scholarly journals Genotypes and Characteristics of Phenamacril-Resistant Mutants in Fusarium asiaticum

Plant Disease ◽  
2016 ◽  
Vol 100 (8) ◽  
pp. 1754-1761 ◽  
Author(s):  
Bin Li ◽  
Zhitian Zheng ◽  
Xiumei Liu ◽  
Yiqiang Cai ◽  
Xuewei Mao ◽  
...  
Keyword(s):  
Point Mutations ◽  
Core Region ◽  
Wild Type ◽  
Head Blight ◽  
Pathogen Population ◽  
Resistance Level ◽  
The Core ◽  
Fusarium Asiaticum ◽  
Resistant Mutants ◽  
Moderate Resistance

Fusarium asiaticum is a critical pathogen of Fusarium head blight (FHB) in the southern part of China. The fungicide phenamacril has been extensively used for controlling FHB in recent years, which reduced both FHB severity and mycotoxin production. Our previous report indicated that resistance of F. asiaticum to phenamacril was related to mutations in myosin5. A recent article revealed that the resistance level of phenamacril-resistant mutants was associated with the genotypes of myosin5 in these mutants. In total, we obtained 239 resistant isolates by fungicide domestication, and 82 resistant mutants were randomly selected for further study. Of these mutants, 25.6, 7.3, and 67.1% showed low resistance (LR), moderate resistance (MR), and high resistance (HR), respectively, to phenamacril determined by 50% effective concentration values. Point mutations A135T, V151M, P204S, I434M, A577T, R580G/H, or I581F led to LR. Point mutations S418R, I424R, and A577G were responsible for MR and point mutations K216R/E, S217P/L, or E420K/G/D conferred HR. Interestingly, all of the mutations concentrated in the myosin5 motor domain and mutations conferring HR occurred at codon 217 and 420, which we called the core region. Homology modeling revealed that mutations far from the core region led to a lower resistance degree. Phenotype assays revealed that the most highly resistant mutants did not significantly change pathogenicity but decreased conidia production compared with the wild type, which may slow down the formation of the resistant pathogen population in the fields.

scholarly journals Genotypes and Phenotypic Characterization of Field Fusarium asiaticum Isolates Resistant to Carbendazim in Anhui Province of China

Plant Disease ◽  
2015 ◽  
Vol 99 (3) ◽  
pp. 342-346 ◽  
Author(s):  
Yu Chen ◽  
Xue Yang ◽  
Chun-Yan Gu ◽  
Ai-Fang Zhang ◽  
Tong-Chun Gao ◽  
...  
Keyword(s):  
Natural Populations ◽  
Point Mutations ◽  
Anhui Province ◽  
Phenotypic Characterization ◽  
Head Blight ◽  
Single Spore ◽  
Tubulin Gene ◽  
Fusarium Asiaticum ◽  
Moderate Resistance

Fusarium asiaticum is a causal agent of Fusarium head blight (FHB) of wheat in the southern part of China. Carbendazim has been extensively used for controlling FHB for more than 30 years, leading to the widespread carbendazim-resistant isolates in all major wheat-producing provinces in China, especially in Anhui Province. F. asiaticum isolates were collected throughout Anhui Province between 2010 and 2012 to monitor their sensitivity to carbendazim. In total, 74 of 899 single-spore isolates F. asiaticum were found to be resistant to carbendazim. Resistant isolates were collected from all of the sampled sites except Hefei of Anhui Province. The overall frequency of carbendazim resistance was shown to be 8.2%. Of the 74 isolates, 1, 68, and 5 had low resistance (LR), moderate resistance (MR) ,and high resistance (HR), respectively, to carbendazim. Five types of point mutations (F167Y, E198L, E198K, F200Y, and E198Q) in the β2-tubulin gene conferring resistance to carbendazim were detected in the field-resistant isolates with frequencies of 89.2, 2.7, 4.1, 2.7, and 1.4%, respectively. The point mutations at codon 167, 198, or 200 of the β2-tubulin gene were correlated with different levels of carbendazim resistance. Some of the sensitive and resistant isolates appeared to possess different biological characteristics; however, these might not be due to resistance. Because carbendazim resistance was generally widespread throughout Anhui Province, the sensitivity of F. asiaticum populations to carbendazim should be constantly monitored for the development of carbendazim resistance in natural populations.

