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1.
Mutants ofUstilago maydis with low resistance to tridemorph isolated in a mutation frequency of 7x 10-6 after UV-irradiation and selection on media containing 25 μg ml-1 tridemorph. Genetic analysis with nine such mutant isolates resulted in the identification of two unlinked chromosomal loci,U/tdm- 1 andU/tdm- 2. TheU/tdm mutations are responsible for low resistance levels to tridemorph (resistance factor, Rf, of 3 or 5 based on effective concentration causing a 50% reduction in the growth rate (EC50) or minimal inhibitory concentration (MIC) values, respectively) and low to moderate level of resistance to fenpropimorph (Rf 10 or 16 based on MIC or EC50, respectively) and fenpropidin (Rf 5 or 11 based on MIC or EC50, respectively). Haploid strains carrying bothU/tdm mutations exhibit higher levels of resistance to the above fungicides, indicating interallelic interaction between nonallelic genes. Crosses between mutants carrying theU/tdm- genes with compatible isolates carrying theU/fpm- 1 orU/fpm- 2 mutations, which were found in previous work to carry fenpropimorph resistance, yielded in all cases a large number of recombinants with wild-type sensitivity, indicating that the mutant genes involved were not allelic. Cross-resistance studies with the inhibitors of C-14 demethylase showed that. the U/tdm-mutations were responsible for increased sensitivity to the triazoles triadimefon, triadimenol, propiconazole and flusilazole, and to the pyridine pyrifenox. Study of gene effect on the fitness ofU. maydis showed thatU/tdm-mutations appeared to be pleiotropic, having more or less adverse effects on growth rate in liquid culture and pathogenicity on young corn plants.  相似文献   

2.
Fenpropimorph-resistant mutants of Ustilago maydis were obtained at high frequency (30 × 10−6) after UV-irradiation followed by selection on media containing fenpropimorph (50 μ g mL−1). Genetic analysis of 30 such mutants resulted in the identification of two unlinked chromosomal loci, the U/fpm -1 locus with two allelic genes ( U/fpm- 1A and U/fpm -1B) and the U/fpm -2 locus. The mutant genes U/fpm- 1A and U/fpm -2 are responsible for high resistance levels (Rf: 75–100 or 257–286 based on MICs or ED50s, respectively), while the U/fpm -1B mutation gives only a small reduction (approximately 7–10-fold) in fenpropimorph sensitivity. Cross-resistance studies with other SBIs showed that the major gene ( U/fpm- 1A and U/fpm -2) mutants were cross-resistant to the related compound fenpropidin (Rf: 15–20 or 53–66 based on MICs or ED50s values, respectively) and to tridemorph (Rf: 5 or 7.1–9.5 based on MICs or ED50s values, respectively), but not to the inhibitors of steps of ergosterol biosynthesis preceding the Δ14-reductase. The minor gene ( U/fpm -1B) mutants also had low-level resistance (approximately 5-fold) to tridemorph and to fenpropidin, but in contrast with the major gene mutants they were 2–10 times more sensitive to the triazoles studied (triadimefon, triadimenol, propiconazole and flusilazole) and to the pyridine, pyrifenox.
Studies of the fitness of U. maydis mutants showed that in major gene mutants, resistance was not associated with changes in growth rate in liquid culture or pathogenicity on young maize plants. The minor gene mutation reduced significantly the growth rate in liquid culture and the pathogenicity, either in homozygous or heterozygous condition in dikaryotic mycelium.  相似文献   

