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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 (>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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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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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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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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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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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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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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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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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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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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Olczak, Adriana A., Jonathan W. Olson, and Robert J. Maier. "Oxidative-Stress Resistance Mutants of Helicobacter pylori." Journal of Bacteriology 184, no. 12 (2002): 3186–93. http://dx.doi.org/10.1128/jb.184.12.3186-3193.2002.
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ABSTRACT Within a large family of peroxidases, one member that catalyzes the reduction of organic peroxides to alcohols is known as alkyl hydroperoxide reductase, or AhpC. Gene disruption mutations in the gene encoding AhpC of Helicobacter pylori (ahpC) were generated by screening transformants under low-oxygen conditions. Two classes of mutants were obtained. Both types lack AhpC protein, but the major class (type I) isolated was found to synthesize increased levels (five times more than the wild type) of another proposed antioxidant protein, an iron-binding, neutrophil-activating protein (NapA). The other class of mutants, the minor class (type II), produced wild-type levels of NapA. The two types of AhpC mutants differed in their frequencies of spontaneous mutation to rifampin resistance and in their sensitivities to oxidative-stress chemicals, with the type I mutants exhibiting less sensitivity to organic hydroperoxides as well as having a lower mutation frequency. The napA promoter regions of the two types of AhpC mutants were identical, and primer extension analysis revealed their transcription start site to be the same as for the wild type. Gene disruption mutations were obtained in napA alone, and a double mutant strain (ahpC napA) was also created. All four of the oxidative-stress resistance mutants could be distinguished from the wild type in oxygen sensitivity or in some other oxidative-stress resistance phenotype (i.e., in sensitivity to stress-related chemicals and spontaneous mutation frequency). For example, growth of the NapA mutant was more sensitive to oxygen than that of the wild-type strain and both of the AhpC-type mutants were highly sensitive to paraquat and to cumene hydroperoxide. Of the four types of mutants, the double mutant was the most sensitive to growth inhibition by oxygen and by organic peroxides and it had the highest spontaneous mutation frequency. Notably, two-dimensional gel electrophoresis combined with protein sequence analysis identified another possible oxidative-stress resistance protein (HP0630) that was up-regulated in the double mutant. However, the transcription start site of the HP0630 gene was the same for the double mutant as for the wild type. It appears that H. pylori can readily modulate the expression of other resistance factors as a compensatory response to loss of a major oxidative-stress resistance component.
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Gao, Yue, Gaoyang Qu, Shengnan Huang, et al. "Comparison between Germinated Seed and Isolated Microspore EMS Mutagenesis in Chinese Cabbage (Brassica rapa L. ssp. pekinensis)." Horticulturae 8, no. 3 (2022): 232. http://dx.doi.org/10.3390/horticulturae8030232.
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Mutagenesis is an important tool for breeding and genomic research. In this study, the germinated seeds and isolated microspores of a double haploid line ‘FT’ were treated with EMS, respectively, with the aim of comparing the effects of the two approaches on generating mutants in Chinese cabbage. For microspore EMS mutagenesis, the isolated microspores were treated with 0.12% EMS for 20 min, a total of 1268 plantlets were obtained, and 15 M1 mutants were screened with a mutation frequency of 1.2%. For seed EMS mutagenesis, 7800 germinated seeds were treated with 0.8% EMS for 12 h, and a total of 701 M2 mutants were screened, with a mutation frequency of 18.78%. In total, 716 mutants with heritable morphological variation including leaf color, leaf shape, leafy head, bolting, and fertility, were obtained from the EMS mutagenesis experiments. Homozygous mutant plants could be screened from M1 lines by microspore mutagenesis, and M2 lines by seed mutagenesis. The mutation frequency was higher in seed mutagenesis than in microspore mutagenesis. Based on these results, we propose that seed EMS mutagenesis is more suitable to generate a large-scale mutant library, and the microspore EMS mutagenesis is conducive to rapidly obtaining homozygous mutants.
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McDonald, J. P., and R. Rothstein. "Unrepaired heteroduplex DNA in Saccharomyces cerevisiae is decreased in RAD1 RAD52-independent recombination." Genetics 137, no. 2 (1994): 393–405. http://dx.doi.org/10.1093/genetics/137.2.393.
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Abstract A direct repeat recombination assay between SUP4 heteroalleles detects unrepaired heteroduplex DNA (hDNA) as sectored colonies. The frequency of unrepaired heteroduplex is dependent on the mismatch and is highest in a construct that generates C:C or G:G mispairs and lowest in one that generates T:G or C:A mispairs. In addition, unrepaired hDNA increases for all mismatches tested in pms1 mismatch repair-deficient strains. These results support the notion that hDNA is formed across the SUP4 repeats during the recombination event and is then subject to mismatch repair. The effects of various repair and recombination defective mutations on this assay were examined. Unrepaired heteroduplex increases significantly only in rad52 mutant strains. In addition, direct repeat recombination is reduced 2-fold in rad52 mutant strains, while in rad51, rad54, rad55 and rad57 mutants direct repeat recombination is increased 3-4-fold. Mutations in the excision repair gene, RAD1, do not affect the frequency of direct repeat recombination. However, the level of unrepaired heteroduplex is slightly decreased in rad1 mutant strains. Similar to previous studies, rad1 rad52 double mutants show a synergistic reduction in direct repeat recombination (35-fold). Interestingly, unrepaired heteroduplex is reduced 4-fold in the double mutants. Experiments with shortened repeats suggest that the reduction in unrepaired heteroduplex is due to decreased hDNA tract length in the double mutant strain.
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Rader, Bethany A., Christopher Wreden, Kevin G. Hicks, Emily Goers Sweeney, Karen M. Ottemann, and Karen Guillemin. "Helicobacter pylori perceives the quorum-sensing molecule AI-2 as a chemorepellent via the chemoreceptor TlpB." Microbiology 157, no. 9 (2011): 2445–55. http://dx.doi.org/10.1099/mic.0.049353-0.
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Helicobacter pylori moves in response to environmental chemical cues using a chemotaxis two-component signal-transduction system. Autoinducer-2 (AI-2) is a quorum-sensing signal produced by the LuxS protein that accumulates in the bacterial environment in a density-dependent manner. We showed previously that a H. pylori luxS mutant was defective in motility on soft agar plates. Here we report that deletion of the luxS gene resulted in swimming behaviour with a reduced frequency of stops as compared to the wild-type strain. Stopping frequency was restored to wild-type levels by genetic complementation of the luxS mutation or by addition of synthetic 4,5-dihydroxy-2,3-pentanedione (DPD), which cyclizes to form AI-2. Synthetic DPD also increased the frequency of stops in wild-type H. pylori, similar to the behaviour induced by the known chemorepellent HCl. We found that whereas mutants lacking the chemoreceptor genes tlpA, tlpC or tlpD responded to an exogenous source of synthetic DPD, the chemoreceptor mutant tlpB was non-responsive to a gradient or uniform distribution of the chemical. Furthermore, a double mutant lacking both tlpB and luxS exhibited chemotactic behaviour similar to the tlpB single mutant, whereas a double mutant lacking both tlpB and the chemotransduction gene cheA behaved like a nonchemotactic cheA single mutant, supporting the model that tlpB functions in a signalling pathway downstream of luxS and upstream of cheA. We conclude that H. pylori perceives LuxS-produced AI-2 as a chemorepellent via the chemoreceptor TlpB.
