comparable. The results indicate that significant alterations in the pattern of gp50 expression continue to occur at a late stage of cerebellar development. In particular, the increase in immunocytochemical staining of the granule cells after P25 is striking in that by this time most major events associated with cerebellar development are essentially complete. 相似文献
35.
Frank Thévenod Martine Dehlinger-Kremer Thomas P. Kemmer Anna-Luise Christian Barry V. L. Potter Irene Schulz 《The Journal of membrane biology》1989,109(2):173-186
Summary We have measured Ca2+ uptake and Ca2+ release in isolated permeabilized pancreatic acinar cells and in isolated membrane vesicles of endoplasmic reticulum prepared from these cells. Ca2+ uptake into cells was monitored with a Ca2+ electrode, whereas Ca2+ uptake into membrane vesicles was measured with45Ca2+. Using inhibitors of known action, such as the H+ ATPase inhibitors NBD-Cl and NEM, the Ca2+ ATPase inhibitor vanadate as well as the second messenger inositol 1,4,5-trisphosphate (IP3) and its analog inositol 1,4,5-trisphosphorothioate (IPS3), we could functionally differentiate two non-mitochondrial Ca2+ pools. Ca2+ uptake into the IP3-sensitive Ca2+ pool (IsCaP) occurs by a MgATP-dependent Ca2+ uptake mechanism that exchanges Ca2+ for H+ ions. In the absence of ATP Ca2+ uptake can occur to some extent at the expense of an H+ gradient that is established by a vacuolar-type MgATP-dependent H+ pump present in the same organelle. The other Ca2+ pool takes up Ca2+ by a vanadate-sensitive Ca2+ ATPase and is insensitive to IP3 (IisCaP). The IsCaP is filled at higher Ca2+ concentrations (10–6 mol/liter) which may occur during stimulation. The low steady-state [Ca2+] of 10–7 mol/liter is adjusted by the IisCaP.It is speculated that both Ca2+ pools can communicate with each other, the possible mechanism of which, however, is at present unknown. 相似文献
36.
Russell G. Snell Leslie M. Thompson Danilo A. Tagle Tracey L. Holloway Glenn Barnes Helen G. Harley Lodewijk A. Sandkuijl Marcy E. MacDonald Francis S. Collins James F. Gusella Peter S. Harper Duncan J. Shaw 《American journal of human genetics》1992,51(2):357-362
We report both a recombination event that places the Huntington disease gene proximal to the marker D4S98 and an extended linkage-disequilibrium study that uses this marker and confirms the existence of disequilibrium between it and the HD locus. We also report the cloning of other sequences in the region around D4S98, including a new polymorphic marker R10 and conserved sequences that identify a gene in the region of interest. 相似文献
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The formation of complexes of vanadate with 2-phosphoglycerate and 3-phosphoglycerate have been studied using 51V nuclear magnetic resonance spectroscopy. Signals attributed to two 2,3-diphosphoglycerate analogues, 2-vanadio-3-phosphoglycerate and 2-phospho-3-vanadioglycerate, were detected but were not fully resolved from signals of inorganic vanadate and the anhydride formed between vanadate and the phosphate ester moieties of the individual phosphoglycerates. Equilibrium constants for formation of the two 2,3-bisphosphate analogues were estimated as 2.5 M-1 for 2-vanadio-3-phosphoglycerate and 0.2 M-1 for 2-phospho-3-vanadioglycerate. The results of the binding study are fully consistent with non-cooperativity in the binding of vanadiophosphoglycerate to the two active sites of phosphoglycerate mutase (PGM). 2-Vanadio-3-phosphoglycerate was found to bind to the dephospho form of phosphoglycerate mutase with a dissociation constant of about 1 x 10(-11) M at pH 7 and 7 x 10(-11) M at pH 8. Three signals attributed to histidine residues were observed in the 1H NMR spectrum of phosphoglycerate mutase. Two of these signals and also an additional signal, tentatively attributed to a tryptophan, underwent a chemical shift change when the vanadiophosphoglycerate complex was bound to the enzyme. The results obtained here are in accord with these vanadate-phosphoglycerate complexes being much more potent inhibitors of phosphoglycerate mutase than either monomeric or dimeric vanadate. The dissociation constant of 10(-11) M for 2-vanadio-3-phosphoglycerate is about 4 orders of magnitude smaller than the Km for PGM, a result in accordance with the vanadiophosphoglycerates being transition state analogues for the phosphorylation of PGM by 2,3-diphosphoglycerate.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
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Nicoletta zini Patrizia Sabatelli Irene Faenza Andrea Ognibene Nadir M. Maraldi 《The Histochemical journal》1996,28(7):495-504
Summary Some key elements of signal transduction have been identified within the nucleus and demonstrated to be responsive to specific
agonists in numerous cell types. In particular, mitogenic stimuli have been reported to induce, a transient increase of the
nuclear phospholipase C β1 activity, causing the release of inositide-derived second messengers, whereas differentiating stimuli induced a decrease
of the enzyme activity and an increase of nuclear phosphatidylinositol 4,5-bisphosphate (PIP2). Recently, we reported evidence, in human osteosarcoma Saos-2 cell lines, on the presence of specific nuclear phospholipase
C isoforms and on the activation of phospholipase C β1 in the nucleus following the exposure to interleukin-1α. In this study we report immunocytochemical ultrastructural evidence on quantitative variations of PIP2 and phospholipase C β1 amounts in the nucleus of Saos-2 cells at different times of exposure to interleukin-1α. After short periods of culture in the presence of the agonist, the intranuclear amount of PIP2 is decreased, while a translocation of phospholipase C β1 occurs from the cytoplasm to the nucleus, in correspondence with the increased hydrolyzing activity of the enzyme. After
longer periods of incubation with interleukin-1α, on the other hand, the intranuclear amount of PIP2 is restored to initial level, while the amount of phospholipase C β1 is increased both at the nuclear and cytoplasmic level, when its activation is no longer effective. The results, compared
with those obtained in other cell types responsive to given agonists, account for a cell-specific modulation of signal transduction
based on polyphosphoinositide breakdown at the nuclear level. 相似文献
40.
Patricia Kramer Jennifer Yount Thomas Mitchell Dante LaMorticella Roque Carrero-Valenzuela Everett Lovrien Irene Maumenee Michael Litt 《Genomics》1996,35(3):539
Congenital cataracts are one of the most common major eye abnormalities and often lead to blindness in infants. At least a third of all cases are familial. Within this group, highly penetrant, autosomal dominant forms of congenital cataracts (ADCC) are most common. ADCC is a genetically heterogeneous group of disorders, in which at least eight different loci have been identified for nine clinically distinct forms. Among these, Armitageet al.(Nature Genet.9: 37–40, 1995) mapped a gene for cerulean blue cataracts to chromosome 17q24. Bodkeret al.(Am. J. Med. Genet.37: 54–59, 1990) described a large family with cerulean blue cataracts, in which the affected daughter of affected first cousins was presumed to be homozygous for the purported gene. We report linkage in this family to the region on chromosome 22q that includes two β crystallin genes (CRYBB2, CRYBB3) and one pseudogene (CRYBB2P1). The affected female in question is homozygous at all markers. 相似文献