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Genetics of streptomycin resistance in methicillin-sensitive multiply-resistant Staphylococcus aureus.

Streptomycin resistance was detected in 17 of 20 multiply-resistant Staphylococcus aureus isolates from a hospital in a southeastern Nigerian town. The isolates were uniformly sensitive to methicillin, erythromycin, gentamicin, mupirocin, ciprofloxacin and vancomycin but produced beta-lactamase and were resistant to other antimicrobial agents and harbored different plasmids which ranged in size and number from 1.0 to c, 40 kb and one to six respectively. Curing and transfer experiments demonstrated that streptomycin resistance (Smr) was located on plasmids in 15 of the 17 isolates. 16 Smr plasmids were isolated and characterized. They belonged to three distinct groups based on size and resistance phenotypes. Eight 4.4 kb plasmids encoded Smr only, three 4.7 kb plasmids encoded resistance to streptomycin and chloramphenicol (SmCm) and five 23.8 kb plasmids encoded resistance to streptomycin, kanamycin, neomycin, cadmium and beta-lactamase production (CPKNS). Restriction endonuclease analysis demonstrated that the 4.4 kb Smr plasmids were similar to one another and indistinguishable from pUB109, an incompatibility group 5 Smr plasmid, suggesting that they may also belong to incompatibility group 5. The SmCm and the CPKNS plasmid groups also gave identical restriction patterns with single and double enzyme digests. Further transfer experiments with one of the SmCm plasmids led to the isolation of a 4.4 kb Smr plasmid which was indistinguishable from the other 4.4 kb plasmids, suggesting that the SmCm plasmids are natural recombinants between a streptomycin and chloramphenicol resistance plasmid. The results demonstrate a multiple origin of streptomycin resistance in the S. aureus population studied.

Drug Resistance, Microbial↗

Whole-genome profiling of antimicrobial resistance and virulence determinants in extensively-drug resistant Pseudomonas aeruginosa isolates causing ventilator associated pneumonia in Egypt.

Among critically ill ICU patients under prolonged mechanical ventilation, Pseudomonas aeruginosa is one of the most common cause of ventilator-associated pneumonia (VAP), with antimicrobial pressure leading to emergence of multidrug, extensively drug and pandrug-resistant (PDR) strains. In Egypt, very little genomic data exist on P. aeruginosa associated with VAP. This study aimed at characterizing the antimicrobial resistance (AMR) determinants, virulence repertoire, MGEs, and sequence types of two highly drug-resistant Pseudomonas aeruginosa isolates, including one pandrug-resistant colistin-resistant isolate and one extensively drug-resistant colistin-susceptible isolate from respiratory tract of Egyptian ICU patients suffering from VAP. The two isolates were identified conventionally and confirmed to the species level using MALDI-TOF MS. Antibiotic susceptibility was assessed using the VITEK-2 Compact system and the broth microdilution method. Genome analysis was performed using PATRIC, ResFinder, CARD, and Mobile Element Finder. For both isolates, resistance was found to all antibiotics routinely tested, however, one isolate had high-level colistin resistance (MIC > 64 µg/mL), while the other isolate was still colistin susceptible. Whole-genome sequencing identified two rare sequence types, ST2023 and ST2685, both 6.5-7.6 Mb in size with a 66% GC content. The presence of 21 MGEs in the SRR36105565 genome shows that it has high genomic flexibility, including a broader resistome than other strains, such as blaVIM-2 and OXA variants, aminoglycoside-modifying enzymes, crpP, and disinfectant-resistance markers. Both isolates retained large virulence determinants including Type III and Type VI secretion systems, alginate regulation genes, quorum-sensing networks, and siderophore biosynthesis clusters. It also represents one of the first genomic studies of VAP associated PDR P. aeruginosa from Egypt. The combination of widespread AMR with intact virulence supports the potential value of future genomic surveillance efforts and improved antimicrobial stewardship in local ICUs.

Pneumonia, Ventilator-Associated↗

Transduction of antibiotic resistance including imipenem resistance by wild type phages from nosocomial strains of Pseudomonas aeruginosa.

