Bibliografías: "Mutant frequency"

1

Curry, John, Larissa Karnaoukhova, Gabriel C. Guenette, and Barry W. Glickman. "Influence of Sex, Smoking and Age on Human hprt Mutation Frequencies and Spectra." Genetics 152, no. 3 (1999): 1065–77. http://dx.doi.org/10.1093/genetics/152.3.1065.

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Abstract Examination of the literature for hprt mutant frequencies from peripheral T cells yielded data from 1194 human subjects. Relationships between mutant frequency, age, sex, and smoking were examined, and the kinetics were described. Mutant frequency increases rapidly with age until about age 15. Afterward, the rate of increase falls such that after age 53, the hprt mutant frequency is largely stabilized. Sex had no effect on mutant frequency. Cigarette smoking increased mean mutant frequency compared to nonsmokers, but did not alter age vs. mutant frequency relationships. An hprt in vivo mutant database containing 795 human hprt mutants from 342 individuals was prepared. No difference in mutational spectra was observed comparing smokers to nonsmokers, confirming previous reports. Sex affected the frequency of deletions (&gt;1 bp) that are recovered more than twice as frequently in females (P = 0.008) compared to males. There is no indication of a significant shift in mutational spectra with age for individuals older than 19 yr, with the exception of A:T → C:G transversions. These events are recovered more frequently in older individuals.

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2

Tanimoto, Koichi, Haruyoshi Tomita, Shuhei Fujimoto, Katsuko Okuzumi, and Yasuyoshi Ike. "Fluoroquinolone Enhances the Mutation Frequency for Meropenem-Selected Carbapenem Resistance in Pseudomonas aeruginosa, but Use of the High-Potency Drug Doripenem Inhibits Mutant Formation." Antimicrobial Agents and Chemotherapy 52, no. 10 (2008): 3795–800. http://dx.doi.org/10.1128/aac.00464-08.

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ABSTRACT The mutation frequency for carbapenem resistance in Pseudomonas aeruginosa strains that were selected with carbapenems was enhanced in the presence of subinhibitory concentrations of fluoroquinolones. The mutants showed either a loss of OprD activity or increased mexAB-oprM expression. The highest mutant isolation frequency was obtained by selection with meropenem, while doripenem inhibited mutant growth.

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3

Magin, Gregory K., Steven H. Robison, Nancy Breslin, Richard Jed Wyatt, and Robert C. Alexander. "DNA repair and mutant frequency in schizophrenia." Mutation Research/DNA Repair 255, no. 3 (1991): 241–46. http://dx.doi.org/10.1016/0921-8777(91)90027-m.

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4

Alexander, R. C., G. K. Magin, S. H. Robison, and R. J. Wyatt. "DNA repair and mutant frequency in schizophrenia." Schizophrenia Research 6, no. 2 (1992): 96. http://dx.doi.org/10.1016/0920-9964(92)90100-j.

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5

Nishimura, Kenji, Shanna K. Johansen, Takashi Inaoka, et al. "Identification of the RsmG Methyltransferase Target as 16S rRNA Nucleotide G527 and Characterization of Bacillus subtilis rsmG Mutants." Journal of Bacteriology 189, no. 16 (2007): 6068–73. http://dx.doi.org/10.1128/jb.00558-07.

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ABSTRACT The methyltransferase RsmG methylates the N7 position of nucleotide G535 in 16S rRNA of Bacillus subtilis (corresponding to G527 in Escherichia coli). Disruption of rsmG resulted in low-level resistance to streptomycin. A growth competition assay revealed that there are no differences in fitness between the rsmG mutant and parent strains under the various culture conditions examined. B. subtilis rsmG mutants emerged spontaneously at a relatively high frequency, 10−6. Importantly, in the rsmG mutant background, high-level-streptomycin-resistant rpsL (encoding ribosomal protein S12) mutants emerged at a frequency 200 times greater than that seen for the wild-type strain. This elevated frequency in the emergence of high-level streptomycin resistance was facilitated by a mutation pattern in rpsL more varied than that obtained by selection of the wild-type strain.