3.
Mutants of Botrytis cinerea and Ustilago maydis highly resistant to fludioxonil were isolated at a high frequency, after nitrosoguanidine or UV mutagenesis, respectively, and selection on media containing fludioxonil. Tests on the response of mutant strains to high osmotic pressure resulted in the identification of two fludioxonil-resistant phenotypes (FLDosm/s and FLDosm/r), regarding the sensitivity to high osmolarity. Approximately 95% of fludioxonil-resistant mutants were found to be more sensitive to high osmotic pressure than the wild-type parent strains. Genetic analysis of phenylpyrrole-resistance in the phytopathogenic basidiomycete U. maydis, showed that fludioxonil-resistance was coded by three unlinked chromosomal loci (U/fld-1, U/fld-2 and U/fld-3), from which only the U/fld-1 mutation coded an osmotic sensitivity similar to that of the wild-types. Cross-resistance studies with fungicides from other chemical groups showed that the mutations for resistance to phenylpyrroles affect the sensitivity of mutant strains to the aromatic hydrocarbon and dicarboximide fungicides, but not to the benzimidazoles, anilinopyrimidines, phenylpyridinamines, hydroxyanilides or the sterol biosynthesis inhibiting fungicides. A study of fitness parameters in the wild-type and fludioxonil-resistant mutants of B. cinerea, showed that all osmotic sensitive (B/FLDosm/s) isolates had significant reductions in the characteristics determining saprophytic fitness such as mycelial growth, sporulation, conidial germination and sclerotial production. Contrary to that, with the exception of mycelial growth, the fitness parameters were unaffected or only slightly affected in most of the osmotic resistant (B/FLDosm/r) isolates. Tests on cucumber seedlings showed that the osmotic-sensitive strains were significantly less pathogenic compared with the wild-type and B/FLDosm/r strains of B. cinerea. Preventative applications of the commercial products Saphire 50 WP (fludioxonil) and Rovral 50 WP (iprodione) were effective against lesion development on cotyledons by the wild-type and the mutant strains of B. cinerea that were resistant to the anilinopyrimidine cyprodinil (B/CPL-27) and to the hydroxyanilide fenhexamid (B/FNH-21), but ineffective, even at high concentrations, against disease caused by the fludioxonil-resistant isolates (B/FLD) and a mutant strain resistant to the dicarboximide iprodione (B/IPR-1). Experiments on the stability of the fludioxonil-resistant phenotype showed a reduction of resistance, mainly in osmotic-sensitive isolates, when the mutants were grown on inhibitor-free medium. A rapid recovery of the high resistance was observed after mutants were returned to the selection medium. Studies on the competitive ability of mutant isolates against the wild-type parent strain of B. cinerea, by applications of a mixed conidial population, showed that, in vitro, all mutants were less competitive than the wild-type strain. However, the competitive ability of osmotic-resistant mutants was higher than the osmotic-sensitive ones. Furthermore, competition tests, in planta, showed a significant reduction of the frequency of both phenylpyrrole-resistant phenotypes, with a respective increase in the population of the wild-type strain of the pathogen.  相似文献   

4.

Sensitivity and inherent resistance risk of Alternaria solani to fludioxonil, cross-resistance profiles and the potential implications of resistance mutations on fitness parameters were investigated. Fludioxonil was highly effective against a wild type A. solani field strain both in vitro (EC50?=?0.05 μg/mL) and in preventive applications on artificially inoculated tomato fruit. Mutants with low [Resistance factor (Rf): 15 based on EC50], medium (Rf: 150–300) and high (Rf: > 1000) levels of phenylpyrrole resistance were isolated from the wild type strain at high frequencies following mutagenesis with UV irradiation and selection on fludioxonil containing medium. Resistant isolates retained their resistance levels even after 9 subcultures on fungicide-free growth medium while they could express their resistant phenotypes in planta. Investigation of cross-resistance relationships showed that fludioxonil resistance mutations also reduce the sensitivity of mutant strains to the aromatic hydrocarbon fungicide quintozene as well as the dicarboximides iprodione and vinclozolin. No cross-resistance was observed between fludioxonil and fungicides with different modes of action such as the sterol biosynthesis inhibitors (DMIs) imazalil and flusilazole and the carboxamide boscalid. All fludioxonil resistant isolates were more sensitive to the anilinopyrimidine pyrimethanil, while only two isolates were less sensitive to the QoI pyraclostrobin compared to the wild-type strain. Study of fitness determining parameters showed that resistance mutation(s) had no adverse effects on mycelial growth, conidial germination and sensitivity to osmotic stress while they had a pleiotropic effect on virulence and conidia production in resistant mutants. Results of the present study indicate that fludioxonil is a highly effective fungicide against A. solani, while the risk of resistance development to this fungicide is considered to be medium making fludioxonil an ideal alternative to high risk fungicides such as boscalid and pyraclostrobin whose performance against early blight has already been compromised by resistance development.