In this report we describe transduction of antibiotic resistance determinants by three wild type bacteriophages isolated from three Pseudomonas aeruginosa strains. The strains showed evident plaques of a lysis caused by a bacteriophage. The strains were identified as lysogenic among 31 imipenem (IMP)-resistant P. aeruginosa strains isolated at the National Institute of Oncology in Bratislava. The carbenicillin (CAR) resistance determinant was transduced by all the three phages to four P. aeruginosa recipients-PAO-1670, ML-M-88, ML-1292 and ML-1008. The gentamicin (GEN) resistance was transduced to ML-1008 only. The kanamycin (KAN) resistance was transduced in the following systems (combinations): "phage AP-37 to M-88", "phage AP-38 to PAO-1670, ML-1292 and M-88", and "phage AP-40 to M-88". The IMP resistance determinant was transduced by all the three phages to P. aeruginosa recipient strains. All transductant colonies were tested for the presence of directly not selected but co-transduced resistance determinants. Whereas transductants selected on media with IMP were resistant to five antibiotics (IMP, CAR, streptomycin (STR), KAN and GEN), transductants selected on CAR, KAN, STR, or GEN were resistant to a block of four of these antibiotics but not to IMP.

Anti-Bacterial Agents↗

Genetics of resistance to anthracnose and identification of AFLP and RAPD markers linked to the resistance gene in PI 320937 germplasm of lentil (Lens culinaris Medikus).

Anthracnose, caused by Colletotrichum truncatum, is a major disease problem and production constraint of lentil in North America. The research was conducted to examine the resistance to anthracnose in PI 320937 lentil and to identify molecular markers linked to the resistance gene in a recombinant inbred line (RIL) population developed from a cross of Eston lentil, the susceptible parent, and PI 320937, the resistant parent. A total of 147 F(5:6) RILs were evaluated for resistance to anthracnose in the greenhouse using isolate 95B36 of C. truncatum. Bulked segregant analysis (BSA) strategy was employed and two contrasting DNA bulks were constructed based on greenhouse inoculation of F(5)-derived F(6) RILs. DNA from the parents and bulks were screened with 700 RAPD primers and seven AFLP primer combinations. Analysis of segregation data indicated that a major dominant gene was responsible for resistance to anthracnose while variations in the resistance level among RILs could be the influences of minor genes. We designate the major gene as LCt-2. MapMaker analysis produced two flanking RAPD markers OPEO6(1250) and UBC-704(700) linked to LCt-2 locus in repulsion (6.4 cM) and in coupling (10.5 cM), respectively. Also, three AFLP markers, EMCTTACA(350) and EMCTTAGG(375) in coupling, and EMCTAAAG(175) in repulsion, were linked to the LCt-2 locus. These markers could be used to tag the LCt-2 locus and facilitate marker-assisted selection for resistance to anthracnose in segregating populations of lentil in which PI 320937 was used as the source of resistance. Also, a broader application of the linked RAPD markers was also demonstrated in Indianhead lentil, widely used as a source of resistance to anthracnose in the breeding program at the Crop Development Centre, University of Saskatchewan. Further selection within the few F(5:6) lines should be effective in pyramiding one or several of the minor genes into the working germplasm of lentil, resulting in a more durable and higher level of resistance.

Chromosome Segregation↗

Resistance gene-analog polymorphism markers co-segregating with the YR5 gene for resistance to wheat stripe rust.

