Gene markers generating polygenic resistance in melon-Fusarium wilt-FOM1.2 interaction pathosystem.

Abstract

Developing melon genotypes with resistance to Fusarium oxysporum f. sp. Melonis-(FOM) race1.2 is a major goal in any breeding program. In this study, we identified the role of 11 gene markers that contribute to polygenic resistance during the FOM1.2-melon interaction. qRT-PCR analysis elucidated upregulation of candidate marker genes AMT, DXPR, Fom-2, GLUC, GalS, GRF3, MLO, PRK, RuBlsCo, TLP and WRKY in resistant 'Shante-F1' and 'Khatouni', and susceptible 'Shante-T' and 'Shahabadi' at 7, 14 and 21 days post-inoculation (dpi). We also studied changes in defence-related enzyme activity: chitinase (CHI), β-1,3-glucanase (GLU) and peroxidase (POX) in melon roots. AMT, GLUC and DXPR transcripts were upregulatied in leaf and root tissues of the resistant 'Shante-F1' and 'Shahabadi'. Transcript levels for GalS and GRF3 increased 6.77- and 6.83-fold in roots of 'Shante-F1' at 7 dpi, whereas in PRK, TLP and WRKY theye increased by 7.84-, 5.15- and 12.26-fold at 14 dpi, respectively. However, transcript levels increased by 5.18-fold for Fom-2 and 8.46-fold for MLO at 21 dpi. Also, RBC transcript level peaked at 14 dpi with 4.9-fold increase in leaves of resistant genotypes, whereas AMT increased 2.94-fold at 21 dpi, and GLUC and DXPR increased 7.11- and 2.91-fold at 14 dpi in 'Shante-F', respectively. Defence-related-enzyme activity was also upregulated three-fold in resistant varieties. The dynamic shifts in the melon transcriptome induced by FOM1.2 emphasize that resistance mechanisms are predominantly regulated through signalling pathways involving CHI, GLU, and POX defence response. Surprisingly, the AMT gene, basically resistant to downy mildew, Pseudoperonospora cubensis; GLUC, MLO and PRK resistant to powdery mildew (Sphaerotheca fusca); TLP and WRKY resistant to Phytophthora blight (Phytophthora capsici); and GRF3 and RBC resistant to root knot nematodes (Meloidogyne spp.) were upregulated in resistant genotypes, indicating a dual role of these genes in resistance to more than one disease at a time.