  相似文献   

5.
水稻稻瘟病菌对烯肟菌胺的抗性风险评估及抗性机制初探   总被引：2，自引：0，他引：2  
 采用菌丝生长速率法测定了100株采自我国主要水稻产区的水稻稻瘟病菌对烯肟菌胺的敏感性, 结果表明, 其EC50分布于0.011 1~0.295 6 μg·mL-1, 平均EC50=(0.078 6±0.056 1) μg·mL-1。供试菌株对烯肟菌胺的敏感性分布呈单侧峰曲线, 未出现抗药性亚群体, 可将该曲线作为稻病瘟菌对烯肟菌胺的敏感性基线。通过室内药剂驯化获得了7株抗药突变体, 突变频率为1.11×10-4, 其中2株高抗突变体NJ0811-I和A10的抗性水平大于1 000倍, 抗药性性状能稳定遗传, 致病力显著弱于其亲本菌株;5株低抗突变体抗性水平在2.05～4.55倍之间, 抗药稳定性差, 适合度与亲本无显著性差异。交互抗药性结果表明, 烯肟菌胺与嘧菌酯存在正交互抗药性, 与田间防治稻瘟病常用药剂稻瘟灵、异稻瘟净无交互抗药性。综合分析表明, 稻瘟病菌对烯肟菌胺可能存在低到中等抗性风险。进一步克隆了抗药突变体及其亲本的cytb基因, CYTB氨基酸序列比对结果表明, 2株高抗突变体均在143位由甘氨酸突变为丝氨酸(G143S), 建立了高抗菌株的AS-PCR分子检测方法;而5株低抗突变体cytb基因未发生点突变, 推测可能存在其他的抗性分子机制。  相似文献   

6.
The genetics of the responses of the barley powdery mildew pathogen,Erysiphe graminis f.sp.hordei, to three morpholine-type fungicides were studied. Resistances to a phenylpropylamine fungicide, fenpropidin, and to a morpholine, fenpropimorph, co-segregated in crosses of a sensitive isolate, DH14, with each of two resistant ones, CC151 and CC152. In the cross CC151×DH14, the results were consistent with resistance to both fungicides being controlled by a single gene, at a locus namedFenl. In the other cross, CC152×DH14, the genetics of resistance were more complicated; the data were consistent with the segregation of two complementary, unlinked genes which each conferred resistance to both fungicides. Fenpropidin-resistant progeny of CC151×DH14 were significantly more resistant to fenpropimorph than were fenpropidin-resistant progeny of CCI 52×DH14, although the resistant progeny of the two crosses did not differ significantly in their level of fenpropidin resistance. Fenpropidin-resistant progeny of CC151×DH14 were significantly more resistant to another morpholine, tridemorph, than were fenpropidin-sensitive progeny, but this was not the case for CC152×DH14. Resistance to triadimenol, a C14 demethylation-inhibitor (DMI) fungicide, segregated in both crosses. Triadimenol resistance appeared to be controlled by one gene in each cross and was not associated with morpholine resistance. CC151×DH14 also segregated for eight avirulence genes. Two of these matched theMla6 resistance, while one gene matched a previously unknown resistance in a Pallas near-isogenic line, P17, which also carries a known resistance gene,Mlk. Fenl was not significantly linked to the triadimenol resistance gene,Tdl(a), or to any of the eight avirulence genes.Avr a6 1, Avr a12 ,Avr La ,Avr p17 andTdl(a) were linked, as wereAvr a 10 andAvr k .Abbreviations ED50 median effective dose - Fpd fenpropidin - Fpm fenpropimorph - PCA principal components analysis - Tdm tridemorph  相似文献   