The Yr5 gene confers resistance to all races of the stripe rust pathogen ( Puccinia striiformis f. sp. tritici) of wheat in the United States. To develop molecular markers for Yr5, a BC(7):F(3) population was developed by backcrossing the Yr5 donor ' Triticum spelta album' (TSA) with the recurrent parent 'Avocet Susceptible' (AVS). Seedlings of the Yr5 near-isogenic lines (AVS/6* Yr5), AVS, TSA, and the BC(7):F(3) lines were tested with North American races of P. striiformis f. sp. tritici under controlled greenhouse conditions. The single gene was confirmed by a 1:2:1 segregation ratio for homozygous-resistant, heterozygous and homozygous-susceptible BC(7):F(3) lines. Genomic DNA was extracted from the parents (the Yr5 near-isogenic line and AVS) and 202 BC(7):F(3) lines. The resistance gene-analog polymorphism (RGAP) technique was used to identify molecular markers. The parents and the homozygous-resistant and homozygous-susceptible BC(7):F(3) bulks were used to identify putative RGAP markers for Yr5. Association of the markers with Yr5 was determined using segregation analysis with DNA from the individual BC(7):F(3) lines. Of 16 RGAP markers confirmed by segregation analysis with 109 BC(7):F(3) lines, and nine of the markers confirmed with an additional 93 BC(7):F(3) lines, three markers co-segregated with the resistance allele and three markers co-segregated with the susceptibility allele at the Yr5 locus. The other four markers were tightly linked to the locus. Analysis of a set of Chinese Spring nulli-tetrasomic lines with three markers that co-segregated with, or were linked to, the susceptibility allele confirmed that the Yr5 locus is on chromosome 2B. Of five RGAP markers that were cloned and sequenced, markers Xwgp-17 and Xwgp-18 that co-segregated with the Yr5 locus were co-dominant and had 98% homology with each other in both DNA and translated amino-acid sequences. The two markers had 97% homology with a resistance gene-like sequence from Aegilops ventricosa and had significant homology with many known plant resistance genes, resistance gene analogs and expressed sequence tags (ESTs) from wheat and other plant species. The markers Xwgp-17 and Xwgp-18 also had significant homology with the NB-ARC domain that is in several genes for plant resistance to diseases, nematode cell death and human apoptotic signaling. These markers should be useful to clone Yr5 and combine Yr5 with other genes for durable and superior resistance for the control of stripe rust.

Amino Acid Sequence↗

Comparative mapping of Phytophthora resistance loci in pepper germplasm: evidence for conserved resistance loci across Solanaceae and for a large genetic diversity.

Phytophthora capsici Leonian, known as the causal agent of the stem, collar and root rot, is one of the most serious problems limiting the pepper crop in many areas in the world. Genetic resistance to the parasite displays complex inheritance. Quantitative trait locus (QTL) analysis was performed in three intraspecific pepper populations, each involving an unrelated resistant accession. Resistance was evaluated by artificial inoculations of roots and stems, allowing the measurement of four components involved in different steps of the plant-pathogen interaction. The three genetic maps were aligned using common markers, which enabled the detection of QTLs involved in each resistance component and the comparison of resistance factors existing among the three resistant accessions. The major resistance factor was found to be common to the three populations. Another resistance factor was found conserved between two populations, the others being specific to a single cross. This comparison across intraspecific germplasm revealed a large variability for quantitative resistance loci to P. capsici. It also provided insights both into the allelic relationships between QTLs across pepper germplasm and for the comparative mapping of resistance factors across the Solanaceae.

Capsicum↗

Mapping QTL associated with resistance to Fusarium head blight in the Nanda2419 x Wangshuibai population. I. Type II resistance.

Scab disease caused by Fusarium spp. has been a major concern for both wheat producers and consumers. Deployment of scab-resistant varieties is the major strategy to curb this disease. To identify the scab resistance genes in wheat cv. Wangshuibai, we produced a F(6:7) recombinant inbred line (RIL) population by crossing Wangshuibai with the scab-susceptible cultivar Nanda2419. The RILs were evaluated for scab resistance in the field by single floret inoculation in two replicates in 2002 and one replicate in 2003. The number of diseased spikelets (NDS) and the length of diseased rachides (LDR) were investigated to reflect the Type II resistance. Among 654 simple sequence repeat (SSR) markers surveyed, 326 were found to be polymorphic between the parents. A partial molecular map was constructed with these markers that covered over 2,210 cM of the wheat genome. Six chromosome regions showed association with both NDS and LDR in a one-way anova analysis, even though the variation explained by them varied between the two traits. Eight intervals were detected for their association with Type II resistance through interval mapping, five of which were not identified in single-point analysis. The quantitative trait loci (QTL) with large effects were the ones in the interval of Xgwm533-3-Xgwm533-1 on chromosome 3B and in the interval of Xwmc539-Xbarc024 on chromosome 6B, whose alleles favoring resistance originate from Wangshuibai. In addition, a QTL whose resistance allele originated from Nanda2419 was consistently detected in the interval of Xs1021m-Xgwm47-1 on chromosome 2B. These results suggest that Wangshuibai is the major source for Type II resistance in this population. The markers associated with these QTL would facilitate the use of scab-resistant genes of Wangshuibai in scab resistance breeding programs of wheat.