An alkaline phosphatase mutant of Pseudomonas aeruginosa. 1. Effects of regulatory, structural, and environmental shifts on enzyme function

1978 ◽  
Vol 24 (4) ◽  
pp. 427-432 ◽  
Author(s):  
M. L. Marceau-Day ◽  
D. F Day ◽  
J. M. Ingram
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Alkaline Phosphatase ◽  
Core Region ◽  
Significant Activity ◽  
Wild Type ◽  
Glycerol Phosphate ◽  
The Core ◽  
Nitrophenyl Phosphate ◽  
Mutant Cells

An alkaline phosphatase mutant of Pseudomonas aeruginosa exhibiting both regulatory and catalytic changes was isolated. Under repression conditions (i.e. high inorganic phosphate (Pi)) the mutant culture produced an alkaline phosphatase (APase) displaying significant activity against both β-glycerol phosphate (βGP) and p-nitrophenyl phosphate (pNPP), while the wild type displayed no activity directed towards these substrates under the same conditions. In vivo, the mutant enzyme's ratio of specific activities was 45:1 in favour of βGP versus pNPP, whereas this ratio was reversed to 1:9 βGP versus pNPP for the same enzyme isolated from mutant cells. In addition, the kinetic parameters and stability requirements for the mutant-derived enzyme was altered in comparison with those of the wild type. A study of lipopolysaccharide(LPS) preparations from both the mutant and wild type indicated the mutant to be deficient in the core region of its LPS. The authors propose that the modifications in the catalytic activity of the mutant enzyme, demonstrated in vivo, are due to a change in the enzyme's microenvironment.

Abscisic acid resistant mutants in the fern Ceratopteris: characterization and genetic analysis

1985 ◽  
Vol 63 (9) ◽  
pp. 1582-1585 ◽  
Author(s):  
Leslie G. Hickok
Keyword(s):  
Abscisic Acid ◽  
Genetic Analysis ◽  
Sexual Differentiation ◽  
Double Mutant ◽  
Acid Resistance ◽  
The Other ◽  
Additive Effects ◽  
Wild Type ◽  
Resistant Mutants ◽  
Moderate Resistance

Abscisic acid normally inhibits growth and male sexual differentiation (antheridia formation) in gametophytes of the fern Ceratopteris. Abscisic acid resistant mutants show increased growth and sexual differentiation in comparison with the wild type when cultured in the presence of abscisic acid. Two different mutants that confer resistance to the effects of abscisic acid have been fully characterized. One shows moderate resistance and the other strong resistance. The mutations involve separate but linked loci. Recombination between the loci yields double mutant (cis) recombinants that exhibit additive effects and show exceptional levels of abscisic acid resistance.

scholarly journals Isolation of Rifampin-Resistant Mutants ofListeria monocytogenes and Their Characterization byrpoB Gene Sequencing, Temperature Sensitivity for Growth, and Interaction with an Epithelial Cell Line

1999 ◽  
Vol 37 (9) ◽  
pp. 2913-2919 ◽  
Author(s):  
Robert Morse ◽  
Karen O’Hanlon ◽  
Mumtaz Virji ◽  
Matthew D. Collins
Keyword(s):  
Type Strain ◽  
Wild Type Strain ◽  
Point Mutations ◽  
Gene Sequencing ◽  
Epithelial Cell Line ◽  
Wild Type ◽  
Partial Sequencing ◽  
Resistant Mutants ◽  
Oflisteria Monocytogenes ◽  
Rna Polymerase Holoenzyme

The sequence of the rpoB gene from Listeria monocytogenes was determined. Rifampin-resistant (Rifr) mutants arising from L. monocytogenes cultures exposed to rifampin were isolated, and by partial sequencing of their rpoB genes, seven different point mutations affecting five different amino acids (473Asp→Asn or Gly, 479Gly→Asp, 483His→Tyr or Leu, 528Ile→Phe, and 530Ser→Tyr), which led to MICs of 0.5 to 100 μg/ml for the organisms, were determined. These mutants showed various deficiencies for growth at 42°C, with only one being comparable to the wild-type strain. The interaction of these Rifr mutants with human Caco-2 cells was examined by using an immunofluorescence technique. Three mutants failed to interact, while three showed a reduced interaction compared to that of the wild type. It is believed that these pleiotropic phenotypes have arisen as a result of mutations within the DNA-dependent RNA polymerase holoenzyme.

scholarly journals Molecular Regions Controlling the Activity of Cng Channels

2001 ◽  
Vol 118 (2) ◽  
pp. 183-192 ◽  
Author(s):  
Holger Möttig ◽  
Jana Kusch ◽  
Thomas Zimmer ◽  
Annette Scholle ◽  
Klaus Benndorf
Keyword(s):  
Energy Difference ◽  
Core Region ◽  
The Other ◽  
Wild Type ◽  
The Core ◽  
Retinal Photoreceptors ◽  
Channel Opening ◽  
Main Portion ◽  
The Difference ◽  
Α Subunits