7.
Demethylation inhibitor (DMI) fungicides are used to control brown rot in stone fruit worldwide. However, their specific mode of action can select resistant isolates of Monilinia fructicola. Monilinia fructicola resistant to DMI fungicides are associated with a fitness cost in the absence of selective pressure, indicating that the sensitive population can be re-established when discontinuing the fungicide in the field. This work aimed to build up the sensitive population of M. fructicola after discontinuing the use of tebuconazole for successive crop seasons. The sensitivity of M. fructicola to tebuconazole was assessed in four commercial peach orchards in Paraná and São Paulo States from 2012/13 to 2015/16. Different fungicide programmes were used and DMI fungicides were discontinued from 2013/14. The sensitivity of M. fructicola to tebuconazole was assessed by a mycelial growth assay in vitro and by determining the frequency of the G461S mutation in the MfCYP51 gene. The isolates from Paraná had high sensitivity to the fungicide across all seasons and the frequency of the G461S mutation remained below 5%. The isolates from São Paulo were highly resistant in the 2012/13 season; however, there was a gradual decline until 2015/16. In addition, the G461S mutation frequency in Sao Paulo State was about 80% in the 2012/13 season, but reduced until it was completely undetectable in 2015/16. These results provide evidence that resistance can be managed in orchards with high selective pressure to tebuconazole after discontinuing the use of the fungicide for at least 3 years.  相似文献   

8.
BACKGROUND: Resistance to carbendazim and other benzimidazole fungicides in Botrytis cinerea (Pers. ex Fr.) and most other fungi is usually conferred by mutation(s) in a single chromosomal β‐tubulin gene, often with several allelic mutations. In Fusarium graminearum Schwade, however, carbendazim resistance is not associated with a mutation in the corresponding β‐tubulin gene. RESULTS: The β‐tubulin gene conferring carbendazim resistance in B. cinerea was cloned and connected with two homologous arms of the β‐tubulin gene of F. graminearum by using a double‐joint polymerase chain reaction (PCR). This fragment was transferred into F. graminearum via homologous double crossover at the site where the β‐tubulin gene of F. graminearum is normally located (the β‐tubulin gene of F. graminearum had been deleted). The transformants were confirmed and tested for their sensitivity to carbendazim. CONCLUSION: The β‐tubulin gene conferring carbendazim resistance in B. cinerea could not express this resistance in F. graminearum, as transformants were still very sensitive to carbendazim. Copyright © 2010 Society of Chemical Industry  相似文献   

9.
The molecular basis of resistance to benzimidazole fungicides with laboratory and field mutant isolates of Botrytis cinerea was investigated. After chemical mutagenesis with N-methyl-N-nitrosogouanidine (NMNG) two different benzimidazole-resistant phenotypes were isolated on media containing carbendazim or a mixture of carbendazim and diethofencarb. The mutant isolates from the fungicide-mixture-containing medium were moderately resistant to carbendazim with wild-type tolerance to diethofencarb while mutant isolates from carbendazim-containing medium were highly resistant to carbendazim but sensitive to diethofencarb. The studied field isolates were highly resistant to benzimidazoles and sensitive to diethofencarb. Study of fitness characteristics of benzimidazole highly-resistant isolates showed that the resistance mutation(s) had no apparent effect on fitness-determining parameters. Contrary to this, the moderately benzimidazole-resistant strains, with no increased diethofencarb sensitivity, had a significant reduction in certain ecological fitness-determining characteristics. Analysis of the sequence of the β-tubulin gene revealed two amino acid replacements in the highly benzimidazole-resistant mutants compared to that of the wild-type parent strain. One was the glutamic acid (GAG) to alanine (GCG) change at position 198 (E198A), identified in both laboratory and field highly benzimidazole-resistant isolates, a mutation previously implicated in benzimidazole resistance. The second was a novel benzimidazole resistance mutation of glutamic acid (GAG) to glycine (GGG) substitution at the same position 198 (E198G), identified in a highly benzimidazole-resistant laboratory mutant strain. Molecular analysis of the moderately benzimidazole-resistant strains revealed no mutations at the β-tubulin gene. A novel diagnostic PCR-RFLP assay utilising a BsaI restriction site present in the benzimidazole-sensitive (E198) but absent in both resistant genotypes (E198G and E198A) was developed for the detection of both amino acid replacements at the β-tubulin gene.  相似文献   