Chromosome Mapping↗

Identification and mapping of resistance gene analogs (RGAs) in Prunus: a resistance map for Prunus.

The genetically anchored physical map of peach is a valuable tool for identifying loci controlling economically important traits in Prunus. Breeding for disease resistance is a key component of most breeding programs. The identification of loci for pathogen resistance in peach provides information about resistance loci, the organization of resistance genes throughout the genome, and permits comparison of resistance regions among other genomes in the Rosaceae. This information will facilitate the breeding of resistant species of Prunus. A candidate gene approach was implemented for locating resistance loci in the genome of peach. Candidate genes representing NBS-LRR, kinase, transmembrane domain classes, as well as, pathogen response (PR) proteins and resistance-associated transcription factors were hybridized to a peach BAC library and mapped by using the peach physical map database and the Genome Database for Rosaceae (GDR). A resistance map for Prunus was generated and currently contains 42 map locations for putative resistance regions distributed among 7 of the 8 linkage groups.

Amino Acid Sequence↗

High-resolution mapping of a new brown planthopper (BPH) resistance gene, Bph18(t), and marker-assisted selection for BPH resistance in rice (Oryza sativa L.).

Brown planthopper (BPH) is a destructive insect pest of rice in Asia. Identification and the incorporation of new BPH resistance genes into modern rice cultivars are important breeding strategies to control the damage caused by new biotypes of BPH. In this study, a major resistance gene, Bph18(t), has been identified in an introgression line (IR65482-7-216-1-2) that has inherited the gene from the wild species Oryza australiensis. Genetic analysis revealed the dominant nature of the Bph18(t) gene and identified it as non-allelic to another gene, Bph10 that was earlier introgressed from O. australiensis. After linkage analysis using MapMaker followed by single-locus ANOVA on quantitatively expressed resistance levels of the progenies from an F2 mapping population identified with marker allele types, the Bph18(t) gene was initially located on the subterminal region of the long arm of chromosome 12 flanked by the SSR marker RM463 and the STS marker S15552. The corresponding physical region was identified in the Nipponbare genome pseudomolecule 3 through electronic chromosome landing (e-landing), in which 15 BAC clones covered 1.612 Mb. Eleven DNA markers tagging the BAC clones were used to construct a high-resolution genetic map of the target region. The Bph18(t) locus was further localized within a 0.843-Mb physical interval that includes three BAC clones between the markers R10289S and RM6869 by means of single-locus ANOVA of resistance levels of mapping population and marker-gene association analysis on 86 susceptible F2 progenies based on six time-point phenotyping. Using gene annotation information of TIGR, a putative resistance gene was identified in the BAC clone OSJNBa0028L05 and the sequence information was used to generate STS marker 7312.T4A. The marker allele of 1,078 bp completely co-segregated with the BPH resistance phenotype. STS marker 7312.T4A was validated using BC2F2 progenies derived from two temperate japonica backgrounds. Some 97 resistant BC2F2 individuals out of 433 screened completely co-segregated with the resistance-specific marker allele (1,078 bp) in either homozygous or heterozygous state. This further confirmed a major gene-controlled resistance to the BPH biotype of Korea. Identification of Bph18(t) enlarges the BPH resistance gene pool to help develop improved rice cultivars, and the PCR marker (7312.T4A) for the Bph18(t) gene should be readily applicable for marker-assisted selection (MAS).

Alleles↗

Powdery mildew resistance and Lr34/Yr18 genes for durable resistance to leaf and stripe rust cosegregate at a locus on the short arm of chromosome 7D of wheat.