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Galli, Alvaro, Tiziana Cervelli, and Robert H. Schiestl. "Characterization of the Hyperrecombination Phenotype of the pol3-t Mutation of Saccharomyces cerevisiae." Genetics 164, no. 1 (2003): 65–79. http://dx.doi.org/10.1093/genetics/164.1.65.
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Abstract The DNA polymerase δ (Pol3p/Cdc2p) allele pol3-t of Saccharomyces cerevisiae has previously been shown to increase the frequency of deletions between short repeats (several base pairs), between homeologous DNA sequences separated by long inverted repeats, and between distant short repeats, increasing the frequency of genomic deletions. We found that the pol3-t mutation increased intrachromosomal recombination events between direct DNA repeats up to 36-fold and interchromosomal recombination 14-fold. The hyperrecombination phenotype of pol3-t was partially dependent on the Rad52p function but much more so on Rad1p. However, in the double-mutant rad1Δ rad52Δ, the pol3-t mutation still increased spontaneous intrachromosomal recombination frequencies, suggesting that a Rad1p Rad52p-independent single-strand annealing pathway is involved. UV and γ-rays were less potent inducers of recombination in the pol3-t mutant, indicating that Pol3p is partly involved in DNA-damage-induced recombination. In contrast, while UV- and γ-ray-induced intrachromosomal recombination was almost completely abolished in the rad52 or the rad1 rad52 mutant, there was still good induction in those mutants in the pol3-t background, indicating channeling of lesions into the above-mentioned Rad1p Rad52p-independent pathway. Finally, a heterozygous pol3-t/POL3 mutant also showed an increased frequency of deletions and MMS sensitivity at the restrictive temperature, indicating that even a heterozygous polymerase δ mutation might increase the frequency of genetic instability.
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Feil, Helene, William S. Feil, and Steven E. Lindow. "Contribution of Fimbrial and Afimbrial Adhesins of Xylella fastidiosa to Attachment to Surfaces and Virulence to Grape." Phytopathology® 97, no. 3 (2007): 318–24. http://dx.doi.org/10.1094/phyto-97-3-0318.
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The role of fimbrial and afimbrial adhesins of Xylella fastidiosa in biofilm formation was assessed by visualization of cell aggregates of mutant strains after incubation on glass surfaces. FimA- or FimF- fimbrial mutants adhered as solitary cells at a slightly lesser frequency to glass surfaces than the parental strain; however, cell aggregates were not formed, unlike the wild-type strain. Conversely, whereas the XadA- and HxfB- nonfimbrial mutants also exhibited a much lower frequency of adherence to glass surfaces than the wild-type strain, most of the cells retained on the surfaces were in cell aggregates of different sizes, much like that of the parental strain. Neither fimbrial or afimbrial mutants formed a mature biofilm on the sides of flasks of broth cultures, unlike the dense biofilm formed by the wild-type strain. Although FimA- and FimF- mutants did not form cell aggregates on glass surfaces when incubated as individual strains, aggregates of a FimA- or FimF- mutant were observed when co-incubated with either a XadA- mutant or HxfB- mutant, respectively. These results are consistent with a model in which the fimbrial adhesins FimA and FimF are involved preferentially in cell-to-cell aggregate formation whereas the afimbrial adhesions XadA and HxfB preferentially contribute to initial cell binding to surfaces, whereupon further cell aggregation can occur. In each of five separate experiments, FimA, FimF, XadA, and HxfB mutants of X. fastidiosa all were less virulent to grape than the corresponding wild-type strain. Fimbrial and afimbrial mutants might produce a reduced biofilm within vessels of grape and, hence, be deficient in various cell-density-dependent traits required for movement through the plant and, thus, virulence.
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Shinohara, Miki, Emi Shita-Yamaguchi, Jean-Marie Buerstedde, Hideo Shinagawa, Hideyuki Ogawa, and Akira Shinohara. "Characterization of the Roles of the Saccharomyces cerevisiae RAD54 Gene and a Homologue of RAD54, RDH54/TID1, in Mitosis and Meiosis." Genetics 147, no. 4 (1997): 1545–56. http://dx.doi.org/10.1093/genetics/147.4.1545.
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Abstract The RAD54 gene, which encodes a protein in the SW12/SNF2 family, plays an important role in recombination and DNA repair in Saccharomyces cerevisiae. The yeast genome project revealed a homologue of RAD54, RDH54/TID1. Properties of the rdh54/tid1 mutant and the rad54 rdh54/tid1 double mutant are shown for mitosis and meiosis. The rad54 mutant is sensitive to the alkylating agent, methyl methanesulfonate (MMS), and is defective in interchromosomal and intrachromosomal gene conversion. The rdh54/tid1 single mutant, on the other hand, does not show any significant deficiency in mitosis. However, the rad54 rdh54/tid1 mutant is more sensitive to MMS and more defective in interchromosomal gene conversion than is the rad54 mutant, but shows the same frequency of intrachromosomal gene conversion as the rad54 mutant. These results suggest that RDH54/TID1 is involved in a minor pathway of mitotic recombination in the absence of RAD54. In meiosis, both single mutants produce viable spores at slightly reduced frequency. However, only the rdh54/tid1 mutant, but not the rad54 mutant, shows significant defects in recombination: retardation of the repair of meiosis-specific double-strand breaks (DSBs) and delayed formation of physical recombinants. Furthermore, the rad54 rdh54/tid1 double mutant is completely defective in meiosis, accumulating DSBs with more recessed ends than the wild type and producing fewer physical recombinants than the wild type. These results suggest that one of the differences between the late stages of mitotic recombination and meiotic recombination might be specified by differential dependency on the Rad54 and Rdh54/Tid1 proteins.
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NIE, PU-YAN, and PEI-AI ZHANG. "EVOLUTIONARY GRAPHS WITH FREQUENCY DEPENDENT FITNESS." International Journal of Modern Physics B 23, no. 04 (2009): 537–43. http://dx.doi.org/10.1142/s0217979209049905.
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Evolutionary graph theory was recently proposed by Lieberman et al. in 2005. In the previous papers about evolutionary graphs (EGs), the fitness of the residents in the EGs is in general assumed to be unity, and the fitness of a mutant is assumed to be a constant r. We aim to extend EG to general cases in this paper, namely, the fitness of a mutant is heavily dependent upon frequency. The corresponding properties for these new EGs are analyzed, and the fixation probability is obtained for large population.
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Martínez-González, Brenda, María Eugenia Soria, Lucía Vázquez-Sirvent, et al. "SARS-CoV-2 Mutant Spectra at Different Depth Levels Reveal an Overwhelming Abundance of Low Frequency Mutations." Pathogens 11, no. 6 (2022): 662. http://dx.doi.org/10.3390/pathogens11060662.
