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1.
Phosphatidylcholine biosynthesis in celery cell suspension cultures with altered sterol compositions
Cell suspension cultures of celery were treated with the plant growth regulator, paclobutrazol. Lipid analysis revealed that use of this xenobiotic had little effect on the quantity or acyl quality of the major phospholipid classes or on the actual amounts of free sterol present in the cell. It did however, cause dramatic changes in the free sterol profile exhibited by treated cultures. In this respect, an increase in 14α-methylsterols was observed.
The synthesis of phosphatidylcholine in celery cell suspension cultures with altered free sterol compositions was studied using two radiolabelled biosynthetic precursors, [3 H-methyl]choline and [3 H-methyl]methionine. The studies showed that the rate of phosphatidylcholine biosynthesis via the CDP-base pathway proceeded at a slower rate in paclobutrazol treated cultures. Accumulation of label phosphocholine was observed arising from reduced CTP:cholinephosphatecytidylyltransferase activity. In contrast, phosphatidylcholine biosynthesis via the sequential methylation of ethanolamine derivatives appeared to be enhanced in cells that had an unusually high 14α-methylsterol content. From these investigations it may be postulated that the biosynthesis of phosphatidylcholine in Apium graveolens suspension cultures may be regulated by membrane sterol composition. 相似文献
The synthesis of phosphatidylcholine in celery cell suspension cultures with altered free sterol compositions was studied using two radiolabelled biosynthetic precursors, [
2.
In guinea pigs between days 41-46 of pregnancy prenatal growth has been manipulated by alteration of nutritional state. Three methods were used. Uterine artery ligation at day 30 of pregnancy depressed fetal growth rate by greater than 50% and was associated with falls in plasma insulin, IGF-1, cortisol, thyroid hormone, glucose, acetate and free fatty acid concentrations and rises in that of IGF-2, glucagon and amino acids. Fetal plasma was inhibitory to sulphate incorporation into pig costal cartilage. Complete food withdrawal from pregnant guinea pigs for 2 days at days 43-44 of pregnancy caused mild fetal growth retardation and similar changes in plasma constituents, except in that plasma IGF-2 concentrations were now depressed and plasma was not inhibitory to sulphate incorporation into pig costal cartilage. Production of hypoglycaemia by 4-times-daily maternal injections of glucose between days 41-46 of pregnancy accelerated fetal growth rate. It also elevated fetal plasma concentrations of insulin, IGF-1, IGF-2, sulphation-promoting activity, thyroid hormones, glucose and free fatty acids and depressed that of glucagon and amino acids. Fetal growth rate during the experimental period showed a good correlation with plasma glucose, insulin and IGF-1 and, to a certain extent, with sulphation-promoting activity. It did not correlate closely with fetal plasma IGF-2 concentration. Hepatic glycogen concentrations showed a good correlation with plasma IGF-2 levels. 相似文献
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Abstract Growth of wild-type Escherichia coli strain MRE600 was severely affected up to 9 h following treatment with the anthracycline doxorubicin (15 μM), however, after 9 h, the cells became resistant. The onset of resistance coincided with some changes in the relative proportions of total saturated, monounsaturated and cyclopropane fatty acids. The anionic lipid content in E. coli strain HDL11 is under lac control and synthesis can be induced by incubation with the lac inducer IPTG. HDL11, with low levels of anionic phospholipid, was unaffected by doxorubicin (100 μM) over 9 h, with only slight inhibition of growth seen over 24 h. When the anionic lipid content of HDL11 was increased, there was a slight increase in the efficacy of doxorubicin, providing evidence for a membrane-based step in doxorubicin action. 相似文献
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Recent studies with mammalian tissues have shown thatphosphatidylcholine (PC) plays a key role in signal transduction mechanismsinvolved in cell proliferation and differentiation. This investigation attemptsto show if PC has a role in gibberellin-stimulated plant signal transduction.With respect to cell differentiation, GA3-treatment caused an overallincrease in the elongation ratio exhibited by the cells. The effects ofGA3 on the biosynthetic route of PC were investigated. Carbon fluxthrough the CDP-base pathway was significantly reduced upon GA3treatment. Whereas, radiolabelling studies with tritiated methionine showed aGA3 concentration-dependent increase in the flux of intermediatesthrough the methyltransferase pathway indicating a possible link betweenmethyltransferase-derived PC and cell differentiation. 相似文献
7.