10.
BACKGROUND: QoI fungicides, inhibitors of mitochondrial respiration, are considered to be at high risk of resistance development. In several phytopathogenic fungi, resistance is caused by mutations (most frequently G143A) in the mitochondrial cytochrome b (cytb) gene. The genetic and molecular basis of QoI resistance were investigated in laboratory and field mutants of Botryotinia fuckeliana (de Bary) Whetz. exhibiting in vitro reduced sensitivity to trifloxystrobin. RESULTS: B. fuckeliana mutants highly resistant to trifloxystrobin were obtained in the laboratory by spontaneous mutations in wild‐type strains, or from naturally infected plants on a medium amended with 1–3 mg L?1 trifloxystrobin and 2 mM salicylhydroxamic acid, an inhibitor of alternative oxidase. No point mutations were detected, either in the complete nucleotide sequences of the cytb gene or in those of the aox and Rieske protein genes of laboratory mutants, whereas all field mutants carried the G143A mutation in the mitochondrial cytb gene. QoI resistance was always maternally inherited in ascospore progeny of sexual crosses of field mutants with sensitive reference strains. CONCLUSIONS: The G143A mutation in cytb gene is confirmed to be responsible for field resistance to QoIs in B. fuckeliana. Maternal inheritance of resistance to QoIs in progeny of sexual crosses confirmed that it is caused by extranuclear genetic determinants. In laboratory mutants the heteroplasmic state of mutated mitochondria could likely hamper the G143A detection, otherwise other gene(s) underlying different mechanisms of resistance could be involved. Copyright © 2012 Society of Chemical Industry  相似文献   

11.
The distribution of ABC (ATP-binding cassette) transporter genes among several taxonomically distinct phytopathogenic fungi was investigated by Southern blot hybridization, polymerase chain reaction assays and partial sequencing. Consensus sequences of the ABC transporter gene, which might be concerned with multidrug resistance against fungicides and with pathogenicity in phytopathogenic fungi, were found in all of the examined phytopathogenic fungi, which belonged to the Mastigomycotina, Ascomycotina, Basidiomycotina and Deuteromycotina. Received 24 August 2000/ Accepted in revised form 5 December 2000  相似文献   

12.
X. Cui  J. Shao  X. Lu  Q. Meng  X. Liu 《Plant pathology》2014,63(6):1365-1373
A total of 1511 isolates of Phytophthora capsici were collected from farms with no history of exposure to the carboxylic acid amide (CAA) fungicides in 32 provinces in China during 2006 to 2013. All 1511 isolates were assayed for mating type and 403 were assayed for sensitivity to dimethomorph (DMM) and metalaxyl. The DMM EC50 values ranged from 0·126 to 0·339 μg mL?1. Both A1 and A2 mating types were detected on the same farms in four provinces and with a 1:1 ratio. Most isolates were sensitive to metalaxyl but a few exhibited intermediate resistance or resistance to metalaxyl. The segregation of DMM resistance and sensitivity among 337 progeny obtained from hybridization or self‐crossing in vitro indicated that the resistance of P. capsici to DMM is controlled by two dominant genes. Eighteen progeny that were derived from hybridization differed in DMM sensitivity and in fitness. Some progeny were as fit as parental isolates. Given the distribution of mating types and therefore the potential for sexual reproduction, the control of resistance by two dominant genes, and the fitness of hybrid progeny, the risk of P. capsici populations developing DMM resistance in China is substantial.  相似文献   