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Populations of RNA viruses are composed of complex and dynamic mixtures of variant genomes that are termed mutant spectra or mutant clouds. This applies also to SARS-CoV-2, and mutations that are detected at low frequency in an infected individual can be dominant (represented in the consensus sequence) in subsequent variants of interest or variants of concern. Here we briefly review the main conclusions of our work on mutant spectrum characterization of hepatitis C virus (HCV) and SARS-CoV-2 at the nucleotide and amino acid levels and address the following two new questions derived from previous results: (i) how is the SARS-CoV-2 mutant and deletion spectrum composition in diagnostic samples, when examined at progressively lower cut-off mutant frequency values in ultra-deep sequencing; (ii) how the frequency distribution of minority amino acid substitutions in SARS-CoV-2 compares with that of HCV sampled also from infected patients. The main conclusions are the following: (i) the number of different mutations found at low frequency in SARS-CoV-2 mutant spectra increases dramatically (50- to 100-fold) as the cut-off frequency for mutation detection is lowered from 0.5% to 0.1%, and (ii) that, contrary to HCV, SARS-CoV-2 mutant spectra exhibit a deficit of intermediate frequency amino acid substitutions. The possible origin and implications of mutant spectrum differences among RNA viruses are discussed.
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Xie, Yali, Chris Counter, and Eric Alani. "Characterization of the Repeat-Tract Instability and Mutator Phenotypes Conferred by a Tn3 Insertion in RFC1, the Large Subunit of the Yeast Clamp Loader." Genetics 151, no. 2 (1999): 499–509. http://dx.doi.org/10.1093/genetics/151.2.499.
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Abstract The RFC1 gene encodes the large subunit of the yeast clamp loader (RFC) that is a component of eukaryotic DNA polymerase holoenzymes. We identified a mutant allele of RFC1 (rfc1::Tn3) from a large collection of Saccharomyces cerevisiae mutants that were inviable when present in a rad52 null mutation background. Analysis of rfc1::Tn3 strains indicated that they displayed both a mutator and repeat-tract instability phenotype. Strains bearing this allele were characterized in combination with mismatch repair (msh2Δ, pms1Δ), double-strand break repair (rad52), and DNA replication (pol3-01, pol30-52, rth1Δ/rad27Δ) mutations in both forward mutation and repeat-tract instability assays. This analysis indicated that the rfc1::Tn3 allele displays synthetic lethality with pol30, pol3, and rad27 mutations. Measurement of forward mutation frequencies in msh2Δ rfc1:Tn3 and pms1Δ rfc1:Tn3 strains indicated that the rfc1::Tn3 mutant displayed a mutation frequency that appeared nearly multiplicative with the mutation frequency exhibited by mismatch-repair mutants. In repeat-tract instability assays, however, the rfc1::Tn3 mutant displayed a tract instability phenotype that appeared epistatic to the phenotype displayed by mismatch-repair mutants. From these data we propose that defects in clamp loader function result in DNA replication errors, a subset of which are acted upon by the mismatch-repair system.
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Fischetti, V. A., M. Jarymowycz, K. F. Jones, and J. R. Scott. "Streptococcal M protein size mutants occur at high frequency within a single strain." Journal of Experimental Medicine 164, no. 4 (1986): 971–80. http://dx.doi.org/10.1084/jem.164.4.971.
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Streptococcal M protein, the antiphagocytic molecule on the surface of the organism, was previously found to exhibit extensive size heterogeneity between as well as within M serotypes. In this study, methods were devised to isolate M protein size mutants within a laboratory-grown culture. We were able to isolate three independent M protein deletion mutants and one additional mutant, which was derived from the first deletion mutant. We found that these deletion mutants occur at a frequency of approximately 1 in 2 X 10(3) CFUs in culture. Functional studies revealed that the deletion mutants were able to survive as well as the parental strain in human blood. They also had the determinants necessary to absorb opsonic antibodies as well as the parent. Pepsin digestion experiments localized the deletions within the N-terminal half of the M molecule, which is distal to the cell wall surface. This is the region of the molecule in which extensive sequence repeats are found. This is consistent with the suggestion that the size changes may be the result of homologous recombination between the repeat regions in the gene. These results support the idea that strains showing M protein size variation within successive clinical isolates from single patients may be derived from the initial infecting organisms, and are not the result of separate unrelated acquisitions of the same serotype. This size change may be important in the survival of the streptococcus in vivo.
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Wang, Hai-xin, Li Zhang, Zi-teng Liang, et al. "Infectivity and antigenicity of pseudoviruses with high-frequency mutations of SARS-CoV-2 identified in Portugal." Archives of Virology 167, no. 2 (2022): 459–70. http://dx.doi.org/10.1007/s00705-021-05327-0.
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AbstractSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has had a major impact on global human health. During the spread of SARS-CoV-2, weakened host immunity and the use of vaccines with low efficacy may result in the development of more-virulent strains or strains with resistance to existing vaccines and antibodies. The prevalence of SARS-CoV-2 mutant strains differs between regions, and this variation may have an impact on the effectiveness of vaccines. In this study, an epidemiological investigation of SARS-CoV-2 in Portugal was performed, and the VSV-ΔG-G* pseudovirus system was used to construct 12 spike protein epidemic mutants, D614G, A222V+D614G, B.1.1.7, S477N+D614G, P1162R+D614G+A222V, D839Y+D614G, L176F+D614G, B.1.1.7+L216F, B.1.1.7+M740V, B.1.258, B.1.258+L1063F, and B.1.258+N751Y. The mutant pseudoviruses were used to infect four susceptible cell lines (Huh7, hACE2-293T-293T, Vero, and LLC-MK2) and 14 cell lines overexpressing ACE2 from different species. Mutant strains did not show increased infectivity or cross-species transmission. Neutralization activity against these pseudoviruses was evaluated using mouse serum and 11 monoclonal antibodies. The neutralizing activity of immunized mouse serum was not significantly reduced with the mutant strains, but the mutant strains from Portugal could evade nine of the 11 monoclonal antibodies tested. Neutralization resistance was mainly caused by the mutations S477N, N439K, and N501Y in the spike-receptor binding domain. These findings emphasize the importance of SARS-CoV-2 mutation tracking in different regions for epidemic prevention and control.
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Melton, D. W., A. M. Ketchen, F. Nunez, et al. "Cells from ERCC1-deficient mice show increased genome instability and a reduced frequency of S-phase-dependent illegitimate chromosome exchange but a normal frequency of homologous recombination." Journal of Cell Science 111, no. 3 (1998): 395–404. http://dx.doi.org/10.1242/jcs.111.3.395.
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The ERCC1 protein is essential for nucleotide excision repair in mammalian cells and is also believed to be involved in mitotic recombination. ERCC1-deficient mice, with their extreme runting and polyploid hepatocyte nuclei, have a phenotype that is more reminiscent of a cell cycle arrest/premature ageing disorder than the classic DNA repair deficiency disease, xeroderma pigmentosum. To understand the role of ERCC1 and the link between ERCC1-deficiency and cell cycle arrest, we have studied primary and immortalised embryonic fibroblast cultures from ERCC1-deficient mice and a Chinese hamster ovary ERCC1 mutant cell line. Mutant cells from both species showed the expected nucleotide excision repair deficiency, but the mouse mutant was only moderately sensitive to mitomycin C, indicating that ERCC1 is not essential for the recombination-mediated repair of interstrand cross links in the mouse. Mutant cells from both species had a high mutation frequency and the level of genomic instability was elevated in ERCC1-deficient mouse cells, both in vivo and in vitro. There was no evidence for an homologous recombination deficit in ERCC1 mutant cells from either species. However, the frequency of S-phase-dependent illegitimate chromatid exchange, induced by ultra violet light, was dramatically reduced in both mutants. In rodent cells the G1 arrest induced by ultra violet light is less extensive than in human cells, with the result that replication proceeds on an incompletely repaired template. Illegitimate recombination, resulting in a high frequency of chromatid exchange, is a response adopted by rodent cells to prevent the accumulation of DNA double strand breaks adjacent to unrepaired lesion sites on replicating DNA and allow replication to proceed. Our results indicate an additional role for ERCC1 in this process and we propose the following model to explain the growth arrest and early senescence seen in ERCC1-deficient mice. In the absence of ERCC1, spontaneously occurring DNA lesions accumulate and the failure of the illegitimate recombination process leads to the accumulation of double strand breaks following replication. This triggers the p53 response and the G2 cell cycle arrest, mediated by increased expression of the cyclin-dependent kinase inhibitor p21(cip1/waf1). The increased levels of unrepaired lesions and double strand breaks lead to an increased mutation frequency and genome instability.
