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At least 19 recordsLinked to original sources
PubMed1987

Genetic control of immune responsiveness: a review of its use as a tool for selection for disease resistance.

Disease resistance and immune responsiveness have been traits generally ignored by animal breeders. Recent advances in immunology and molecular biology have opened new avenues towards our understanding of genetic control of these traits. The major histocompatibility gene complex (MHC) appears to play a central role in all immune functions and disease resistance. The need to understand the relationship between immune responsiveness, disease resistance and production traits is discussed in this review. Antagonistic relationships might prevent simultaneous improvement of all of these traits by conventional breeding methods. It is suggested that genetic engineering methods may allow the simultaneous improvement of disease resistance and production traits in domestic animals. Genes of the MHC will be especially good candidates for genetic engineering experiments to improve domestic species.

Animals↗
PubMed2005

Acquired immunity and stochasticity in epidemic intervals impede the evolution of host disease resistance.

Disease can generate intense selection pressure on host populations, but here we show that acquired immunity in a population subject to repeated disease outbreaks can impede the evolution of genetic disease resistance by maintaining susceptible genotypes in the population. Interference between the life-history schedule of a species and periodicity of the disease has unintuitive effects on selection intensity, and stochasticity in outbreak period further reduces the rate of spread of disease-resistance alleles. A general age-structured population genetic model was developed and parameterized using empirical data for phocine distemper virus (PDV) epizootics in harbor seals. Scenarios with acquired immunity had lower levels of epizootic mortality compared with scenarios without acquired immunity for the first PDV outbreaks, but this pattern was reversed after about five disease cycles. Without acquired immunity, evolution of disease resistance was more rapid, and long-term population size variation is efficiently dampened. Acquired immunity has the potential to significantly influence rapid evolutionary dynamics of a host population in response to age-structured disease selection and to alter predicted selection intensities compared with epidemiological models that do not consider such feedback. This may have important implications for evolutionary population dynamics in a range of human, agricultural, and wildlife disease settings.

Aging↗
PubMed1990

Compounds from plants that regulate or participate in disease resistance.

Disease resistance is multifactorial. The response phase includes: synthesis of phytoalexins, i.e. low molecular weight antimicrobial compounds which accumulate at sites of infection; systemically produced enzymes which degrade pathogens, e.g. chitinases, beta-1,3-glucanases and proteases; systemically produced enzymes which generate antimicrobial compounds and protective biopolymers, e.g. peroxidases and phenoloxidases; biopolymers which restrict the spread of pathogens, e.g. hydroxyproline-rich glycoproteins, lignin, callose; and compounds which regulate the induction and/or activity of the defence compounds, e.g. elicitors of plant and microbial origin, immunity signals from immunized plants and compounds which release immunity signals. Disease resistance in plants is not determined by the presence or absence of genes for resistance mechanisms, it is determined by the speed and degree of gene expression and the activity of the gene products. It is likely, therefore, that all plants have the genetic potential for resistance. This potential can be expressed systemically (immunization) after restricted inoculation with pathogens, attenuated pathogens or selected non-pathogens, or treatment with chemical substances that are produced by immunized plants or chemicals which release such signals. Immunization is effective against diseases caused by fungi, bacteria and viruses, and it has been successfully tested in the laboratory and field. Advances in science have provided information and technology to enhance resistance to plant pests. Pesticides are part of this technology, but they also contribute to a complex world problem which threatens our environment and hence our survival. The future will see the restriction of pesticide use and a greater reliance on resistant plants generated using immunization and other biological control technologies, genetic engineering and classical plant breeding. However, as with past and current technology, we will have created unique problems. The survival of our planet depends upon anticipating these problems and meeting the challenge of their solution.

Breeding↗
PubMed1997

Bacterial avirulence proteins as triggers of plant disease resistance.

Disease resistance in plants is often characterized by matching resistance and avirulence genes in host and pathogen, respectively. It has recently been shown that expression of bacterial avirulence genes in plants induces resistance gene-dependent defense reactions. The finding that avirulence proteins act inside plant cells represents a major advance in our understanding of host-pathogen specificity.

Bacteria↗
PubMed1998

Disease resistance gene homologs correlate with disease resistance loci of Arabidopsis thaliana.