13.
浙江省果蔬灰葡萄孢对啶酰菌胺的抗性   总被引：1，自引：0，他引：1  
以2004—2006年从浙江、江苏等地采集的灰葡萄孢对啶酰菌胺的敏感性基线[EC50 = (1.07 ± 0.11) mg/L]为依据,采用菌丝生长速率法连续监测了浙江省果蔬灰葡萄孢群体对啶酰菌胺的敏感性变化。结果表明:浙江省果蔬灰葡萄孢对啶酰菌胺的抗性发展迅速,2012—2013年和2017—2018年的平均EC50值分别为 (5.23 ± 7.79) 和 (24.30 ± 49.33) mg/L。其中,2012—2013年的抗药性菌株频率为15.3%,且均为低水平抗性 (LR) 菌株;而2017—2018年的抗药性频率上升至53.2%,并出现了7.5%的中等水平抗性 (MR) 菌株和1.3%的高水平抗性 (HR) 菌株。啶酰菌胺抗性菌株的菌丝生长速率、产孢量、产菌核数和致病力与敏感菌株相比均无显著差异。抗药性分子机制研究表明:啶酰菌胺抗性菌株的琥珀酸脱氢酶B亚基 (SDH B) 均发生了点突变,共包括H272R、P225F和N230I 3种类型,其中H272R型突变占88.5%;其SDH A和SDH D均未发生点突变;而SDH C的突变 (G85A + I93V + M158V + V168I) 与对药剂敏感性之间无明显联系。  相似文献   

14.
自1976年以来,三唑酮一直就是我国防治小麦白粉病的主要药剂.1991年首次在山东省发现抗性菌株,之后其他地区也相继有抗药性菌株的报道.本实验室从1995年就开始监测小麦白粉菌对三唑酮的抗药性,研究结果表明,平均抗性水平和抗性菌株的频率均总体呈上升趋势[1-3].  相似文献   

15.
After chemical mutagenesis with N-methyl-N-nitrosoguanidine (MNNG) two phenotypes that were highly or moderately resistant to fenhexamid, were isolated from a wild-type strain of Botrytis cinerea, at a mutation frequency of 0.9 × 10–5. Resistance factors, based on EC50 values, were 460–570 and 10–15, respectively. The mutation(s) for resistance to fenhexamid did not affect the sensitivity of mutant strains to the benzimidazole benomyl, the phenylpyridinamine fluazinam, the anilinopyrimidine cyprodinil, the guanidine iminoctadine or to the sterol-biosynthesis-inhibiting fungicides fenarimol, fenpropimorph and tridemorph. On the contrary, an increased sensitivity (EC50 ratios of 0.2–0.6) of fenhexamid-resistant strains to the phenylpyrrole fludioxonil and the dicarboximide iprodione was observed. Study of fitness parameters of fenhexamid-resistant isolates of both phenotypic classes showed that these mutation(s) had no effect on mycelial growth and sensitivity to high osmolarity, but they did affect one or more of some other characteristics, such as sporulation, conidial germination and sclerotia production. In tests on cucumber seedlings under greenhouse conditions, all highly fenhexamid-resistant isolates tested presented decreased infection ability compared with the wild-type. Preventive applications of a commercial formulation of fenhexamid, Teldor 50 WP, were effective against lesion development on cotyledons by the wild-type, but ineffective, even in high concentrations, against disease caused by the fenhexamid-resistant isolates. The risk of resistance problems arising during commercial use of fenhexamid is discussed.  相似文献   

