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1
Poisson-like fluctuation patterns of revertants of leucine auxotrophy (leu-500) in Salmonella typhimurium caused by delay in mutant cell division.鼠伤寒沙门氏菌中亮氨酸营养缺陷型(leu-500)回复突变体的类泊松波动模式是由突变细胞分裂延迟引起的。
Genetics. 1994 Jun;137(2):353-9. doi: 10.1093/genetics/137.2.353.
2
Reduced leu operon expression in a miaA mutant of Salmonella typhimurium.鼠伤寒沙门氏菌miaA突变体中亮氨酸操纵子表达降低。
J Bacteriol. 1988 Nov;170(11):5125-33. doi: 10.1128/jb.170.11.5125-5133.1988.
3
Occurrence of leu+ revertants under starvation cultures in Escherichia coli is growth-dependent.在大肠杆菌的饥饿培养条件下,亮氨酸营养缺陷型回复突变株的出现取决于生长情况。
BMC Genet. 2002 Apr 25;3:6. doi: 10.1186/1471-2156-3-6.
4
The origin of His+ revertants of Salmonella typhimurium obtained on selective medium.
Res Microbiol. 1992 Sep;143(7):711-9. doi: 10.1016/0923-2508(92)90066-w.
5
Promoter mutation causing catabolite repression of the Salmonella typhimurium leucine operon.导致鼠伤寒沙门氏菌亮氨酸操纵子分解代谢阻遏的启动子突变。
J Bacteriol. 1984 Jun;158(3):948-53. doi: 10.1128/jb.158.3.948-953.1984.
6
New class of streptomycin-resistant mutants incompatible with supX suppressor mutations in Salmonella typhimurium.鼠伤寒沙门氏菌中与supX抑制突变不兼容的新型链霉素抗性突变体。
J Bacteriol. 1974 Dec;120(3):1315-21. doi: 10.1128/jb.120.3.1315-1321.1974.
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Conditional lethality of cell shape mutations of Salmonella typhimurium: rodA and mre mutants are lethal on solid but not in liquid medium.
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8
A search for a general phenomenon of adaptive mutability.对适应性可变性普遍现象的探索。
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9
Transcription attenuation is the major mechanism by which the leu operon of Salmonella typhimurium is controlled.转录衰减是鼠伤寒沙门氏菌亮氨酸操纵子被调控的主要机制。
J Mol Biol. 1983 Jan 25;163(3):377-94. doi: 10.1016/0022-2836(83)90064-5.
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[The nature of the emergence of His+-revertants in Salmonella typhimurium].
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引用本文的文献

1
Toxic effect and adaptation in Scenedesmus intermedius to anthropogenic chloramphenicol contamination: genetic versus physiological mechanisms to rapid acquisition of xenobiotic resistance.中型栅藻对人为氯霉素污染的毒性效应与适应性:快速获得异生物质抗性的遗传与生理机制
Ecotoxicology. 2009 Jul;18(5):481-7. doi: 10.1007/s10646-009-0303-8. Epub 2009 Mar 25.
2
Spontaneous mutations in bacteria: chance or necessity?细菌中的自发突变:是偶然还是必然?
Genetica. 1996 Jan;97(1):87-101. doi: 10.1007/BF00132585.

本文引用的文献

1
Mutations of Bacteria from Virus Sensitivity to Virus Resistance.细菌从对病毒敏感到对病毒抗性的突变。
Genetics. 1943 Nov;28(6):491-511. doi: 10.1093/genetics/28.6.491.
2
ANALYSIS OF UNLINKED SUPPRESSORS OF AN O degrees MUTATION IN SALMONELLA.鼠伤寒沙门氏菌O度突变非连锁抑制子的分析
Proc Natl Acad Sci U S A. 1963 Jul;50(1):140-8. doi: 10.1073/pnas.50.1.140.
3
The directed mutation controversy and neo-Darwinism.定向突变争议与新达尔文主义。
Science. 1993 Jan 8;259(5092):188-94. doi: 10.1126/science.7678468.
4
Transduction of Escherichia coli trp genes in Salmonella typhimurium and effect of N-methyl-N'-nitro-N-nitrosoguanidine on transduction with heterogenotic DNA.大肠杆菌色氨酸基因在鼠伤寒沙门氏菌中的转导以及N-甲基-N'-硝基-N-亚硝基胍对异源DNA转导的影响。
J Gen Microbiol. 1983 Feb;129(2):321-35. doi: 10.1099/00221287-129-2-321.
5
Escherichia coli DNA topoisomerase I mutants have compensatory mutations in DNA gyrase genes.大肠杆菌DNA拓扑异构酶I突变体在DNA促旋酶基因中存在补偿性突变。
Cell. 1982 Nov;31(1):43-51. doi: 10.1016/0092-8674(82)90403-2.
6
Mutations in the gene coding for Escherichia coli DNA topoisomerase I affect transcription and transposition.编码大肠杆菌DNA拓扑异构酶I的基因发生突变会影响转录和转座。
Proc Natl Acad Sci U S A. 1981 May;78(5):2747-51. doi: 10.1073/pnas.78.5.2747.
7
Autolysin(s) of Bacillus subtilis as dechaining enzyme.枯草芽孢杆菌的自溶素作为解链酶
J Bacteriol. 1970 Aug;103(2):494-9. doi: 10.1128/jb.103.2.494-499.1970.
8
DNA supercoiling and suppression of the leu-500 promoter mutation.DNA超螺旋与亮氨酸-500启动子突变的抑制
J Bacteriol. 1985 Nov;164(2):947-9. doi: 10.1128/jb.164.2.947-949.1985.
9
Adaptive evolution that requires multiple spontaneous mutations. I. Mutations involving an insertion sequence.需要多个自发突变的适应性进化。I. 涉及插入序列的突变。
Genetics. 1988 Dec;120(4):887-97. doi: 10.1093/genetics/120.4.887.
10
Mutation and selection in bacterial populations: alternatives to the hypothesis of directed mutation.细菌群体中的突变与选择:对定向突变假说的替代观点
Proc Natl Acad Sci U S A. 1989 Apr;86(8):2775-8. doi: 10.1073/pnas.86.8.2775.