The α subunits of CNG channels of retinal photoreceptors (rod) and olfactory neurons (olf) are proteins that consist of a cytoplasmic NH2 terminus, a transmembrane core region (including the segments S1–S6), and a cytoplasmic COOH terminus. The COOH terminus contains a cyclic nucleotide monophosphate binding domain NBD) that is linked by the C-linker (CL) to the core region. The binding of cyclic nucleotides to the NBD promotes channel opening by an allosteric mechanism. We examined why the sensitivity to cGMP is 22 times higher in olf than in rod by constructing chimeric channels and determining the [cGMP] causing half maximum channel activity (EC50). The characteristic difference in the EC50 value between rod and olf was introduced by the NH2 terminus and the core-CL region, whereas the NBD showed a paradoxical effect. The difference of the free energy difference Δ(ΔG) was determined for each of these three regions with all possible combinations of the other two regions. For rod regions with respect to corresponding olf regions, the open channel conformation was destabilized by the NH2 terminus (Δ(ΔG) = −1.0 to −2.0 RT) and the core-CL region (Δ(ΔG) = −2.0 to −2.9 RT), whereas it was stabilized by the NBD (Δ(ΔG) = 0.3 to 1.1 RT). The NH2 terminus deletion mutants of rod and olf differed by Δ(ΔG) of only 0.9 RT, whereas the wild-type channels differed by the much larger value of 3.1 RT. The results show that in rod and olf, the NH2 terminus, the core-CL region, and the NBD differ by characteristic Δ(ΔG) values that do not depend on the specific composition of the other two regions and that the NH2 terminus generates the main portion of Δ(ΔG) between the wild-type channels.

scholarly journals Biological Characteristics and Molecular Mechanisms of Fludioxonil Resistance in Fusarium graminearum in China

Plant Disease ◽  
2020 ◽  
Vol 104 (9) ◽  
pp. 2426-2433
Author(s):  
F. Zhou ◽  
D. X. Li ◽  
H. Y. Hu ◽  
Y. L. Song ◽  
Y. C. Fan ◽  
...  
Keyword(s):  
Fusarium Graminearum ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Stop Codon ◽  
Point Mutations ◽  
Premature Stop Codon ◽  
Cross Resistance ◽  
Alternative Mechanism ◽  
Head Blight ◽  
Resistant Mutants

Fusarium graminearum is the primary causal agent of Fusarium head blight (FHB) of wheat. The phenylpyrrole fungicide fludioxonil is not currently registered for the management of FHB in China. The current study assessed the fludioxonil sensitivity of a total of 53 F. graminearum isolates collected from the six most important wheat-growing provinces of China during 2018 and 2019. The baseline fludioxonil sensitivity distribution indicated that all of the isolates were sensitive, exhibiting a unimodal cure with a mean effective concentration for 50% inhibition value of 0.13 ± 0.12 μg/ml (standard deviation). Five fludioxonil-resistant mutants were subsequently induced by exposure to fludioxonil under laboratory conditions. Ten successive rounds of subculture in the absence of the selection pressure indicated that the mutation was stably inherited. However, the fludioxonil-resistant mutants were found to have reduced pathogenicity, higher glycerol accumulation, and higher osmotic sensitivity than the parental wild-type isolates, indicating that there was a fitness cost associated with fludioxonil resistance. In addition, the study also found a positive cross resistance between fludioxonil, procymidone, and iprodione, but not with other fungicides such as boscalid, carbendazim, tebuconazole, and fluazinam. Sequence analysis of four candidate target genes (FgOs1, FgOs2, FgOs4, and FgOs5) revealed that the HBXT2R mutant contained two point mutations that resulted in amino acid changes at K223T and K415R in its FgOs1 protein, and one point mutation at residue 520 of its FgOs5 protein that resulted in a premature stop codon. Similarly, the three other mutants contained point mutations that resulted in changes at the K192R, K293R, and K411R residues of the FgOs5 protein but none in the FgOs2 and FgOs4 genes. However, it is important to point out that the FgOs2 and FgOs4 expression of all the fludioxonil-resistant mutants was significantly (P < 0.05) downregulated compared with the sensitive isolates (except for the SQ1-2 isolate). It was also found that one of the resistant mutants did not have changes in any of the sequenced target genes, indicating that an alternative mechanism could also lead to fludioxonil resistance.