16.
BACKGROUND: It is possible that a single nucleotide polymorphism (SNP) (G143A mutation) in the cytochrome b gene could confer resistance to quinone outside inhibiting (QoI) fungicides (strobilurins) in rice blast fungus because this mutation caused a high level of resistance to fungicides such as azoxystrobin in Pyricularia grisea Sacc. and other fungal plant pathogens. The aim of this study was to survey Magnaporthe oryzae B Couch sp. nov. isolates in Japan for resistance to QoIs, and to try to develop molecular detection methods for QoI resistance. RESULTS: A survey on the QoI resistance among M. oryzae isolates from rice was conducted in Japan. A total of 813 single‐spore isolates of M. oryzae were tested for their sensitivity to azoxystrobin using a mycelial growth test on PDA. QoI fungicide resistance was not found among these isolates. The introduction of G143A mutation into a plasmid containing the cytochrome b gene sequence of rice blast fungus was achieved by site‐directed mutagenesis. Molecular diagnostic methods were developed for identifying QoI resistance in rice blast fungus using the plasmid construct. CONCLUSION: As the management of rice blast disease is often dependent on chemicals, the rational design of control programmes requires a proper understanding of the fungicide resistance phenomenon in field populations of the pathogen. Mutation of the cytochrome b gene of rice blast fungus would be specifically detected from diseased leaves and seeds using the molecular methods developed in this study. Copyright © 2009 Society of Chemical Industry  相似文献   

17.
In this study, the sensitivity of 218 isolates of Colletotrichum musae to imazalil and thiabendazole was evaluated, as well the fitness and competitive ability of less sensitive isolates. There was a positive correlation between the sensitivity to the two fungicides, but the isolates were more sensitive to imazalil. The estimated effective concentration of the fungicide able to inhibit mycelial growth by 50% (EC50) was used to select four isolates with the lowest and the highest values for both fungicides, which were considered as sensitive (S) and less sensitive (LS), respectively. The level of sensitivity was maintained after 10 successive transfers on fungicide-free medium. Both fungicides were effective in controlling the disease caused by S isolates of C. musae in detached banana fruit when recommended doses were used. However, only imazalil was able to control the disease caused by LS isolates. For both fungicides, analysis of fitness-related variables (mycelial growth, sporulation, germination, and virulence) showed no difference between the groups of S and LS isolates, but a large variation was observed within the group. The LS isolates to thiabendazole that showed a mutation (F200Y) in the β-tubulin gene did not have fitness penalties. Our results allow a better understanding of the sensitivity and fitness of isolates of C. musae from Brazil, and demonstrate the importance of periodic monitoring to determine the frequency of LS isolates in populations, aiming at more effective management of anthracnose in banana orchards in Brazil.  相似文献   

18.
为评价西瓜蔓枯病菌对啶酰菌胺的抗性风险,了解其抗性机理,室内通过药剂驯化方法获得2株啶酰菌胺的抗性突变体XF21-3和YC60-1,测定了抗性突变体的生物学特性,并通过对Sdh B基因片段的测序比对,分析了西瓜蔓枯病菌对啶酰菌胺的抗性机理。生物测定结果表明:啶酰菌胺对2株抗性突变体的EC50值分别为108和124 μg/mL,抗性倍数（RR）分别为1 007和1 347,均为高抗菌株;抗性突变体的菌丝生长速率和产孢量均大于亲本菌株,但其致病性与亲本菌株无显著差异,对外界环境渗透压的敏感性低于亲本菌株;此外,啶酰菌胺与萎锈灵、戊唑醇、乙霉威及醚菌酯之间均不存在交互抗性,但与噻呋酰胺之间存在交互抗性。Sdh B基因片段测序及比对结果表明,高抗性突变体中Sdh B亚基277位上的氨基酸所对应的碱基由CAC突变为TAC,即由组氨酸（His）突变为酪氨酸（Tyr）。研究表明,西瓜蔓枯病菌在药剂选择压力下容易形成啶酰菌胺的抗性群体,且抗性突变体的离体适合度高于亲本菌株,此外,啶酰菌胺与同类型杀菌剂噻呋酰胺之间存在交互抗性,因此认为西瓜蔓枯病菌对啶酰菌胺具有中等抗性风险;同时进一步验证了Sdh B亚基277位上的氨基酸突变（His→Tyr,CAC→TAC）是西瓜蔓枯病菌对啶酰菌胺产生抗性的原因。  相似文献   