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6

Gnanamurthy, S., and D. Dhanavel. "Effect of EMS on Induced Morphological Mutants and Chromosomal Variation in Cowpea (Vigna unguiculata (L.) Walp)." International Letters of Natural Sciences 22 (August 2014): 33–43. http://dx.doi.org/10.18052/www.scipress.com/ilns.22.33.

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Effect of EMS (ethyl methane sulphonate) on induced morphological mutants and chromosomal variation in cowpea was studied using five different doses of mutagen along with a control in randomized blocked design with three replications. The morphological mutants there are two types of viable and chlorophyll mutants. Viable mutant contains tall, dwarf, early maturity, late maturity, leaf mutants pod mutant and flower mutants. The frequency of chlorophyll mutant contains albino, xantha and viridis. This concentration can damage or modify important components of plant cells and have been reported to affect the morphology, anatomy, biochemistry and physiology of plants differentially depending on the concentration level. These effects include changes in the cellular structure and metabolism of the plants e.g., dilation of thylakoid membranes, alteration in photosynthesis, modulation of the antioxidative system and accumulation of phenolic compounds. The morphological and chromosomal variation was found to be mutagen sensitive in somatic cells of cowpea. It was found to increase with increasing the concentration of EMS in Cowpea plants. The chemical mutagen like ethyl methane sulphonate induces high frequency of chromosomal changes like anaphasic bridge; anaphasic laggard, anaphasic bridge and clumbing of chromosome were including control plants also observed.

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7

Gnanamurthy, S., and D. Dhanavel. "Effect of EMS on Induced Morphological Mutants and Chromosomal Variation in Cowpea (<i>Vigna unguiculata</i> (L.) Walp)." International Letters of Natural Sciences 22 (August 5, 2014): 33–43. http://dx.doi.org/10.56431/p-i0xny2.

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Effect of EMS (ethyl methane sulphonate) on induced morphological mutants and chromosomal variation in cowpea was studied using five different doses of mutagen along with a control in randomized blocked design with three replications. The morphological mutants there are two types of viable and chlorophyll mutants. Viable mutant contains tall, dwarf, early maturity, late maturity, leaf mutants pod mutant and flower mutants. The frequency of chlorophyll mutant contains albino, xantha and viridis. This concentration can damage or modify important components of plant cells and have been reported to affect the morphology, anatomy, biochemistry and physiology of plants differentially depending on the concentration level. These effects include changes in the cellular structure and metabolism of the plants e.g., dilation of thylakoid membranes, alteration in photosynthesis, modulation of the antioxidative system and accumulation of phenolic compounds. The morphological and chromosomal variation was found to be mutagen sensitive in somatic cells of cowpea. It was found to increase with increasing the concentration of EMS in Cowpea plants. The chemical mutagen like ethyl methane sulphonate induces high frequency of chromosomal changes like anaphasic bridge; anaphasic laggard, anaphasic bridge and clumbing of chromosome were including control plants also observed.

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8

Ingham, Neil J., Navid Banafshe, Clarisse Panganiban, et al. "Inner hair cell dysfunction in Klhl18 mutant mice leads to low frequency progressive hearing loss." PLOS ONE 16, no. 10 (2021): e0258158. http://dx.doi.org/10.1371/journal.pone.0258158.

