AUTHOR=Drizou Fryni , Bruce Toby J. A. , Ray Rumiana V. , Graham Neil S. 

TITLE=Infestation by Myzus persicae Increases Susceptibility of Brassica napus cv. “Canard” to Rhizoctonia solani AG 2-1

JOURNAL=Frontiers in Plant Science

VOLUME=Volume 9 - 2018

YEAR=2018

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2018.01903

DOI=10.3389/fpls.2018.01903

ISSN=1664-462X

ABSTRACT=Plants have the ability to defend themselves against herbivorous insects and plant pathogens.  Understanding the complicated interactions triggering plant defence mechanism is of great interest as it may allow the development of more effective and sustainable disease control methods.  Myzus persicae and Rhizoctonia solani anastomosis group (AG) 2-1 are two important organisms attacking oilseed rape (OSR), causing disease and reduced yields. At present, is unclear how these two interact with each other and with OSR defences and therefore the aim of the present study was to gain a better insight into the indirect interaction between aphids and pathogen. In separate experiments, we assessed the effect of AG 2-1 infection on aphid performance, measured as growth rate and population increase and then the effect of aphid infestation on AG 2-1 by quantifying disease and the amount of fungal DNA in plant stems and compost for two OSR varieties, ‘Canard’ and ‘Temple’. Additionally, we examined the expression of genes related to jasmonic acid (JA) and salicylic acid (SA) defence pathways. There was no significant effect of AG 2-1 infection on M. persicae performance. However, aphid infestation in one of the varieties, ‘Canard’, resulted in significantly increased disease symptoms caused by AG 2-1, although, the amount of fungal DNA was not significantly different between treatments. Expression of LOX3 and MYC2 was elevated under AG 2-1 treatment but downregulated in plants with both aphids and pathogen. Therefore it seems plausible that alterations in the JA signalling due to aphid infestation resulted in the increased susceptibility to AG 2-1.