19.
The objective of this work was to estimate the risk of a decrease in the efficacy of biocontrol as a result of selection pressure exerted by biocontrol agents on Botrytis cinerea, focusing on pyrrolnitrin, an antibiotic identified in diverse biocontrol agents having an effect on B. cinerea. To evaluate a possible decrease in sensitivity to pyrrolnitrin, 10 successive generations of five isolates of B. cinerea were produced in vitro in the presence of a sublethal dose (10 μg L?1) of the antibiotic. For one isolate, a significant reduction in the sensitivity to pyrrolnitrin at the fifth generation was observed with a resistance factor of c. 11. The production of 10 additional generations for four of these isolates, with increasing doses of pyrrolnitrin (100–4000 μg L?1), resulted in the development of variants of B. cinerea with high levels of resistance to the antibiotic (RF > 1000) and a reduced sensitivity in vitro to a pyrrolnitrin‐producing bacterium. Reverse adaptation of resistant variants after 10 additional generations in the absence of selection pressure was not observed, suggesting stability of the resistance. Comparison of the pyrrolnitrin‐resistant generations and their sensitive parental isolates for mycelial growth, sporulation and aggressiveness on plant tissues revealed that the high level of resistance to pyrrolnitrin resulted in a high fitness cost. Mycelial growth was reduced between 1·7 to 3·6 times and sporulation reduced 3·8 to 6·6 times that of sensitive parental isolates. Similarly, aggressiveness was 7 to 10 and 3 to 10 times lower for resistant isolates on tomato and apple, respectively. This study provides evidence that a fungal plant pathogen is able to gradually build up resistance to an antibiotic produced by a biocontrol agent.  相似文献   

20.
 Laboratory mutants of Cochliobolus heterostrophus resistant to iprodione were obtained after chemical mutageneses. All the mutants were able to grow on the medium amended with iprodione 100 μg/ml. They showed positive cross-resistance to procymidone and fludioxonil and were sensitive to high osmolarity. Crosses between the mutant and a wild-type strain revealed that the fungicide resistance and osmotic sensitivity traits were inherited by their offspring in a 1 : 1 mutant/wild type ratio, indicating that the mutant phenotypes in these strains were due to alteration at a single gene locus. Results from allelism tests indicated that three genes (Dic1, Dic2, Dic3) conferred the mutant phenotypes. Among them, Dic1 mutant strains were classified into three types on the basis of their phenotypes. The first type was moderately resistant to the fungicides and less sensitive to osmotic stress than the other Dic1 mutant strains. The second type showed moderate fungicide resistance, but growth was inhibited under lower osmotic stress (50 mM KCl). The other Dic1 mutant strains grew well on medium containing iprodione and fludioxonil even at a concentration of 100 μg/ml and were highly sensitive to osmotic stress. The Dic2 and Dic3 mutant strains had moderate resistance to the fungicides with low-level osmotic sensitivity. The Dic1 gene was epistatic to Dic2 and Dic3 for fungicide resistance and hypostatic to them for osmotic sensitivity. These results suggest that the osmoregulatory system is involved in fungicide resistance in laboratory mutants of C. heterostrophus. Received: March 14, 2002 / Accepted: August 13, 2002  相似文献   

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