The disease resistance genes RPS2 of Arabidopsis and N of tobacco, among other recently cloned resistance genes, share several conserved sequences. Degenerate oligonucleotide primers, based on conserved sequences in the nucleotide binding site (NBS) and a weak hydrophobic domain of RPS2 and N, were used to amplify homologous sequences from Arabidopsis thaliana. Amplification products were obtained that were similar in sequence to the disease resistance genes RPS2, RPM1, N and L6. The Arabidopsis CIC-YAC library was used to identify the position of the disease resistance homologs on the Arabidopsis genome. Their map positions could be correlated with the disease resistance loci RPS5, RAC1, RPP9, CAR1, RPP7, RPW2, RPP1, RPP10, RPP14, RPP5, RPP4, RPS2, RPW6, HRT, RPS4, RPP8, RPP21, RPP22, RPP23, RPP24 and TTR1. This method was therefore not only successful in the identification of sequences located within gene clusters that are involved in disease resistance, but could also contribute to the cloning of disease resistance genes from Arabidopsis.

Amino Acid Sequence↗
PubMed1998

Treatment of resistant disease.

Resistant AML encompasses two groups of patients: those with refractory leukemia and those whose leukemia has relapsed. Refractory leukemia is disease that does not respond to initial induction chemotherapy with cytarabine and an anthracycline. Patients with refractory leukemia are likely to have disease with adverse cytogenetics, a history of antecedent hematologic disturbance, adverse immunophenotypic features, and expression of multiple drug resistance. On the other hand, relapsed leukemia is leukemia that recurs following a CR. The duration of CR greatly affects the patient's prognosis and response to additional treatment. Patients with relapsed leukemia are heterogeneous with variable pretreatment characteristics.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1998

Impact of genetics on disease resistance.

The genetics of a bird or flock has a profound impact on its ability to resist disease, because genetics define the maximum achievable performance level. Careful attention should be paid to genetics as an important component of a comprehensive disease management program including high-level biosecurity, sanitation, and appropriate vaccination programs. Some specific genes (e.g., the MHC) are known to play a role in disease resistance, but resistance is generally a polygenic phenomenon. Future research directions will expand knowledge of the impact of genetics on disease resistance by identifying non-MHC genetic control of resistance and by further elucidating mechanisms regulating expression of genes related to immune response.

Animals↗
PubMed2002

[Analysis and mapping of homologous sequences of barley disease resistance gene Mlo and maize disease resistance gene Hm1 in rice].

The encoding products of the disease resistance (R) gene of barley, Mlo, and the maize R gene, Hm1, do not contain the recognizable structural domains of most of the known plant R gene products. The two genes do not comply with the gene-for-gene theory in the response to pathogen infection either. Two sequences, OsMlo-1 and DFR-1 which were homologous to the barley Mlo and maize Hm1, respectively, were isolated from rice. The OsMlo-1 was mapped between two molecular markers, RZ667 and RG424, and located at a distance of 20.6 centi-Morgan (cM) from RZ667 and 6.0 cM from RG424 on rice chromosome 6. The DFR-1 was flanked by molecular markers R2635 and RG462 with an estimated genetic distance of 11.3 cM from R2635 and 23.9 cM from RG462 on rice chromosome 1. Using other published rice molecular linkage maps as references, it was found that the chromosomal locations of OsMlo-1 and DFR-1 were correspondence with two previously identified rice blast resistant QTLs (quantitative trait loci), respectively. The results suggest that the genes homologous to barley Mlo and maize Hm1 in rice may be involved in defense responses induced by pathogen infection.

Chromosome Mapping↗
PubMed2002

The RAR1 interactor SGT1, an essential component of R gene-triggered disease resistance.

Plant disease resistance (R) genes trigger innate immune responses upon pathogen attack. RAR1 is an early convergence point in a signaling pathway engaged by multiple R genes. Here, we show that RAR1 interacts with plant orthologs of the yeast protein SGT1, an essential regulator in the cell cycle. Silencing the barley gene Sgt1 reveals its role in R gene-triggered, Rar1-dependent disease resistance. SGT1 associates with SKP1 and CUL1, subunits of the SCF (Skp1-Cullin-F-box) ubiquitin ligase complex. Furthermore, the RAR1-SGT1 complex also interacts with two COP9 signalosome components. The interactions among RAR1, SGT1, SCF, and signalosome subunits indicate a link between disease resistance and ubiquitination.

