Abstract
A disease test at different leaf layers (plant stages) of homologous rust and heterologous rust species were studied. The result from homologous rust species showed that those quantitative trait loci (QTLs) (Rphq2 and Rphq11) which were effective at seedling stage were also effective across all plant stages with gradually decreasing effect as plants grew older. Rphq3 which had consistent effect in all leaf layers confirmed the same result, that it is a plant stage independent QTL. For heterologous rusts, the effect of Rnhq-V was studied on three rust species; P. hordei-murini (Phm), P. hordei-secalini (Phs) and P. triticina isolate ‘Flamingo’ at three stages (leaf layers). Infection frequencies are higher at seedling stage and dramatically decrease as plants grow older in all three rust species tested on both SusPtrit and Su-Rnhq-V. The difference between lines tends to be reduced with higher leaf layer in all three tested inappropriate rust species. However, this would be not because of less effectiveness of the Rnhq. Key words: Plant stage, homologous rust, heterologous rust.
Highlights
Developmental conditions of the host plant may determine the outcome of pathogen infection; on the other hand, pathogen infection can change the developmental program of the host (Haffner et al, 2015; Grant and Jones, 2009)
Compared with SusPtrit, latency period (LP) differences were slightly larger for QTL-Near-isogenic lines (NILs) (201 to 240 h), Vada NILs (218 to 258 h) and L94-NILs (205 to 248 h) across all leaf layers
From first leaf to third leaf layers, Rphq2 has longer relative latency period (RLP) than Rphq3 and up to second leaf layers compared to Rphq11 on NILs with SusPtrit genetic background
Summary
Developmental conditions of the host plant may determine the outcome of pathogen infection; on the other hand, pathogen infection can change the developmental program of the host (Haffner et al, 2015; Grant and Jones, 2009). Resistance to infectious pathogens appears at different stages of host development, varies with plant age or tissue maturity, may be specific or broad-spectrum and is driven by diverse mechanisms, depending on plant pathogen interactions (DeveleyRiviere and Galiana, 2007). These responses of plants to infectious pathogens include basal response through transcription of genes in response to pathogen-associated molecular pattern recognition, hypersensitive response at the site of infection, systemic acquired resistance making the entire plant resistant to infection, jasmonic acid response and non-host immunity (Boyajyan et al, 2014). Many studies have been published on this phenomenon and reported for large number of crop plants
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