Chromium resistance genetic element flanked by XerC/XerD recombination sites and its distribution in environmental and clinical Acinetobacter strains

2018 ◽  
Vol 365 (8) ◽  
Author(s):  
Sofia Mindlin ◽  
Anatoliy Petrenko ◽  
Mayya Petrova
Keyword(s):  
Genetic Element ◽  
Chromium Resistance

scholarly journals GERMLINE HYPERMUTABILITY IN DROSOPHILA AND ITS RELATION TO HYBRID DYSGENESIS AND CYTOTYPE

Genetics ◽  
1981 ◽  
Vol 98 (3) ◽  
pp. 565-587
Author(s):  
William R Engels
Keyword(s):  
Cell Survival ◽  
Chromosomal Rearrangements ◽  
Stable State ◽  
Hybrid Dysgenesis ◽  
Mutation Rates ◽  
Female Sterility ◽  
Genetic Element ◽  
Two Generations ◽  
The Mean ◽  
P Factor

ABSTRACT In its hypermutable state, an unstable singed allele, snw, mutates in the germline to two other alleleic forms at a total frequency usually between 40 and 60%. In its stable state, the mutation rate of snw is essentially zero. Its state depends on an extrachromosomal condition indistinguishable from a property called cytotype previously studied as a component of hybrid dysgenesis. Of the two known systems of hybrid dysgenesis, denoted P-M and I-R, snw hypermutability is determined by the P-M system and appears to be independent of the I-R system. Cytotype, as defined by the control of snw mutability, is self-reproducing in the cytoplasm or nucleoplasm of the germline through at least two generations. However, it is not entirely autonomous, being ultimately determined by the chromosomes after sufficiently many generations of backcrossing. This combination of chromosomal and extrachromosomal transmission agrees well with previous studies on cytotype. Temperature differences have little effect on the mean mutation rates, but they have a pronounced effect on the intrinsic variance among individuals. The latter effect suggests that high temperatures reduce germ-cell survival during the development of dysgenic flies. Chromosomal rearrangements produce no apparent effects on the behavior of snw. Hypermutability is thought to be caused by the excision or other alteration of an inserted genetic element in the snw gene. This element might be a copy of the "P factor," which is though to be a mobile sequence capable of causing female sterility and other dysgenic traits in the P-M system.

HLA-DQB2: transitional pseudogene or cryptic genetic element?

1991 ◽  
Vol 32 ◽  
pp. 17
Author(s):  
Lakshmi K. Gaur ◽  
P. Thurtle ◽  
G.T. Nepom
Keyword(s):  
Genetic Element

scholarly journals A putative mobile genetic element carrying a novel type IIF restriction-modification system (PluTI)

2010 ◽  
Vol 38 (9) ◽  
pp. 3019-3030 ◽  
Author(s):  
Feroz Khan ◽  
Yoshikazu Furuta ◽  
Mikihiko Kawai ◽  
Katarzyna H. Kaminska ◽  
Ken Ishikawa ◽  
...  
Keyword(s):  
Mobile Genetic Element ◽  
Genetic Element ◽  
Modification System ◽  
Restriction Modification System ◽  
Restriction Modification

Specificity of Chromosome Damage Caused by the Rex Element of Drosophila melanogaster

Genetics ◽  
1996 ◽  
Vol 144 (1) ◽  
pp. 109-115 ◽  
Author(s):  
Leonard G Robbins
Keyword(s):  
Drosophila Melanogaster ◽  
Early Development ◽  
X Chromosome ◽  
Ribosomal Rna ◽  
Chromosome Damage ◽  
Genetic Element ◽  
Single Chromosome ◽  
Experimental Cross ◽  
Rdna Array ◽  
Early Embryos

Abstract Rex is a multicopy genetic element that maps within an X-linked ribosomal RNA gene (rDNA) array of D. melanogaster. Acting maternally, Rex causes recombination between rDNA arrays in a few percent of early embryos. With target chromosomes that contain two rDNA arrays, the exchanges either delete all of the material between the two arrays or invert the entire intervening chromosomal segment. About a third of the embryos produced by Rex homozygotes have cytologically visible chromosome damage, nearly always involving a single chromosome. Most of these embryos die during early development, displaying a characteristic apoptosis-like phenotype. An experiment that tests whether the cytologically visible damage is rDNA-specific is reported here. In this experiment, females heterozygous for Rex and an rDNA-deficient X chromosome were crossed to males of two genotypes. Some of the progeny from the experimental cross entirely lacked rDNA, while all of the progeny from the control cross had at least one rDNA array. A significantly lower frequency of early-lethal embryos in the experimental cross, proportionate to the fraction of rDNA-deficient embryos, demonstrates that Rex preferentially damages rDNA.

scholarly journals A Salmonella Phage-P22 Mutant Defective in Abortive Transduction

Genetics ◽  
1997 ◽  
Vol 145 (1) ◽  
pp. 17-27 ◽  
Author(s):  
Nicholas R Benson ◽  
John Roth
Keyword(s):  
Protein S ◽  
Lytic Infection ◽  
Genetic Element ◽  
Bacterial Dna ◽  
Phage Mutant ◽  
Viral Particles ◽  
Phage Dna ◽  
Phage P22 ◽  
Mutant Locus ◽  
Salmonella Phage

In the course of a lytic infection the Salmonella phage P22 occasionally encapsulates bacterial DNA instead of phage DNA. Thus, phage lysates include two classes of viral particles. Phage particles carrying bacterial DNA are referred to as transducing particles and deliver this DNA to a host as efficiently as particles carrying phage DNA. Once injected, the transduced DNA can either recombine with the recipient chromosome to form a “complete” transductant, or it can establish itself as an expressible, nonreplicating genetic element and form an “abortive” transductant. In this work, we describe a P22-phage mutant with reduced ability to form abortive transductants. The mutation responsible for this phenotype, called tdx-1, was found as one of two mutations contributing to the high-transducing phenotype of the P22-mutant HT12/4. In addition, the tdx-1 mutation is lethal when combined with an erf-am mutation. The tdx-1 mutation has been mapped to a region of the P22 genome that encodes several injected proteins and may involve more than one mutant locus. The phenotypes of the tdx-1 mutation suggest that the Tdx protein(s) normally assist in the circularization of the P22 genome and also contribute to the formation of DNA circles thought to be required for abortive transduction.

scholarly journals Assembly of a fragmented ribonucleotide reductase by protein interaction domains derived from a mobile genetic element

2010 ◽  
Vol 39 (4) ◽  
pp. 1381-1389 ◽  
Author(s):  
Mikael Crona ◽  
Connor Moffatt ◽  
Nancy C. Friedrich ◽  
Anders Hofer ◽  
Britt-Marie Sjöberg ◽  
...  
Keyword(s):  
Protein Interaction ◽  
Ribonucleotide Reductase ◽  
Mobile Genetic Element ◽  
Genetic Element ◽  
Interaction Domains
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