Amino Acid Motifs↗
PubMedDate not supplied

Estimating disease resistance in insects: phenoloxidase and lysozyme-like activity and disease resistance in the cricket Gryllus texensis.

An animal's ability to resist disease is usually estimated by measuring one or more components of the immune system. There is an assumption that these assays of immunity measure an animal's ability to mount an effective immune response. This paper tests this assumption by examining the relationship between two common estimates of insect immunocompetence, phenoloxidase and lysozyme-like enzyme activity, and resistance to three common insect bacterial pathogens: Serratia marcescens, Serratia liquefaciens, and Bacillus cereus. There was a correlation (Spearman's rs=0.33, p<0.001, n=190 pairs) between total phenoloxidase and baseline lysozyme-like activity within individuals. However, total phenoloxidase and baseline lysozyme-like activity levels did not predict which male crickets would survive any of the three bacterial challenges. Lysozyme-like activity increased after an immune challenge (Friedman, 33.72, p<0.001), and the greater the increase, the greater the chance that the cricket would survive S. marcescens (slope=0.15, chi 2=8.2, p=0.005) or B. cereus (slope=0.8, chi 2=6.4, p=0.01). The crickets with a greater total hemolymph protein concentration were also more likely to survive a challenge with any of the three bacterial pathogens than the crickets with lower total hemolymph protein concentrations (S. liquefaciens: slope=0.02, chi 2=9.2, p=0.002; B. cereus: slope=0.02, chi 2=6.5, p=0.01; S. marcescens: slope=0.03, chi 2=7.8, p=0.005). Because of the complexity of the immune system, empirical tests of the relationship between assays of immunity and resistance to a range of actual pathogens are important for correctly interpreting these measures.

Animals↗
PubMed2003

The impact zone: genomics and breeding for durable disease resistance.

Durable disease resistance is a major but elusive goal of many crop improvement programs. Genomic approaches will have a significant impact on efforts to ameliorate plant diseases by increasing the definition of and access to genepools available for crop improvement. This approach will involve the detailed characterization of the many genes that confer resistance, as well as technologies for the precise manipulation and deployment of resistance genes. Genomic studies on pathogens are providing an understanding of the molecular basis of specificity and the opportunity to select targets for more durable resistance. There are, however, several biological and societal issues that will have to be resolved before the full impact of genomics on breeding for disease resistance is realized.

Breeding↗
PubMedDate not supplied

Immunological basis of differences in disease resistance in the chicken.

Genetic resistance to diseases is a multigenic trait governed mainly by the immune system and its interactions with many physiologic and environmental factors. In the adaptive immunity, T cell and B cell responses, the specific recognition of antigens and interactions between antigen presenting cells, T cells and B cells are crucial. It occurs through a network of mediator proteins such as the molecules of the major histocompatibility complex (MHC), T cell receptors, immunoglobulins and secreted proteins such as the cytokines and antibodies. The diversity of these proteins that mainly is due to an intrinsic polymorphism of the genes causes phenotypic variation in disease resistance. The well-known linkage of MHC polymorphism and Marek's disease resistance difference represents a classic model revealing immunological factors in resistance differences and diversity of mediator molecules. The molecular bases in any resistance variation to infectious pathogens are vaguely understood. This paper presents a review of the major immune mediators involved in resistance and susceptibility to infectious diseases and their functional mechanisms in the chicken. The genetic interaction of disease resistance with production traits and the environment is mentioned.

Animals↗
PubMed2006

Promoter mutations of an essential gene for pollen development result in disease resistance in rice.

Disease resistance and sexual reproductive development are generally considered as separate biological processes, regulated by different sets of genes. Here we show that xa13, a recessive allele conferring disease resistance against bacterial blight, one of the most devastating rice diseases worldwide, plays a key role in both disease resistance and pollen development. The dominant allele, Xa13, is required for both bacterial growth and pollen development. Promoter mutations in Xa13 cause down-regulation of expression during host-pathogen interaction, resulting in the fully recessive xa13 that confers race-specific resistance. The recessive xa13 allele represents a new type of plant disease resistance.

Alleles↗
PubMed1997

NDR1, a pathogen-induced component required for Arabidopsis disease resistance.