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Inaoka, Takashi, Koji Kasai, and Kozo Ochi. "Construction of an In Vivo Nonsense Readthrough Assay System and Functional Analysis of Ribosomal Proteins S12, S4, and S5 in Bacillus subtilis." Journal of Bacteriology 183, no. 17 (2001): 4958–63. http://dx.doi.org/10.1128/jb.183.17.4958-4963.2001.
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ABSTRACT To investigate the function of ribosomal proteins and translational factors in Bacillus subtilis, we developed an in vivo assay system to measure the level of nonsense readthrough by utilizing the LacZ-LacI system. Using the in vivo nonsense readthrough assay system which we developed, together with an in vitro poly(U)-directed cell-free translation assay system, we compared the processibility and translational accuracy of mutant ribosomes with those of the wild-type ribosome. Like Escherichia coli mutants, most S12 mutants exhibited lower frequencies of both UGA readthrough and missense error; the only exception was a mutant (in which Lys-56 was changed to Arg) which exhibited a threefold-higher frequency of readthrough than the wild-type strain. We also isolated several ribosomal ambiguity (ram) mutants from an S12 mutant. These ram mutants and the S12 mutant mentioned above (in which Lys-56 was changed to Arg) exhibited higher UGA readthrough levels. Thus, the mutation which altered Lys-56 to Arg resulted in aram phenotype in B. subtilis. The efficacy of our in vivo nonsense readthrough assay system was demonstrated in our investigation of the function of ribosomal proteins and translational factors.
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Zuñiga-Castillo, Jacobo, David Romero, and Jaime M. Martínez-Salazar. "The Recombination Genes addAB Are Not Restricted to Gram-Positive Bacteria: Genetic Analysis of the Recombination Initiation Enzymes RecF and AddAB in Rhizobium etli." Journal of Bacteriology 186, no. 23 (2004): 7905–13. http://dx.doi.org/10.1128/jb.186.23.7905-7913.2004.
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ABSTRACT Single-strand gaps (SSGs) and double-strand breaks (DSBs) are the major initiation sites for recombination. In bacteria, the SSGs are repaired by RecFOR, while the DSBs are processed by RecBCD in gram-negative bacteria and AddAB in gram-positive bacteria. Unexpectedly, instead of recBCD genes, the addAB genes were found in members of the α-proteobacteria group (gram negative). Taking Rhizobium etli as a model, the role of recF and addAB genes in homologous recombination and repair of damaged DNA was evaluated. Inactivation of either recF or addA provoked strong sensitivity to UV radiation and mitomycin C, while an additive effect was observed in the recF-addA mutant. The DSBs generated by nalidixic acid caused low viability only in the addA mutant. The recombination frequency of large and small plasmids was reduced in the recF mutant (24- and 36-fold, respectively), whereas a slight decrease (threefold) in the addA mutant was observed. Moreover, an additive effect (47- and 90-fold, respectively) was observed in the double mutant, but it was not as dramatic as that in a recA mutant. Interestingly, the frequency of deletion and Campbell-type recombination was slightly affected in either single or double mutants. These results suggest that another pathway exists that allows plasmid and Campbell-type recombination in the absence of recF and addA genes.
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Canzoniero, Jenna VanLiere, Karen Cravero, and Ben Ho Park. "The Impact of Collisions on the Ability to Detect Rare Mutant Alleles Using Barcode-Type Next-Generation Sequencing Techniques." Cancer Informatics 16 (January 1, 2017): 117693511771923. http://dx.doi.org/10.1177/1176935117719236.
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Barcoding techniques are used to reduce error from next-generation sequencing, with applications ranging from understanding tumor subclone populations to detecting circulating tumor DNA. Collisions occur when more than one sample molecule is tagged by the same unique identifier (UID) and can result in failure to detect very-low-frequency mutations and error in estimating mutation frequency. Here, we created computer models of barcoding technique, with and without amplification bias introduced by the UID, and analyzed the effect of collisions for a range of mutant allele frequencies (1e−6 to 0.2), number of sample molecules (10 000 to 1e7), and number of UIDs (410-414). Inability to detect rare mutant alleles occurred in 0% to 100% of simulations, depending on collisions and number of mutant molecules. Collisions also introduced error in estimating mutant allele frequency resulting in underestimation of minor allele frequency. Incorporating an understanding of the effect of collisions into experimental design can allow for optimization of the number of sample molecules and number of UIDs to minimize the negative impact on rare mutant detection and mutant frequency estimation.
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Altmann, Thomas, Gisela Felix, Alison Jessop, et al. "Ac/Ds transposon mutagenesis in Arabidopsis thaliana: mutant spectrum and frequency of Ds insertion mutants." Molecular and General Genetics MGG 247, no. 5 (1995): 646–52. http://dx.doi.org/10.1007/bf00290357.
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Spormann, Alfred M., and Dale Kaiser. "Gliding Mutants of Myxococcus xanthuswith High Reversal Frequencies and Small Displacements." Journal of Bacteriology 181, no. 8 (1999): 2593–601. http://dx.doi.org/10.1128/jb.181.8.2593-2601.1999.
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ABSTRACT Myxococcus xanthus cells move on a solid surface by gliding motility. Several genes required for gliding motility have been identified, including those of the A- and S-motility systems as well as the mgl and frz genes. However, the cellular defects in gliding movement in many of these mutants were unknown. We conducted quantitative, high-resolution single-cell motility assays and found that mutants defective inmglAB or in cglB, an A-motility gene, reversed the direction of gliding at frequencies which were more than 1 order of magnitude higher than that of wild type cells (2.9 min−1for ΔmglAB mutants and 2.7 min−1 forcglB mutants, compared to 0.17 min−1 for wild-type cells). The average gliding speed of ΔmglABmutant cells was 40% of that of wild-type cells (on average 1.9 μm/min for ΔmglAB mutants, compared to 4.4 μm/min for wild-type cells). The mglA-dependent reversals and gliding speeds were dependent on the level of intracellular MglA protein: mglB mutant cells, which contain only 15 to 20% of the wild-type level of MglA protein, glided with an average reversal frequency of about 1.8 min−1 and an average speed of 2.6 μm/min. These values range between those exhibited by wild-type cells and by ΔmglAB mutant cells. Epistasis analysis of frz mutants, which are defective in aggregation and in single-cell reversals, showed that a frzD mutation, but not a frzE mutation, partially suppressed themglA phenotype. In contrast to mgl mutants,cglB mutant cells were able to move with wild-type speeds only when in close proximity to each other. However, under those conditions, these mutant cells were found to glide less often with those speeds. By analyzing double mutants, the high reversing movements and gliding speeds of cglB cells were found to be strictly dependent on type IV pili, encoded by S-motility genes, whereas the high-reversal pattern ofmglAB cells was only partially reduced by apilR mutation. These results suggest that the MglA protein is required for both control of reversal frequency and gliding speed and that in the absence of A motility, type IV pilus-dependent cell movement includes reversals at high frequency. Furthermore, mglAB mutants behave as if they were severely defective in A motility but only partially defective in S motility.
