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Race Specificity of QTL. Genetic selection and adaptation of Cochliobolus heterostrophus to corn hosts with partial resistance. Kolmer, JA; Leonard, KJ Phytopathology. Vol. 76, no. 8, pp. 774-777. 1986. Recurrently selected for virulence of C. heterostrophus on one line- 316.
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Race Specificity of QTL • Genetic selection and adaptation of Cochliobolus heterostrophus to corn hosts with partial resistance. Kolmer, JA; Leonard, KJ Phytopathology. Vol. 76, no. 8, pp. 774-777. 1986. • Recurrently selected for virulence of C. heterostrophus on one line- 316. P Balint-Kurti QDR lecture
Saw line-specific as well as line-non-specific response. • What does this mean? P Balint-Kurti QDR lecture
Do these dichotomies really exist? P Balint-Kurti QDR lecture
Is quantitative resistance really durable? • This is certainly the received wisdom though no formal studies have been done (?) • Likely to be true • But some major genes Lr34 and Sr2 for instance are durable too. P Balint-Kurti QDR lecture
Do these dichotomies really exist? P Balint-Kurti QDR lecture
True, but major genes might also be developmentally and environmentally influenced. • At temperatures above 28°C, the HR and the restriction response associated with the tobacco N gene are inactive. P Balint-Kurti QDR lecture
Do these dichotomies really exist? P Balint-Kurti QDR lecture
(almost) all available necrotrophic resistance is quantitative P Balint-Kurti QDR lecture
Do these dichotomies really exist? P Balint-Kurti QDR lecture
Quantitative resistance is, by definition, partial • But some (most?) R-genes do not confer complete resistance either. P Balint-Kurti QDR lecture
Lots of examples of this type of thing Randy Wisser P Balint-Kurti QDR lecture
“Ghost” effects • Defeated R-genes still seem to be doing something! P Balint-Kurti QDR lecture
CAVEAT • PERSONAL OPINION! P Balint-Kurti QDR lecture
So are Quantitative resistance genes similar to major R-genes? • Maybe… • Most of the perceived differences are matters of degree • Rcg1, a quantitative gene for anthracnose stalk rot resistance was cloned and found to encode an NBS-LRR gene. • But Rcg1 has an extremely significant effect • What is the difference between a “major” gene and a strong QTL? P Balint-Kurti QDR lecture
Perhaps R-genes that interact weakly with their corresponding Avr genes cause partial resistance? • There is some evidence for this. E.g. weak interations between L gene products in flax and corresponding Avr gene products is associated with weaker HR response • Presumably this happens often during evolution P Balint-Kurti QDR lecture
QTL disproportionately colocalize with RGA in rice P Balint-Kurti QDR lecture
Integrated disease-QTL map of rice • disease QTL • R-genes • RGAs (NBS-LRR) • Lesion mimic genes Randy Wisser Wisser et al., 2005 Genetics Wisser et al. 2005 Genetics 169: 2277 P Balint-Kurti QDR lecture
Questions Are certain genes associated with the dQTL fraction of the genome? Do genes (or groups of genes) condition multiple disease resistance? Randy Wisser P Balint-Kurti QDR lecture
genomic location differential expression defense response literature selection response Examining dQTL-gene associations QTL Many positional candidate genes Chromosome non-QTL fraction QTL fraction total gene dist. enriched in QTL fraction: Resistance (R) genes R-gene analogs (RGAs) Pathogen-induced genes Gene families (n=4/145) P Balint-Kurti QDR lecture Randy Wisser
R-genes can’t be the whole story surely! • What other types of things might cause variations in quantitative resistance? • Structural features • Cell wall • Stomatal density, openness • Preformed defenses • Phytoalexins etc. • Components of the basal defence system? • PAMP receptors? • Effector targets? P Balint-Kurti QDR lecture
Traits affecting leaf wetness may play a role P Balint-Kurti QDR lecture
“race or cultivar-specific resistance mediated by single resistance (R) genes is thought to be of limited value in the field, because of the rapid evolution of new virulent races of the pathogens. On the other hand, nonhost and partial resistance appear more durable. However, the extent to which durable nonhost or partial resistance involves genetic components that are distinct from R genes remains unclear.” P Balint-Kurti QDR lecture
Is quantitative resistance effective against multiple diseases • This area has not been looked at much. • If the resistance mechanism is somewhat general then you might expect it to be effective against a set of similar pathogens. • Mitchell-Olds, T., R. V. James, M. V. Palmer, and P. H. Williams, Genetics of Brassica rapa (syn. campestris). 2. Selection for multiple disease resistance to three fungal pathogens: Peronospora parasitica, Albugo candida, and Leptosphaeria maculans,Heredity, vol. 75 (1995), pp. 362-369 . P Balint-Kurti QDR lecture
Positive correlations among multiple diseases Southern leaf blight Northern leaf blight Gray leaf spot R. J. Wisser P Balint-Kurti QDR lecture
So what use are dQTL? • Knowledge of the location of disease resistance QTL can be used in “Marker Assisted Breeding” (MAS). • MAS uses markers to follow and incorporate into germplasm previously mapped genes for a beneficial phenotype P Balint-Kurti QDR lecture
Jim Holland Catch-22 of MAS If phenotypic data are poor indicators of genotypes, you cannot adequately map QTLs to implement MAS. If phenotypic data are good, you do not need MAS. P Balint-Kurti QDR lecture
Jim Holland The Catch-22 can be avoided if: • A small number of QTLs explain most of the genetic variation, in which case: • High heritability in the QTL mapping phase is optimal to identify QTL markers, then: • Markers can be implemented more easily/cheaply than phenotyping in future selection cycles. P Balint-Kurti QDR lecture
In other words… • MAS makes sense: • If it is difficult/costly to select directly for resistance • Under what circumstances would this happen? • And QTL mapping is accurate. • And the QTL being selected for have reasonably large effects P Balint-Kurti QDR lecture