Rocio Acuna-Hidalgo Denny Schanze Ariana Kariminejad Ann Nordgren Mohamad Hasan Kariminejad Peter Conner Giedre Grigelioniene Daniel Nilsson Magnus Nordenskjöld Anna Wedell Christoph Freyer Anna Wredenberg Dagmar Wieczorek Gabriele Gillessen-Kaesbach Hülya Kayserili Nursel Elcioglu Siavash Ghaderi-Sohi Payman Goodarzi Hamidreza Setayesh Maartje van de Vorst Marloes Steehouwer Rolph Pfundt Birgit Krabichler Cynthia Curry Malcolm G. MacKenzie Kym M. Boycott Christian Gilissen Andreas R. Janecke Alexander Hoischen Martin Zenker 《American journal of human genetics》2014
8.
Jayne Y. Hehir-Kwa Nienke Wieskamp Caleb Webber Rolph Pfundt Han G. Brunner Christian Gilissen Bert B. A. de Vries Chris P. Ponting Joris A. Veltman 《PLoS computational biology》2010,6(4)
Copy number variants (CNVs) have recently been recognized as a common form of genomic variation in humans. Hundreds of CNVs can be detected in any individual genome using genomic microarrays or whole genome sequencing technology, but their phenotypic consequences are still poorly understood. Rare CNVs have been reported as a frequent cause of neurological disorders such as mental retardation (MR), schizophrenia and autism, prompting widespread implementation of CNV screening in diagnostics. In previous studies we have shown that, in contrast to benign CNVs, MR-associated CNVs are significantly enriched in genes whose mouse orthologues, when disrupted, result in a nervous system phenotype. In this study we developed and validated a novel computational method for differentiating between benign and MR-associated CNVs using structural and functional genomic features to annotate each CNV. In total 13 genomic features were included in the final version of a Naïve Bayesian Tree classifier, with LINE density and mouse knock-out phenotypes contributing most to the classifier''s accuracy. After demonstrating that our method (called GECCO) perfectly classifies CNVs causing known MR-associated syndromes, we show that it achieves high accuracy (94%) and negative predictive value (99%) on a blinded test set of more than 1,200 CNVs from a large cohort of individuals with MR. These results indicate that this classification method will be of value for objectively prioritizing CNVs in clinical research and diagnostics. 相似文献
9.
Vissers LE Stankiewicz P Yatsenko SA Crawford E Creswick H Proud VK de Vries BB Pfundt R Marcelis CL Zackowski J Bi W van Kessel AG Lupski JR Veltman JA 《Human genetics》2007,121(6):697-709
Recent molecular cytogenetic data have shown that the constitution of complex chromosome rearrangements (CCRs) may be more
complicated than previously thought. The complicated nature of these rearrangements challenges the accurate delineation of
the chromosomal breakpoints and mechanisms involved. Here, we report a molecular cytogenetic analysis of two patients with
congenital anomalies and unbalanced de novo CCRs involving chromosome 17p using high-resolution array-based comparative genomic
hybridization (array CGH) and fluorescent in situ hybridization (FISH). In the first patient, a 4-month-old boy with developmental
delay, hypotonia, growth retardation, coronal synostosis, mild hypertelorism, and bilateral club feet, we found a duplication
of the Charcot-Marie–Tooth disease type 1A and Smith-Magenis syndrome (SMS) chromosome regions, inverted insertion of the
Miller-Dieker lissencephaly syndrome region into the SMS region, and two microdeletions including a terminal deletion of 17p.
The latter, together with a duplication of 21q22.3-qter detected by array CGH, are likely the unbalanced product of a translocation
t(17;21)(p13.3;q22.3). In the second patient, an 8-year-old girl with mental retardation, short stature, microcephaly and
mild dysmorphic features, we identified four submicroscopic interspersed 17p duplications. All 17 breakpoints were examined
in detail by FISH analysis. We found that four of the breakpoints mapped within known low-copy repeats (LCRs), including LCR17pA,
middle SMS-REP/LCR17pB block, and LCR17pC. Our findings suggest that the LCR burden in proximal 17p may have stimulated the
formation of these CCRs and, thus, that genome architectural features such as LCRs may have been instrumental in the generation
of these CCRs. 相似文献
10.