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Guest, J. R., and I. T. Creaghan. "Further Studies with Lipoamide Dehydrogenase Mutants of Escherichia coli k12." Microbiology 81, no. 1 (2000): 237–45. http://dx.doi.org/10.1099/00221287-81-1-237.
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The immunological properties of ten lipoamide dehydrogenase mutants of Escherichia coli were investigated with antiserum raised against purified lipoamide dehydrogenase. Seven mutants were CRM+ (cross-reacting material present) as they contained lipoamide dehydrogenase proteins exhibiting either complete or partial immunological identity with the wild-type protein. This indicates that at least seven of the mutations affect the lipoamide dehydrogenase structural gene (lpd). The remaining three mutants (CRM-) contained no detectable cross-reacting protein. None of the lpd mutations were sensitive to any of three different amber-suppressors. Genetic analysis by P1-transduction showed that all the lpd mutant sites were clustered very near the distal gene (aceF) of the ace region which specifies the dehydrogenase (aceE) and transacetylase (aceF) components of the pyruvate dehydrogenase multienzyme complex. Calculations based on the recombination frequency between an aceF mutant and the nearest lpd mutant site support the conclusion that apart from the possible presence of a regulatory element, the aceF and lpd genes are contiguous.
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Soria, Xavier, Felip Vilardell, Óscar Maiques, et al. "BRAFV600E Mutant Allele Frequency (MAF) Influences Melanoma Clinicopathologic Characteristics." Cancers 13, no. 20 (2021): 5073. http://dx.doi.org/10.3390/cancers13205073.
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Background: Cutaneous melanoma shows high variability regarding clinicopathological presentation, evolution and prognosis. Methods: Next generation sequencing was performed to analyze hotspot mutations in different areas of primary melanomas (MMp) and their paired metastases. Clinicopathological features were evaluated depending on the degree of variation of the BRAFV600E mutant allele frequency (MAF) in MMp. Results: In our cohort of 14 superficial spreading, 10 nodular melanomas and 52 metastases, 17/24 (71%) melanomas had a BRAFV600E mutation and 5/24 (21%) had a NRASQ61 mutation. We observed a high variation of BRAFV600E MAF (H-BRAFV600E) in 7/17 (41%) MMp. The H-BRAFV600E MMp were all located on the trunk, had lower Breslow and mitotic indexes and predominantly, a first nodal metastasis. Regions with spindled tumor cells (Spin) and high lymphocytic infiltrate (HInf) were more frequent in the H-BRAFV600E patients (4/7; 57%), whereas regions with epithelial tumor cells (Epit) and low lymphocytic infiltrate (LInf) were predominant (6/10; 60%) and exclusive in the low BRAFV600E MAF variation tumors (L-BRAFV600E). The H-BRAFV600E/Spin/HInf MMp patients had better prognostic features and nodal first metastasis. Conclusions: The H-BRAFV600E MMp were located on the trunk, had better prognostic characteristics, such as lower Breslow and mitotic indexes as well as high lymphocytic infiltrate.
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Curtsinger, J. W., and F. M. Sheen. "Frequency-Dependent Viability in Mutant Strains of Drosophila melanogaster." Journal of Heredity 82, no. 2 (1991): 105–9. http://dx.doi.org/10.1093/oxfordjournals.jhered.a111043.
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Lam, C. M. C., C. Chong, and J. T. Y. Wong. "A dinoflagellate mutant with higher frequency of multiple fission." Protoplasma 216, no. 1-2 (2001): 75–79. http://dx.doi.org/10.1007/bf02680134.
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Ribeiro, Ruy M., Sebastian Bonhoeffer, and Martin A. Nowak. "The frequency of resistant mutant virus before antiviral therapy." AIDS 12, no. 5 (1998): 461–65. http://dx.doi.org/10.1097/00002030-199805000-00006.
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Rice, Sederick C., Pamela M. Vacek, Alan H. Homans, et al. "Comparative analysis ofHPRT mutant frequency in children with cancer." Environmental and Molecular Mutagenesis 42, no. 1 (2003): 44–49. http://dx.doi.org/10.1002/em.10171.
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Hakoda, Masayuki, Mitoshi Akiyama, Seishi Kyoizumi, Akio A. Awa, Michio Yamakido, and Masanori Otake. "Increased somatic cell mutant frequency in atomic bomb survivors." Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 201, no. 1 (1988): 39–48. http://dx.doi.org/10.1016/0027-5107(88)90109-1.
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Havekes, Francis W. J., J. Hans de Jong, and Christa Heyting. "Comparative analysis of female and male meiosis in three meiotic mutants of tomato." Genome 40, no. 6 (1997): 879–86. http://dx.doi.org/10.1139/g97-814.
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Female meiosis was analysed in squash preparations of ovules from three meiotic mutants and wild-type plants of tomato. In the completely asynaptic mutant as6, chromosome pairing and chiasma formation were virtually absent in both sexes. In the partially asynaptic mutant asb, with intermediate levels of chromosome pairing at pachytene, there were a higher number of chiasmate chromosome arms in female meiosis than in male meiosis, whereas in the desynaptic mutant as5 there were normal levels of chromosome pairing at pachytene and a similar reduction in chiasma frequency in the two sexes. In wild-type tomato, we found slightly higher numbers of chiasmate chromosome arms in female meiosis than in male meiosis. We propose that the higher female chiasma frequencies in mutant asb and wild-type tomato result from a longer duration of female meiotic prophase. This would allow chromosomes more time to pair and recombine. It is possible that a longer duration of prophase I does not affect mutants as5 and as6, either because the meiotic defect acts before the pairing process begins (in as6) or because it acts at a later stage and involves chiasma maintenance (in as5).Key words: female meiosis, tomato, chiasma, mutant.
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Kawai, Fumitaka, Momoko Shoda, Rie Harashima, Yoshito Sadaie, Hiroshi Hara, and Kouji Matsumoto. "Cardiolipin Domains in Bacillus subtilis Marburg Membranes." Journal of Bacteriology 186, no. 5 (2004): 1475–83. http://dx.doi.org/10.1128/jb.186.5.1475-1483.2004.
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ABSTRACT Recently, use of the cardiolipin (CL)-specific fluorescent dye 10-N-nonyl-acridine orange (NAO) revealed CL-rich domains in the Escherichia coli membrane (E. Mileykovskaya and W. Dowhan, J. Bacteriol. 182: 1172-1175, 2000). Staining of Bacillus subtilis cells with NAO showed that there were green fluorescence domains in the septal regions and at the poles. These fluorescence domains were scarcely detectable in exponentially growing cells of the clsA-disrupted mutant lacking detectable CL. In sporulating cells with a wild-type lipid composition, fluorescence domains were observed in the polar septa and on the engulfment and forespore membranes. Both in the clsA-disrupted mutant and in a mutant with disruptions in all three of the paralogous genes (clsA, ywjE, and ywiE) for CL synthase, these domains did not vanish but appeared later, after sporulation initiation. A red shift in the fluorescence due to stacking of two dye molecules and the lipid composition suggested that a small amount of CL was present in sporulating cells of the mutants. Mass spectrometry analyses revealed the presence of CL in these mutant cells. At a later stage during sporulation of the mutants the frequency of heat-resistant cells that could form colonies after heat treatment was lower. The frequency of sporulation of these cells at 24 h after sporulation initiation was 30 to 50% of the frequency of the wild type. These results indicate that CL-rich domains are present in the polar septal membrane and in the engulfment and forespore membranes during the sporulation phase even in a B. subtilis mutant with disruptions in all three paralogous genes, as well as in the membranes of the medial septa and at the poles during the exponential growth phase of wild-type cells. The results further suggest that the CL-rich domains in the polar septal membrane and engulfment and forespore membranes are involved in sporulation.