鼠伤寒沙门氏菌中亮氨酸营养缺陷型(leu-500)回复突变体的类泊松波动模式是由突变细胞分裂延迟引起的。

Poisson-like fluctuation patterns of revertants of leucine auxotrophy (leu-500) in Salmonella typhimurium caused by delay in mutant cell division.

作者信息

Dijkmans R, Kreps S, Mergeay M

机构信息

Laboratory Genetics and Biotechnology, Vlaamse Instelling voor Technologisch Onderzoek (V.I.T.O.), Mol, Belgium.

出版信息

Genetics. 1994 Jun;137(2):353-9. doi: 10.1093/genetics/137.2.353.

DOI:10.1093/genetics/137.2.353
PMID:8070649
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1205961/
Abstract

Leu+ mutants from Salmonella typhimurium leu-500 strain MA412 arise at high frequencies and mutant colonies appear over a broad range of time on selective plates. This observation suggested that these Leu+ mutants might be induced or "directed."= If such a mechanism was responsible, mutants should originate on selective plates rather than in the preceding culture in nonselective conditions and should give rise to Poisson-like fluctuation curves upon plating of sister cultures on selective medium. Poisson-like distribution profiles were indeed observed for Leu+ mutants of S. typhimurium MA412. However, an explanation for the observed Poisson-like fluctuation patterns without a need for selection-induced mutations was found. Microscopical analysis and cell mass/viable count measurements showed that the size of Leu+ mutant cells was often much larger than those of nonmutants. This size difference was a stable characteristic of a large proportion of Leu+ mutants, was observed both in stationary and growing culture and did not measurably affect the division rates of the cells in nutrient broth. As the transition from normal-sized nonmutant to oversized mutant cells during the nonselective culture phase of the fluctuation experiment may have been accompanied by a period with no or few completed cell division cycles, the number of mutant offspring may have been smaller than that of sibling nonmutants. Such underrepresentation of mutants in the final culture is expected to give rise to Poisson-like fluctuation patterns without invoking "directed" mutations.

摘要

鼠伤寒沙门氏菌leu - 500菌株MA412的亮氨酸(Leu)+突变体以高频率出现,并且在选择性平板上,突变菌落会在很宽的时间范围内出现。这一观察结果表明,这些Leu +突变体可能是被诱导或“定向”产生的。如果存在这样一种机制,那么突变体应该起源于选择性平板上,而不是在非选择性条件下的前一代培养物中,并且当将姐妹培养物接种到选择性培养基上时,应该会产生类似泊松分布的波动曲线。实际上,在鼠伤寒沙门氏菌MA412的Leu +突变体中观察到了类似泊松分布的情况。然而,人们发现了一种无需选择诱导突变就能解释所观察到的类似泊松分布波动模式的原因。显微镜分析和细胞质量/活菌计数测量表明,Leu +突变体细胞的大小通常比非突变体细胞大得多。这种大小差异是很大一部分Leu +突变体的稳定特征,在静止期和生长培养期均能观察到,并且在营养肉汤中对细胞的分裂速率没有明显影响。由于在波动实验的非选择性培养阶段,从正常大小的非突变体向超大突变体细胞的转变可能伴随着一段没有或很少有完整细胞分裂周期的时期,突变后代的数量可能比其非突变的姐妹细胞少。在最终培养物中突变体的这种数量不足预计会产生类似泊松分布的波动模式,而无需引入“定向”突变。