The incorporation of effective and durable disease resistance is an important breeding objective for wheat improvement. The leaf rust resistance gene Lr34 and stripe rust resistance gene Yr18 are effective at the adult plant stage and have provided moderate levels of durable resistance to leaf rust caused by Puccinia triticina Eriks. and to stripe rust caused by Puccinia striiformis Westend. f. sp. tritici. These genes have not been separated by recombination and map to chromosome 7DS in wheat. In a population of 110 F(7) lines derived from a Thatcher x Thatcher isogenic line with Lr34/Yr18, field resistance to leaf rust conferred by Lr34 and to stripe rust resistance conferred by Yr18 cosegregated with adult plant resistance to powdery mildew caused by Blumeria graminis (DC) EO Speer f. sp. tritici. Lr34 and Yr18 were previously shown to be associated with enhanced stem rust resistance and tolerance to barley yellow dwarf virus infection. This chromosomal region in wheat has now been linked with resistance to five different pathogens. The Lr34/Yr18 phenotypes and associated powdery mildew resistance were mapped to a single locus flanked by microsatellite loci Xgwm1220 and Xgwm295 on chromosome 7DS.

Chromosome Mapping↗

Genetic resistance in experimental autoimmune encephalomyelitis. I. Analysis of the mechanism of LeR resistance using radiation chimeras.

Experimental autoimmune encephalomyelitis (EAE) is a cell-mediated autoimmune disease of the central nervous system that has been extensively studied in the rat. The Lewis rat is highly susceptible to the induction of EAE, while the Lewis resistant (LeR) rat is known to be resistant. In this paper, we demonstrate that the LeR rat, which was derived from the Lewis strain by inbreeding of fully resistant animals, is histocompatible with the Lewis strain. Radiation chimeras, a tool for distinguishing between immunologic and nonimmunologic resistance mechanisms, were utilized to analyze the cellular mechanisms involved in genetic resistance to EAE. By transplanting bone marrow cells from LeR rats into irradiated Lewis recipients, Lewis rats were rendered resistant to EAE induction. Likewise, transplanting Lewis bone marrow cells into irradiated LeR recipients rendered LeR rats susceptible. Mixed lymphoid cell chimeras using bone marrow, spleen, and thymus cells in Lewis recipient rats revealed individual lymphoid cell types and cell interactions that significantly affected the incidence and severity of EAE. Our results suggest that LeR resistance is mediated by hematopoietic/immune cells, and that cells located in the spleen appear to play a critical role in the resistance/susceptibility to EAE induction. Depletion of splenic adherent cells did not change the patterns of EAE resistance. In vivo cell mixing studies suggested the presence of a suppressor cell population in the LeR spleen preparations which exerted an inhibitory effect on Lewis autoimmune responses. Thus, the mechanism of LeR resistance appears to be different from that in other EAE-resistant animals.

Animals↗

Glutathione is the antioxidant responsible for resistance to oxidative stress in V79 Chinese hamster fibroblasts rendered resistant to cadmium.

By manipulation of Cd and Zn concentrations in the medium, several phenotypes, differing in the contents of glutathione (GSH) and metallothionein (Mt), were derived from a parental clone of V79 Chinese hamster fibroblast. In some of these phenotypes, resistance to Cd and cross-resistance to oxidative stress was developed. The highest levels of GSH and Mt were found in cells which were rendered resistant to Cd by stepwise increases of Cd and Zn in the cell medium for over 50 passages. Upon removal of Cd/Zn from the medium of these cells or addition of Cd/Zn to the parental cell medium, changes of cellular GSH and Mt levels occurred to different extents. At the same time, changes in the resistance to Cd and H2O2 were observed. Good linear correlations were observed for Mt levels x resistance to Cd and for GSH levels x resistance to H2O2. Poor linear correlations were found for Mt levels x resistance to H2O2 or for GSH levels x resistance to Cd. Moreover, addition of Zn to the medium produced an increase in Mt content without affecting the GSH content. In this case no cross-resistance to oxidative stress was developed. Therefore, Mt which has been shown to be an excellent antioxidant in in vitro experiments, does not seem to play any major role against oxidative stress in Zn and Cd challenged cells. Most of the cross-resistance to oxidative stress in Cd challenged cells seems to be accounted for by the parallel increase in GSH.