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Al- Khafaji, K. A., and A. N. Al- Thwami. "Identification of differences in virulence factors production from mutant isolates of clinical Vibrio cholerae S." Journal of Biotechnology Research Center 5, no. 1 (2011): 61–73. http://dx.doi.org/10.24126/jobrc.2011.5.1.149.
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Antibiotic resistant mutants for rifampicin, streptomycin and klindamycin were isolated from the clinical isolate of Vibrio choleraeS mutated by chemical mutagens. Mutation frequency of V. cholerae S depends on the treatment time and the highest viable count of antibiotic resistant were for Rifampicin after treatment with Acridine orange, Ethedium bromide, Nitrosoguanidine, 5-Florouracil, 2-Bromouracil and cyclophosphamide. One thousand mutant isolates were examined for morphological differences in colony surface, color and diameter. The treatment with AO, NTG, 5-FU, and 2-BU gave opaque to orange color larger diameter about 5-7 mm of Rifampicin resistant mutant isolates at TSA and 25% of these mutant appeared as wrinkled surface. Klindamycin resistant mutants of V. cholerae S were appeared as similar to the wild type while, Streptomycin resistant mutants of appeared as pin- point white smooth colonies on TSA. No differences were seen for oxidase, string test and fermentation pattern for sucrose and lactose. Toxin CoregulatedPili production was differed from high level order designated as +++ to mild ++ and low level designated as + after mutation with 5-FU and 2-BU. However, 15% of rifampicin resistant mutant isolates gave no agglutination phenomena. No proteases activity detected even after 48 hour of incubation; the production of lipases enzyme did not affected; while, mutator isolates produced high level of β- haemolysins about 2.5 fold. About 90% of cyclophosphamide- rifampicin mutant showed homogenized culture with no auto agglutination but high level of proteases. While, only 10% of cyclophosphamide - rifampicin mutants gave slightly auto agglutination and didn’t produce proteases enzyme. The production of both TCP and CT were increased from rough pigment producing mutant isolates comparing with yellow and smooth mutants.
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Struble, Julie M., and Ryan T. Gill. "Reverse Engineering Antibiotic Sensitivity in a Multidrug-Resistant Pseudomonas aeruginosa Isolate." Antimicrobial Agents and Chemotherapy 50, no. 7 (2006): 2506–15. http://dx.doi.org/10.1128/aac.01640-05.
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ABSTRACT Antibiotic resistance is a pervasive and growing clinical problem. We describe an evaluation of a reverse engineering approach for identifying cellular mechanisms and genes that could be manipulated to increase antibiotic sensitivity in a resistant Pseudomonas aeruginosa isolate. We began by chemically mutating a broadly resistant isolate of P. aeruginosa and screening for mutants with increased sensitivity to the aminoglycoside amikacin, followed by performing whole-genome transcriptional profiling of the mutant and wild-type strains to characterize the global changes occurring as a result of the mutations. We then performed a series of assays to characterize the mechanisms involved in the increased sensitivity of the mutant strains. We report four primary results: (i) mutations that increase sensitivity occur at a high frequency (10−2) relative to the frequency of those that increase resistance (10−5 to 10−10) and occur at a frequency 104 higher than the frequency of a single point mutation; (ii) transcriptional profiles were altered in sensitive mutants, resulting in overall expression patterns more similar to those of the sensitive laboratory strain PAO1 than those of the parental resistant strain; (iii) genes found from transcriptional profiling had the more dramatic changes in expression-encoded functions related to cellular membrane permeability and aminoglycoside modification, both of which are known aminoglycoside resistance mechanisms; and finally, (iv) even though we did not identify the specific sites of mutation, several different follow-up MIC assays suggested that the mutations responsible for increased sensitivity differed between sensitive mutants.
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Onda, Masaaki, Katsuhiro Hanada, Hirokazu Kawachi, and Hideo Ikeda. "Escherichia coli MutM Suppresses Illegitimate Recombination Induced by Oxidative Stress." Genetics 151, no. 2 (1999): 439–46. http://dx.doi.org/10.1093/genetics/151.2.439.
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Abstract DNA damage by oxidative stress is one of the causes of mutagenesis. However, whether or not DNA damage induces illegitimate recombination has not been determined. To study the effect of oxidative stress on illegitimate recombination, we examined the frequency of λbio transducing phage in the presence of hydrogen peroxide and found that this reagent enhances illegitimate recombination. To clarify the types of illegitimate recombination, we examined the effect of mutations in mutM and related genes on the process. The frequency of λbio transducing phage was 5- to 12-fold higher in the mutM mutant than in the wild type, while the frequency in the mutY and mutT mutants was comparable to that of the wild type. Because 7,8-dihydro-8-oxoguanine (8-oxoG) and formamido pyrimidine (Fapy) lesions can be removed from DNA by MutM protein, these lesions are thought to induce illegitimate recombination. Analysis of recombination junctions showed that the recombination at Hotspot I accounts for 22 or 4% of total λbio transducing phages in the wild type or in the mutM mutant, respectively. The preferential increase of recombination at nonhotspot sites with hydrogen peroxide in the mutM mutant was discussed on the basis of a new model, in which 8-oxoG and/or Fapy residues may introduce double-strand breaks into DNA.
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Nitzan, N., M. Hazanovsky, M. Tal, and L. Tsror(Lahkim). "Vegetative Compatibility Groups in Colletotrichum coccodes, the Causal Agent of Black Dot on Potato." Phytopathology® 92, no. 8 (2002): 827–32. http://dx.doi.org/10.1094/phyto.2002.92.8.827.
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Black dot of potato, caused by Colletotrichum coccodes, is a disease of growing economic importance, but the degree of genetic diversity and pathogenic differentiation among isolates is unknown. Using nitrate auxotrophic (Nit) mutants, we characterized vegetative compatibility groups (VCG) diversity for C. coccodes for 110 isolates originating from Israel, The Netherlands, and France. We recovered frequencies of nit1 and NitM mutant classes at 38.5 and 7.2%, respectively, and selected 12 isolates as tester isolates. Using these testers, we defined four multimember VCGs at 7.3, 35.5, 20.0, and 10.0% frequency in this sample. Thirty isolates (27.3% of all tested isolates) could not be assigned to any of the major groups, and showed only self-compatibility. The frequency of recovery of Nit mutant sectors was highest in isolates from VCG4, with 50.9 and 13.6% recovery for nit1 and NitM, respectively. However, we did not detect differences in the frequency of mutant classes among the three countries of origin. In pathogenicity tests, isolates from VCG3 were the most aggressive to potato, as expressed by high stem colonization levels and sclerotia density on root and crown. These results suggest that there is significant VCG diversity in this species and that this VCG diversity may be correlated with pathogenic characteristics or specialization.