Emergence of phenotypic variants upon mismatch repair disruption in Pseudomonas aeruginosa

Microbiology ◽  
2004 ◽  
Vol 150 (5) ◽  
pp. 1327-1338 ◽  
Author(s):  
Andrea M. Smania ◽  
Ignacio Segura ◽  
Roberto J. Pezza ◽  
Cecilia Becerra ◽  
Inés Albesa ◽  
...  
Keyword(s):  
Mismatch Repair ◽  
High Frequency ◽  
Type Strain ◽  
Wild Type Strain ◽  
Point Mutations ◽  
Repair System ◽  
Wild Type ◽  
Antibiotic Resistant ◽  
Prolonged Incubation ◽  
Resistant Mutants

MutS is part of the bacterial mismatch repair system that corrects point mutations and small insertions/deletions that fail to be proof-read by DNA polymerase activity. In this work it is shown that the disruption of the P. aeruginosa mutS gene generates the emergence of diverse colony morphologies in contrast with its parental wild-type strain that displayed monomorphic colonies. Interestingly, two of the mutS morphotypes emerged at a high frequency and in a reproducible way and were selected for subsequent characterization. One of them displayed a nearly wild-type morphology while the other notably showed, compared with the wild-type strain, increased production of pyocyanin and pyoverdin, lower excretion of LasB protease and novel motility characteristics, mainly related to swarming. Furthermore, it was reproducibly observed that, after prolonged incubation in liquid culture, the pigmented variant consistently emerged from the mutS wild-type-like variant displaying a reproducible event. It is also shown that these P. aeruginosa mutS morphotypes not only displayed an increase in the frequency of antibiotic-resistant mutants, as described for clinical P. aeruginosa mutator isolates, but also generated mutants whose antibiotic-resistant levels were higher than those measured from spontaneous resistant mutants derived from wild-type cells. It was also found that both morphotypes showed a decreased cytotoxic capacity compared to the wild-type strain, leading to the emergence of invasive variants. By using mutated versions of a tetracycline resistance gene, the mutS mutant showed a 70-fold increase in the reversion frequency of a +1 frameshift mutation with respect to its parental wild-type strain, allowing the suggestion that the phenotypical diversity generated in the mutS population could be produced in part by frameshift mutations. Finally, since morphotypical diversification has also been described in clinical isolates, the possibility that this mutS diversification was related to the high frequency hypermutability observed in P. aeruginosa CF isolates is discussed.

Intramitochondrial Viruses of Reptilian Cell Origin

1972 ◽  
Vol 30 ◽  
pp. 318-319
Author(s):  
Philip D. Lunger ◽  
H. Fred Clark
Keyword(s):  
Particle Production ◽  
Outer Zone ◽  
Density Variation ◽  
Core Region ◽  
Mitochondrial Membranes ◽  
Virus Particles ◽  
The Core ◽  
Vipera Russelli ◽  
Maturation Stages ◽  
Type Particle

In the course of fine structure studies of spontaneous “C-type” particle production in a viper (Vipera russelli) spleen cell line, designated VSW, virus particles were frequently observed within mitochondria. The latter were usually enlarged or swollen, compared to virus-free mitochondria, and displayed a considerable degree of cristae disorganization.Intramitochondrial viruses measure 90 to 100 mμ in diameter, and consist of a nucleoid or core region of varying density and measuring approximately 45 mμ in diameter. Nucleoid density variation is presumed to reflect varying degrees of condensation, and hence maturation stages. The core region is surrounded by a less-dense outer zone presumably representing viral capsid.Particles are usually situated in peripheral regions of the mitochondrion. In most instances they appear to be lodged between loosely apposed inner and outer mitochondrial membranes.

scholarly journals CHROMOSOMAL BASIS OF THE MEROZYGOSITY IN A PARTIALLY DIPLOID MUTANT OF PNEUMOCOCCUS

Genetics ◽  
1975 ◽  
Vol 80 (4) ◽  
pp. 667-678
Author(s):  
Mary Lee S Ledbetter ◽  
Rollin D Hotchkiss
Keyword(s):  
High Efficiency ◽  
Point Mutations ◽  
Resistant Mutant ◽  
Chromosomal Marker ◽  
Structural Abnormality ◽  
C Cells ◽  
Wild Type ◽  
Chromosomal Locus ◽  
Low Efficiency ◽  
Derivatives Of

ABSTRACT A sulfonamide-resistant mutant of pneumococcus, sulr-c, displays a genetic instability, regularly segregating to wild type. DNA extracts of derivatives of the strain possess transforming activities for both the mutant and wild-type alleles, establishing that the strain is a partial diploid. The linkage of sulr-c to strr-61, a stable chromosomal marker, was established, thus defining a chromosomal locus for sulr-c. DNA isolated from sulr-c cells transforms two mutant recipient strains at the same low efficiency as it does a wild-type recipient, although the mutant property of these strains makes them capable of integrating classical "low-efficiency" donor markers equally as efficiently as "high efficiency" markers. Hence sulr-c must have a different basis for its low efficiency than do classical low efficiency point mutations. We suggest that the DNA in the region of the sulr-c mutation has a structural abnormality which leads both to its frequent segregation during growth and its difficulty in efficiently mediating genetic transformation.

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