Plant disease resistance (R) genes confer an ability to resist infection by pathogens expressing specific corresponding avirulence genes. In Arabidopsis thaliana, resistance to both bacterial and fungal pathogens, mediated by several R gene products, requires the NDR1 gene. Positional cloning was used to isolate NDR1, which encodes a 660-base pair open reading frame. The predicted 219-amino acid sequence suggests that NDR1 may be associated with a membrane. NDR1 expression is induced in response to pathogen challenge and may function to integrate various pathogen recognition signals.

Amino Acid Sequence↗
PubMed2001

The sustainability, feasibility and desirability of breeding livestock for disease resistance.

Selective breeding for disease resistance utilises proven animal breeding methods to improve animal health, welfare and productivity. Unsurprisingly, it is receiving more and more attention from livestock breeders. However, there are a number of largely theoretical arguments that have been raised as potential problems in selection for disease resistance. These can be classified under sustainability, feasibility and desirability. This review considers each of these areas in turn. Several examples show that enhanced resistance to disease is stable under natural selection and therefore deliberate selection for disease resistance should also be stable and sustainable. The feasibility of selective breeding depends in part upon the heritability of the trait or traits used to measure disease resistance, as well as the amount of variation among animals. The heritability of traits associated with resistance to many important diseases is often high and considerable variation among animals exists. Consequently, selective breeding for enhanced disease resistance is certainly feasible. The desirability of breeding for disease resistance depends upon whether there are trade-offs with other economically important traits. By and large these remain to be defined. However, even if unfavourable associations exist, breeders can create selection indices that include traits with unfavourable associations and maximise the desired responses while attempting to minimise undesirable effects. In conclusion, so long as one or more diseases exert a significant influence on livestock production, selective breeding will be a useful tool to assist in disease control.

Animals↗
PubMed1989

Selection for disease resistance.

Approaches to disease control are prioritized. Genetic improvement could reduce need for treatment and culling but would not reduce the need for proper management and sanitation. Results of several studies indicate that disease incidence and cost increases with selection for milk yield. The large array of disease resistance mechanisms in animals suggests a large number of loci are involved in disease resistance. A few loci, e.g., the major histocompatibility complex, may account for a major portion of genetic variance in disease. Rate of genetic gain from selection for a major locus alone or in combination with performance is discussed. Four criteria for including traits in a breeding program are outlined, and each is discussed with respect to disease. In spite of low heritabilities for disease traits, genetic variation for disease incidence is economically important and justifies including disease in breeding programs. An industry-wide standard for recording and accumulating field data for disease is lacking. Institutional relationships among segments of the animal breeding and animal health industries are needed to facilitate genetic improvement for disease resistance.

Animals↗
PubMed1997

Patterns of hemopoietic reconstitution in nonobese diabetic mice: dichotomy of allogeneic resistance versus competitive advantage of disease-resistant marrow.

Complete replacement of the immune system via allogeneic bone marrow transplantation is sufficient to prevent diabetes in the nonobese diabetic (NOD) mouse model. In the present study we examined whether mixed allogeneic reconstitution would be sufficient to interrupt the autoimmune process with respect to occurrence of overt diabetes, as well as preexisting autoimmune insulitis. NOD mice were lethally irradiated and reconstituted with a mixture of NOD and B10.BR marrow. A relative resistance to allogeneic bone marrow engraftment was noted in NOD recipients of the mixed bone marrow inoculum, compared with disease-resistant controls. Moreover, unlike disease-resistant controls, all animals that initially repopulated as mixed donor/host chimeras became predominantly allogeneic by 4 mo, suggesting a competitive advantage for long term engraftment for disease-resistant marrow. All but one mouse in the group that engrafted with allogeneic marrow remained free of diabetes for the entire follow-up period (n = 22). Moreover, in all animals examined, virtually all islets were free of insulitis. In contrast, 74% of NOD mice that received similar conditioning and failed to engraft with donor marrow developed acute diabetes and intra-islet insulitis was present in all animals examined. These data suggest that NOD mice exhibit a relative resistance to engraftment compared with disease-resistant recipients. Conversely, animals that initially repopulated as a mixture of syngeneic and donor marrow become converted to virtually all donor by 4 mo. These data provide additional support that a defective stem cell is responsible for autoimmune diabetes in this experimental model.

Animals↗