Animals↗

The resistance to human plasma of Trypanosoma brucei, T. rhodesiense and T. gambiense: III. Clones of two plasma-resistant strains.

Tests for resistance to human plasma were made on six clones of a stabilate of Trypanosoma rhodesiense (LUMP 10) which was calculated to contain about 3,000 resistant trypanosomes per million. Two of the clones were not resistant and four were only subresistant. Tests were also made on 12 lines (clones) of a stabilate of polymorphic trypanosomes isolated from tsetse flies. One of them, ETAT 10, had infected a laboratory worker and was found to be fully resistant to human plasma; the other lines showed only low or moderate resistance. Resistance of a strain to human plasma often depends upon a small minority of resistant trypanosomes. Strains of polymorphic trypanosomes may be classified as fully resistant, moderately resistant, subresistant, or sensitive to human plasma, if they contain respectively, all, some (e.g. one per hundred), very few (e.g. one per million) or no individuals which are resistant.

Animals↗

Hybrid resistance against a natural killer (NK) cell-resistant lymphoma (YWA) is mediated by a T cell-dependent mechanism.

Rejection of the Moloney virus-induced YAC lymphoma of strain A origin by semisynegeneic F1 hybrids has previously been shown to correlate with the levels of natural killer (NK) cell activity in the same F1 hybrids against this target cell line in vitro. In the present study, YAC and another Moloney virus-induced lymphoma,, YWA, derived from the A congenic A.SW strain, were tested for F1 hybrid resistance after s.c. inoculation of small numbers of cells into syngeneic and semisyngeneic F1 mice. While YAC cells invariably grew progressively once they formed a palpable tumor, regression of YWA tumors was frequently observed in both susceptible and resistant genotypes. The hybrid resistance pattern for YAC and YWA differed in one important respect: outcross of the syngeneic host to the A-congenic A.BY strain introduced a strong H-2b-associated resistance factor against YWA, but not against YAC. Compared to YAC, which is highly NK-sensitive and rapidly eliminated from mice with high NK activity, YWA was insensitive to NK-mediated lysis in vitro and [125I] UdR-labelled YWA cells were not eliminated more efficiently from the highly resistant (A.SW X A.BY) F1 then from the parental strain in short-term (4-18h) in vivo rejection assays. It was therefore concluded that the H-2b-associated resistance against YWA was independent of NK cells or other rapidly acting effector mechanisms. Moreover, thymectomy, followed by irradiation and fetal liver reconstitution, completely abolished the resistance against YWA but left the resistance against YAC virtually intact. These data suggest that two lymphomas induced by the same agent can be rejected by different effectors. The NK-resistant YWA lymphoma is rejected by a T-dependent mechanism, while the resistance against the inoculation of the highly NK-sensitive YAC line is T-independent and, in all probability, mediated by NK cells.

Animals↗

Susceptibility of brook charr, Salvelinus fontinalis to the pathogenic haemoflagellate, Cryptobia salmositica, and the inheritance of innate resistance by progenies of resistant fish.

Eighty-seven of 175 laboratory raised F1 generation brook charr (Salvelinus fontinalis) were resistant to experimental Cryptobia salmositica infection. Susceptibility to the pathogen was not related to age nor to route of infection. Plasma of resistant charr lysed the parasite under in vitro conditions while those of susceptible fish did not. Sperm from 4 susceptible and 4 resistant male charr, from 8 F1 families, were used to fertilize eggs from 2 hatchery raised susceptible charr. Susceptibility of progenies (F2 families) was determined 4 weeks after inoculation of the parasite. All progenies (seven F2 families) of 4 susceptible males were susceptible to experimental infection and their plasma did not lyse the parasite. It was presumed that these susceptible progenies were homozygous recessive (rr), and that the resistant allele was dominant. All progenies (two F2 families) of 1 resistant male (presumed RR) and 2 susceptible females were all resistant to infection and their plasma lysed the parasite. The ratio of resistant to susceptible charr in 6 other F2 families from the other 3 resistant males (presumed Rr) and two susceptible females was about 1:1. The results suggest a single Mendelian locus which determines innate resistance to C. salmositica infection in brook charr and that it is possible to breed Cryptobia-resistant fish.