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Kawamoto, Yudai, Hirotaka Toda, Hiroshi Inoue, et al. "Fast and Inexpensive Phenotyping and Genotyping Methods for Evaluation of Barley Mutant Population." Plants 9, no. 9 (2020): 1153. http://dx.doi.org/10.3390/plants9091153.
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To further develop barley breeding and genetics, more information on gene functions based on the analysis of the mutants of each gene is needed. However, the mutant resources are not as well developed as the model plants, such as Arabidopsis and rice. Although genome editing techniques have been able to generate mutants, it is not yet an effective method as it can only be used to transform a limited number of cultivars. Here, we developed a mutant population using ‘Mannenboshi’, which produces good quality grains with high yields but is susceptible to disease, to establish a Targeting Induced Local Lesions IN Genomes (TILLING) system that can isolate mutants in a high-throughput manner. To evaluate the availability of the prepared 8043 M3 lines, we investigated the frequency of mutant occurrence using a rapid, visually detectable waxy phenotype as an indicator. Four mutants were isolated and single nucleotide polymorphisms (SNPs) were identified in the Waxy gene as novel alleles. It was confirmed that the mutations could be easily detected using the mismatch endonuclease CELI, revealing that a sufficient number of mutants could be rapidly isolated from our TILLING population.
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Mikheeva, Lidia E., Oliver Schmitzh, Sergey V. Shestakov, and Hermann Bothe. "Mutants of the Cyanobacterium Anabaena variabilis Altered in Hydrogenase Activities." Zeitschrift für Naturforschung C 50, no. 7-8 (1995): 505–10. http://dx.doi.org/10.1515/znc-1995-7-807.
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Abstract Two mutants of the cyanobacterium Anabaena variabilis impaired in the utilization or formation of molecular hydrogen have been obtained by nitroso-guanidine mutagenesis. Cultures of both mutants did not show alterations in the growth characteristics or in the heterocysts frequency but evolved molecular hydrogen from nitrogenase with enhanced rates. Activity measurements in extracts showed that one mutant (PK84) did not perform Na2S2O4- dependent H2-formation and was, therefore, unable to express an active bidirectional hydrogenase. Both mutants (PK84, PK 17R) were characterized by lower activity of phenazine-methosulphate-dependent H2-uptake when extracts were assayed from younger cultures. In older cells, particularly when grown with nitrate in the medium , this H2-uptake activity was, how ever, enhanced. Both mutants are likely affected in regulatory hydrogenase genes. The mutant PK84 offers perspectives for potential applications in solar energy conversion programs.
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Abhangrao A.K., Jitendra Kumar Sahoo, and Anis Mirza. "Effect of physical mutagens on base population of tuberose (Polyanthus tuberosa L.)." Ecology, Environment and Conservation 28 (2022): 435–39. http://dx.doi.org/10.53550/eec.2022.v28i07s.072.
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An investigation was conducted at the Department of Horticulture, College of Agriculture Parbhani, during which studies on tuberose (Polyanthus tuberosa L.) mutation breeding were explored and promising mutants were isolated. In VM1 generation and VM2 generation, the experimental material was Phule Rajani of tuberose variety treated with five doses of 0.5 Kr, 1Kr, 1.5Kr, 2Kr, and 2.5 Kr. The maximum floral abnormalities were observed in treatment T4 in the VM1 generation, whereas the maximum flower abnormalities were observed in treatment T3 in the VM2 generation. In the VM1 generation, the highest mutation frequency was reported at treatment T3. Treatment T1 had the highest mutation frequency in the VM2 generation. In early mutant characters, the highest percentage of the spectrum was seen in treatment T2 in VM1 and VM2. In both generations, the greatest spectrum percentage was recorded in the flower colour mutant character in treatment T2. In all generations, the greatest spectrum % was recorded in the tiny flower mutant at treatment T4. In both generations of the Big flower mutant, the highest spectrum % was found in treatment T1. In mutant characteristics, the number of petals increased, and the greatest spectrum percentage was seen at treatment T2 in VM1. Maximum generation in VM2 at T1 therapy. In the VM1 generation, the number of spikes increased, and the spectrum % rose. At treatment T2, the number of spikes in the VM2 generation increased. In the VM1 and VM2 generations, the greatest spectrum % was seen in late mutant characters at treatment T5. Both generational variations can be seen.
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Duffy, Brion K., and Geneviève Défago. "Controlling Instability in gacS-gacARegulatory Genes during Inoculant Production of Pseudomonas fluorescens Biocontrol Strains." Applied and Environmental Microbiology 66, no. 8 (2000): 3142–50. http://dx.doi.org/10.1128/aem.66.8.3142-3150.2000.
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ABSTRACT Secondary metabolism in fluorescent pseudomonads is globally regulated by gacS, which encodes a membrane-bound sensor kinase, and gacA, which encodes a transcriptional response regulator. Spontaneous mutation in either gene blocked biosynthesis of the antimicrobial compounds hydrogen cyanide, 2,4-diacetylphloroglucinol, pyoluteorin, and pyrrolnitrin by the model biocontrol strain Pseudomonas fluorescens CHA0. Spontaneous mutants also had altered abilities to utilize several carbon sources and to increase medium pH compared with the wild type, suggesting thatgacS and gacA influence primary as well as secondary bacterial metabolism. Inoculant efficacy for biocontrol was significantly reduced by contamination with regulatory mutants which accumulated during inoculum production. Spontaneous mutants accumulated in all 192 separate liquid cultures examined, typically at a frequency of 1% or higher after 12 days. During scale-up in a simulated industrial fermentation process, mutants increased exponentially and accounted for 7, 23, and 61% of the total viable cells after transfer to 20-, 100-, and 500-ml preparations, respectively. GacS−and GacA− mutants had identical phenotypes and occurred at the same frequency, indicating that the selective pressures for the two mutants were similar. We developed a simple screening method for monitoring inoculant quality based on the distinctive appearance of mutant colonies (i.e., orange color, enlarged diameter, hyperfluorescence). Mutant competitiveness was favored in a nutrient-rich medium with a high electrolyte concentration (nutrient broth containing yeast extract). We were able to control mutant accumulation and to clean up contaminated cultures by using certain mineral amendments (i.e., zinc, copper, cobalt, manganese, and ammonium molybdate) or by diluting media 1/10. Spontaneous mutants and genetic constructs had the same response to culture conditions. Zinc and medium dilution were also effective for improving the genetic stability of other P. fluorescens biocontrol strains obtained from Ghana and Italy.
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Baccari, Clelia, Nabil Killiny, Michael Ionescu, Rodrigo P. P. Almeida, and Steven E. Lindow. "Diffusible Signal Factor–Repressed Extracellular Traits Enable Attachment of Xylella fastidiosa to Insect Vectors and Transmission." Phytopathology® 104, no. 1 (2014): 27–33. http://dx.doi.org/10.1094/phyto-06-13-0151-r.