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Age-related hearing loss in humans (presbycusis) typically involves impairment of high frequency sensitivity before becoming progressively more severe at lower frequencies. Pathologies initially affecting lower frequency regions of hearing are less common. Here we describe a progressive, predominantly low-frequency recessive hearing impairment in two mutant mouse lines carrying different mutant alleles of the Klhl18 gene: a spontaneous missense mutation (Klhl18lowf) and a targeted mutation (Klhl18tm1a(KOMP)Wtsi). Both males and females were studied, and the two mutant lines showed similar phenotypes. Threshold for auditory brainstem responses (ABR; a measure of auditory nerve and brainstem neural activity) were normal at 3 weeks old but showed progressive increases from 4 weeks onwards. In contrast, distortion product otoacoustic emission (DPOAE) sensitivity and amplitudes (a reflection of cochlear outer hair cell function) remained normal in mutants. Electrophysiological recordings from the round window of Klhl18lowf mutants at 6 weeks old revealed 1) raised compound action potential thresholds that were similar to ABR thresholds, 2) cochlear microphonic potentials that were normal compared with wildtype and heterozygous control mice and 3) summating potentials that were reduced in amplitude compared to control mice. Scanning electron microscopy showed that Klhl18lowf mutant mice had abnormally tapering of the tips of inner hair cell stereocilia in the apical half of the cochlea while their synapses appeared normal. These results suggest that Klhl18 is necessary to maintain inner hair cell stereocilia and normal inner hair cell function at low frequencies.

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9

Waddell, D. R., K. Duffy, and G. Vogel. "Cytokinesis is defective in Dictyostelium mutants with altered phagocytic recognition, adhesion, and vegetative cell cohesion properties." Journal of Cell Biology 105, no. 5 (1987): 2293–300. http://dx.doi.org/10.1083/jcb.105.5.2293.

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Mutants that have been selected for defects in phagocytic recognition, adhesion, and vegetative cell-cell cohesion were found to be larger and more highly multinucleate than their parent strain. This defect is associated with the complex mutant phenotype of these mutants since revertants of the mutants coordinately acquire the wild-type phenotype for all of the defects. The larger size and multinuclearity were due to a high frequency of failure of cytokinesis in cells of wild-type size. This was shown by purifying the small cells in mutant populations and observing their growth and cell division. The mutant phenotype is more penetrant during axenic growth. Most of the mutants are not multinucleate when grown on bacteria. Recently, new mutants have been isolated that are also multinucleate when grown on bacteria by a strong selection procedure for non-adhesion to tissue culture dishes. The pleiotropic mutant phenotype and the greater penetrance of the mutant phenotype in axenic culture can be explained by hypothesizing a deficiency in a membrane component of the actomyosin motor that is involved in all of the processes defective in the mutants.

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10

Criss, Alison K., Kevin M. Bonney, Rhoda A. Chang, Paul M. Duffin, Brian E. LeCuyer, and H. Steven Seifert. "Mismatch Correction Modulates Mutation Frequency and Pilus Phase and Antigenic Variation in Neisseria gonorrhoeae." Journal of Bacteriology 192, no. 1 (2009): 316–25. http://dx.doi.org/10.1128/jb.01228-09.

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ABSTRACT The mismatch correction (MMC) system repairs DNA mismatches and single nucleotide insertions or deletions postreplication. To test the functions of MMC in the obligate human pathogen Neisseria gonorrhoeae, homologues of the core MMC genes mutS and mutL were inactivated in strain FA1090. No mutH homologue was found in the FA1090 genome, suggesting that gonococcal MMC is not methyl directed. MMC mutants were compared to a mutant in uvrD, the helicase that functions with MMC in Escherichia coli. Inactivation of MMC or uvrD increased spontaneous resistance to rifampin and nalidixic acid, and MMC/uvrD double mutants exhibited higher mutation frequencies than any single mutant. Loss of MMC marginally enhanced the transformation efficiency of DNA carrying a single nucleotide mismatch but not that of DNA with a 1-kb insertion. Unlike the exquisite UV sensitivity of the uvrD mutant, inactivating MMC did not affect survival after UV irradiation. MMC and uvrD mutants exhibited increased PilC-dependent pilus phase variation. mutS-deficient gonococci underwent an increased frequency of pilin antigenic variation, whereas uvrD had no effect. Recombination tracts in the mutS pilin variants were longer than in parental gonococci but utilized the same donor pilS loci. These results show that gonococcal MMC repairs mismatches and small insertion/deletions in DNA and also affects the recombination events underlying pilin antigenic variation. The differential effects of MMC and uvrD in gonococci unexpectedly reveal that MMC can function independently of uvrD in this human-specific pathogen.

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