Alleles↗

The R1 gene for potato resistance to late blight (Phytophthora infestans) belongs to the leucine zipper/NBS/LRR class of plant resistance genes.

Late blight caused by the oomycete Phytophthora infestans is the most destructive disease in potato cultivation worldwide. New, more virulent P. infestans strains have evolved which overcome the genetic resistance that has been introgressed by conventional breeding from wild potato species into commercial varieties. R genes (for single-gene resistance) and genes for quantitative resistance to late blight are present in the germplasm of wild and cultivated potato. The molecular basis of single-gene and quantitative resistance to late blight is unknown. We have cloned R1, the first gene for resistance to late blight, by combining positional cloning with a candidate gene approach. The R1 gene is member of a gene family. It encodes a protein of 1293 amino acids with a molecular mass of 149.4 kDa. The R1 gene belongs to the class of plant genes for pathogen resistance that have a leucine zipper motif, a putative nucleotide binding domain and a leucine-rich repeat domain. The most closely related plant resistance gene (36% identity) is the Prf gene for resistance to Pseudomonas syringae of tomato. R1 is located within a hot spot for pathogen resistance on potato chromosome V. In comparison to the susceptibility allele, the resistance allele at the R1 locus represents a large insertion of a functional R gene.

Amino Acid Sequence↗

On the response of genetically resistant and susceptible rabbits to the quantitative inhalation of human type tubercle bacilli and the nature of resistance to tuberculosis.

If genetically resistant and susceptible rabbits inhale a certain number of human type tubercle bacilli, no tuberculosis in the lungs of the resistant animals is seen, as a rule several months after infection, while there is a variable and often extensive disease in the susceptible rabbits. The analogy to the presence or absence of active tuberculosis in man infected with the tubercle bacillus is evident. The inhaled tubercle bacilli multiply for but a short time in the resistant rabbits and are usually rapidly and completely destroyed. In the susceptible rabbits, the bacilli multiply profusely for a much longer time and persist in large numbers even months after inhalation. Whatever be the cause of the more rapid destruction of tubercle bacilli in the resistant animal, the resulting more rapid release of the contained antigens enhances the development of allergic sensitivity and antibodies in these animals. The development of an acquired resistance against tubercle bacilli of the human type is sufficiently rapid to affect the genesis of the initial gross primary pulmonary foci that result from the inhalation of a given number of bacilli. The greater the genetic resistance, the fewer the initial primary foci. Variations in genetic resistance are essentially variations in the rate of development of acquired resistance. It is suggested that variations in genetic resistance to inhaled human type tubercle bacilli may affect the prevalence of alveolar phagocytes capable of acquiring adequate resistance to the growth of the bacilli in their cytoplasm. The prevalence of such cells is subject to hormonal and immunological influences.

Animals↗

RFLP mapping of genes conferring complete and partial resistance to blast in a durably resistant rice cultivar.

Moroberekan, a japonica rice cultivar with durable resistance to blast disease in Asia, was crossed to the highly susceptible indica cultivar, CO39, and 281 F7 recombinant inbred (RI) lines were produced by single seed descent. The population was evaluated for blast resistance in the greenhouse and the field, and was analyzed with 127 restriction fragment length polymorphism (RFLP) markers. Two dominant loci associated with qualitative resistance to five isolates of the fungus were tentatively named Pi-5(t) and Pi-7(t). They were mapped on chromosomes 4 and 11, respectively. To identify quantitative trait loci (QTLs) affecting partial resistance, RI lines were inoculated with isolate PO6-6 of Pyricularia oryzae in polycyclic tests. Ten chromosomal segments were found to be associated with effects on lesion number (P < 0.0001 and LOD > 6.0). Three of the markers associated with QTLs for partial resistance had been reported to be linked to complete blast resistance in previous studies. QTLs identified in greenhouse tests were good predictors of blast resistance at two field sites. This study illustrates the usefulness of RI lines for mapping a complex trait such as blast resistance and suggests that durable resistance in the traditional variety, Moroberekan, involves a complex of genes associated with both partial and complete resistance.

Chromosome Mapping↗