Vol. 61 No. 1 (2022)
Articles

Mechanisms of resistance to powdery mildew in cucumber

Mumin Ibrahim TEK
Department of Plan Protection, Faculty of Agriculture, Akdeniz University, The Campus 07059 Konyaalti-Antalya
Bio
Ozer CALIS
Department of Plan Protection, Faculty of Agriculture, Akdeniz University, The Campus 07059 Konyaalti-Antalya
Published May 13, 2022
Keywords
  • Signaling pathway genes,
  • Podosphaera xanthii
How to Cite
[1]
M. I. TEK and O. CALIS, “Mechanisms of resistance to powdery mildew in cucumber”, Phytopathol. Mediterr., vol. 61, no. 1, pp. 119-127, May 2022.

Funding data

Abstract

Podosphaera xanthii causes powdery mildew of cucumber, and is associated with significant yield and quality losses. Development of resistant or tolerant varieties is the most effective and eco-friendly strategy for powdery mildew management. An important host resistance mechanism is based on the recognition of conserved resistance genes, resulting in durable resistance. To determine powdery mildew resistance mechanisms in cucumber, total RNAs were isolated from the powdery mildew resistant cultivar Meltem, the tolerant line VT18, and the susceptible local variety Camlica. Expression levels of nine genes in these plants were analysed by Reverse Transcription Polymerase Chain Reaction (RT-PCR). The host reactions were assessed using microscope observations of stained specimens. Serine/threonine (STN7), transcription factor (WRKY22), serine/threonine-protein kinase (D6PKL1), and serine/threonine receptor kinase (NFP) genes were induced, as positive regulators in defence mechanisms against powdery mildew. Polygalacturonase Inhibitor (PGIP) did not express after P. xanthii inoculation of Camlica, resulting in susceptibility. After inoculation, callose synthase (CALLOSE) and cinnamyl alcohol dehydrogenase (CAD) gene expression levels were increased in resistant Meltem, but Hypersensitive Reaction (HR) and ROS formation were only linked in the tolerant VT18. Powdery mildew development was less in Meltem than in VT18, indicating that cell wall thickening and HR play separate roles in resistance to this disease.

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