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The objective of this study was to map the quantitative trait loci (QTLs) for chip color after harvest (AH), cold storage (CS) and after reconditioning (RC) in diploid potato and compare them with QTLs for starch-corrected chip color. Chip color traits AH, CS, and RC significantly correlated with tuber starch content (TSC). To limit the effect of starch content, the chip color was corrected for TSC. The QTLs for chip color (AH, CS, and RC) and the starch-corrected chip color determined with the starch content after harvest (SCAH), after cold storage (SCCS) and after reconditioning (SCRC) were compared to assess the extent of the effect of starch and the location of genetic factors underlying this effect on chip color. We detected QTLs for the AH, CS, RC and starch-corrected traits on ten potato chromosomes, confirming the polygenic nature of the traits. The QTLs with the strongest effects were detected on chromosomes I (AH, 0 cM, 11.5% of variance explained), IV (CS, 43.9 cM, 12.7%) and I (RC, 49.7 cM, 14.1%). When starch correction was applied, the QTLs with the strongest effects were revealed on chromosomes VIII (SCAH, 39.3 cM, 10.8% of variance explained), XI (SCCS, 79.5 cM, 10.9%) and IV (SCRC, 43.9 cM, 10.8%). Applying the starch correction changed the landscape of QTLs for chip color, as some QTLs became statistically insignificant, shifted or were refined, and new QTLs were detected for SCAH. The QTLs on chromosomes I and IV were significant for all traits with and without starch correction.

Tuber tissue discolorations caused by impact (blackspot bruising) and enzymatic discoloration (ED) after tuber cutting are crucial quality traits of the cultivated potato. To understand the complex genetics of the traits, quantitative trait locus (QTL) analysis using diploid mapping population and diversity array technology (DArT) markers was performed. The phenotypic assessment included the complex evaluation of blackspot bruising susceptibility through two methods: rotating drum (B RD ) and falling bolt (B FB ) in combination with the evaluation of enzymatic discoloration. Because of observed in-practice relationship between bruising susceptibility and tuber starch content (TSC), analysis of starch content-corrected bruising susceptibility (SCB) was performed. QTLs for bruising were detected on chromosomes I, V with both test methods. The rotating drum method enabled the detection of additional QTLs on chromosomes VIII and XII. Analysis of SCB enabled the identification of the major QTL on chromosome V and two weaker QTLs on chromosomes VIII and XII, independently of starch content. The QTL for bruising detected on chromosome I overlapped with the most significant QTL for tuber starch content. This QTL was not significant for starch content-corrected bruising susceptibility, and the effect of the QTL on chromosome V was enhanced for this trait. The QTL analysis of ED revealed the contribution of seven QTLs for the trait, located on six chromosomes, including these detected for the first time: a major locus on chromosome V and minor QTLs on chromosomes VII and X, which were specific for the trait. The QTL for ED on chromosome VIII was co-localized with the marker for polyphenol oxidase (POT32). The phenotypic correlation between bruising and ED was confirmed in QTL analyses of both traits, and the QTLs detected for these traits overlapped on chromosomes I, V, and VIII. Our results should provide a basis for further studies on candidate genes affecting blackspot bruise susceptibility and enzymatic discoloration.