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The hypothesis that a wild-type strain of Xylella fastidiosa would restore the ability of rpfF mutants blocked in diffusible signal factor production to be transmitted to new grape plants by the sharpshooter vector Graphocephala atropunctata was tested. While the rpfF mutant was very poorly transmitted by vectors irrespective of whether they had also fed on plants infected with the wild-type strain, wild-type strains were not efficiently transmitted if vectors had fed on plants infected with the rpfF mutant. About 100-fewer cells of a wild-type strain attached to wings of a vector when suspended in xylem sap from plants infected with an rpfF mutant than in sap from uninfected grapes. The frequency of transmission of cells suspended in sap from plants that were infected by the rpfF mutant was also reduced over threefold. Wild-type cells suspended in a culture supernatant of an rpfF mutant also exhibited 10-fold less adherence to wings than when suspended in uninoculated culture media. A factor released into the xylem by rpfF mutants, and to a lesser extent by the wild-type strain, thus inhibits their attachment to, and thus transmission by, sharpshooter vectors and may also enable them to move more readily through host plants.
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Tsubouchi, Hideo, and Hideyuki Ogawa. "Exo1 Roles for Repair of DNA Double-Strand Breaks and Meiotic Crossing Over inSaccharomyces cerevisiae." Molecular Biology of the Cell 11, no. 7 (2000): 2221–33. http://dx.doi.org/10.1091/mbc.11.7.2221.
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The MRE11, RAD50, andXRS2 genes of Saccharomyces cerevisiaeare involved in the repair of DNA double-strand breaks (DSBs) produced by ionizing radiation and by radiomimetic chemicals such as methyl methanesulfonate (MMS). In these mutants, single-strand DNA degradation in a 5′ to 3′ direction from DSB ends is reduced. Multiple copies of the EXO1 gene, encoding a 5′ to 3′ double-strand DNA exonuclease, were found to suppress the high MMS sensitivity of these mutants. The exo1 single mutant shows weak MMS sensitivity. When an exo1 mutation is combined with anmre11 mutation, both repair of MMS-induced damage and processing of DSBs are more severely reduced than in either single mutant, suggesting that Exo1 and Mre11 function independently in DSB processing. During meiosis, transcription of the EXO1gene is highly induced. In meiotic cells, the exo1mutation reduces the processing of DSBs and the frequency of crossing over, but not the frequency of gene conversion. These results suggest that Exo1 functions in the processing of DSB ends and in meiotic crossing over.
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Raivio, Taneli, Yisrael Sidis, Lacey Plummer, et al. "Frequency of Impaired Fibroblast Growth Factor Receptor 1 Signaling as a Cause of Normosmic Idiopathic Hypogonadotropic Hypogonadism." Molecular Endocrinology 23, no. 12 (2009): 2120–21. http://dx.doi.org/10.1210/mend.23.12.9994.
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ABSTRACT Context FGFR1 mutations have been identified in about 10% of patients with Kallmann syndrome. Recently cases of idiopathic hypogonadotropic hypogonadism (IHH) with a normal sense of smell (nIHH) have been reported. Aims The objective of the study was to define the frequency of FGFR1 mutations in a large cohort of nIHH, delineate the spectrum of reproductive phenotypes, assess functionality of the FGFR1 mutant alleles in vitro, and investigate genotype-phenotype relationships. Design FGFR1 sequencing of 134 well-characterized nIHH patients (112 men and 22 women) and 270 healthy controls was performed. The impact of the identified mutations on FGFR1 function was assessed using structural prediction and in vitro studies. Results Nine nIHH subjects (five males and four females; 7%) harbor a heterozygous mutation in FGFR1 and exhibit a wide spectrum of pubertal development, ranging from absent puberty to reversal of IHH in both sexes. All mutations impair receptor function. The Y99C, Y228D, and I239T mutants impair the tertiary folding, resulting in incomplete glycosylation and reduced cell surface expression. The R250Q mutant reduces receptor affinity for FGF. The K618N, A671P, and Q680X mutants impair tyrosine kinase activity. However, the degree of functional impairment of the mutant receptors did not always correlate with the reproductive phenotype, and variable expressivity of the disease was noted within family members carrying the same FGFR1 mutation. These discrepancies were partially explained by additional mutations in known IHH loci. Conclusions Loss-of-function mutations in FGFR1 underlie 7% of nIHH with different degrees of impairment in vitro. These mutations act in concert with other gene defects in several cases, consistent with oligogenicity.
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Balhadère, Pascale V., Andrew J. Foster, and Nicholas J. Talbot. "Identification of Pathogenicity Mutants of the Rice Blast Fungus Magnaporthe grisea by Insertional Mutagenesis." Molecular Plant-Microbe Interactions® 12, no. 2 (1999): 129–42. http://dx.doi.org/10.1094/mpmi.1999.12.2.129.
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Restriction enzyme-mediated DNA integration (REMI) mutagenesis was used to identify mutants of Magnaporthe grisea impaired in pathogenicity. Three REMI protocols were evaluated and the frequency of REMIs determined. An REMI library of 3,527 M. grisea transformants was generated in three genetic backgrounds, and 1,150 transformants were screened for defects in pathogenicity with a barley cut leaf assay. Five mutants were identified and characterized. Two mutants (2029 and 2050) were impaired in appressorium function. Two other mutants, 125 and 130, were altered in conidial morphology, conidiogenesis, and appressorium function. Mutant 130 was also a methionine auxotroph and methionine auxotrophy co-segregated with the reduction in pathogenicity. An additional mutant, 80, showed reduced pathogenicity on blast-susceptible rice cultivars but was fully pathogenic on barley. The reduction of pathogenicity in mutant 80 was associated with a delay in conidial germination and appressorium development. Genetic analysis suggested single-gene segregation for each mutant, but only two of the mutations co-segregated with the hygromycin resistance marker. The genetic loci in mutants 2029, 2050, 125, 130, and 80 were termed PDE1, PDE2, IGD1, MET1, and GDE1, respectively. pde1 and pde2 were non-allelic to cpkA, a mutation in the catalytic subunit of cyclic AMP (cAMP)-dependent protein kinase A with a very similar phenotype. The results indicate the utility of REMI for studying fungal pathogenicity, but also highlight the requirement for rigorous genetic and phenotypic analysis.
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Bunch, T. A., M. W. Graner, L. I. Fessler, et al. "The PS2 integrin ligand tiggrin is required for proper muscle function in Drosophila." Development 125, no. 9 (1998): 1679–89. http://dx.doi.org/10.1242/dev.125.9.1679.
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Tiggrin is a novel extracellular matrix ligand for the Drosophila PS2 integrins. We have used flanking P elements to generate a precise deletion of tiggrin. Most flies lacking tiggrin die as larvae or pupae. A few adults do emerge and these appear to be relatively normal, displaying only misshapen abdomens and a low frequency of wing defects. Examination of larvae shows that muscle connections, function and morphology are defective in tiggrin mutants. Muscle contraction waves that extend the length of the larvae are much slower in tiggrin mutants. Direct examination of bodywall muscles shows defects in muscle attachment sites, where tiggrin is specifically localized, and muscles appear thinner. Transgenes expressing tiggrin are capable of rescuing tiggrin mutant phenotypes. Transgenes expressing a mutant tiggrin, whose Arg-Gly-Asp (RGD) integrin recognition sequence has been mutated to Leu-Gly-Ala (LGA) show much reduced, but significant, rescuing ability. Cell spreading assays detect no interactions of this mutant tiggrin with PS2 integrins. Therefore, while the RGD sequence is critical for PS2 interactions and full activity in the whole fly, the mutant tiggrin retains some function(s) that are probably mediated by interactions with other ECM molecules or cell surface receptors