CmPMRl and CmPMrs are responsible for resistance to powdery mildew caused by Podosphaera xanthii race 1 in Melon

Advanced Genetic Studies on Powdery Mildew Resistance in TGR-1551

“…Nevertheless, the phenotyping and genotyping of the advanced backcrossed lines allowed us to narrow the resistance interval to a region of approximately 400 kb between HRM markers Oidio3 (chr12: 21,870,304 bp) and Oidio2 (chr12: 22,251,703 bp) ( Table 3 ). This narrowed region is not located within the previously proposed resistance QTL and is also outside the boundaries proposed for other resistance sources such as Edisto27, MR-1, PMR5, WM6, PI 124112, and PI 134198 [ 17 , 19 , 24 , 25 , 26 , 30 , 35 , 36 , 63 ] ( Figure 1 ). Nevertheless, the recessive gene present in TGR-1551 is unique, since no recessive genes conferring resistance to more than one Px race have been reported previously in melons, and this resistance could be conferred by a gene different from those derived from other accessions.…”

“…This QTL from Fukino et al [ 17 ] was strongly linked to the microsatellite markers associated with the QTL derived from TGR-1551 (TJ29, CMBR111, and CMBR150) [ 33 ]. This candidate interval proposed by Fukino et al [ 17 ] has recently been confirmed by Hong et al [ 35 ] and the resistance of MR-1 to race 1 has recently been mapped to the same region [ 19 , 24 ]. More recently, Howlader et al [ 36 ] described three SNP markers associated with specific resistance to race 5 of Px in chromosome 12, in close proximity to the microsatellite markers previously described by Fukino et al [ 17 ] and Beraldo-Hoischen et al [ 33 ].…”

“…The effect of the detected SNPs was calculated with SNPeff ( Supplementary Table S4 ). Regarding other accessions, different candidate resistance genes have recently been proposed using a similar approach [ 19 , 24 , 25 , 35 ]. There were SNPs affecting the coding region of 19 genes located within the candidate region on chromosome 12.…”

“…To date, several genes and QTL associated with resistance to CPM have been mapped in different melon populations derived from several genetic sources, including Pm-x [ 14 ], Pm-x1,5 and Pm-x3 [ 15 ], Pm2F [ 16 ], QTL (AR5) [ 17 ], and Pm-Edisto47-2 [ 18 ] on chromosome 2; qPx1-4 [ 19 ] on chromosome 4; Pm-w [ 20 ], Pm-R [ 21 ], Pm-AN [ 22 ], qPx1-5 [ 19 ], and QTL PmV-1-Pi124112 [ 23 ] on chromosome 5; CmPMrs [ 24 ] and qPx1-10 [ 19 ] on chromosome 10; Pm-y [ 14 ], QTL PmXII-1-Pi124112 [ 23 ], QTL (AR5) [ 17 ], Pm-Edisto47-1 [ 18 ], CmPMR1 [ 24 ], qPx1-12 [ 19 ], qCmPMR-12 [ 25 ], and BPm12.1 [ 26 ] on chromosome 12; and Pm-1 [ 27 ] on LGIX. Most of these resistances are race-specific and controlled by one or two dominant genes.…”

“…Most of these resistances are race-specific and controlled by one or two dominant genes. Epistatic effects have been described between CmPMrs and CmPMR1 QTLs [ 24 ], as well as between qPx1-5 and qPx1-12 [ 19 ]. In addition, several studies reported that Mildew Locus O (MLO) genes act as susceptibility factors in CPM disease and their inactivation of specific MLO genes (knock-out or knock-down) leads to a mediating form of mlo resistance [ 28 , 29 ].…”