Influence of year and genetic factors on chilling injury susceptibility in peach (Prunus persica (L.) Batsch)

Abstract

Chilling injury (CI) is a major physiological problem limiting consumption and export of peach and nectarine (Prunus persica (L.) Batsch). To clarify the genetic basis for chilling injury, inheritance of the major CI symptoms mealiness, flesh browning, flesh bleeding, and flesh leatheriness were examined over three years in two related peach progenies. In addition, genetic relationships among traits and the year-to-year variation in trait performance in these progenies were tracked. Both populations also segregated for Freestone-Melting flesh (F-M) and yellow flesh. There were significant differences in CI symptoms among years. The major gene endoPG, which controls the F-M locus, provides resistance to mealiness in nonmelting flesh fruit. Only fruit with melting flesh can develop mealiness if the tree possesses other genetic susceptibility factors and/or experiences inducing conditions. The F-M locus also greatly influences susceptibility to flesh bleeding, although the physiological mechanism for this disorder is unclear and may be controlled by a different gene closely linked to endoPG. Unlike mealiness, flesh bleeding occurred primarily in non-melting flesh fruit, particularly when the fruit is white-fleshed. Flesh browning incidence was greater in mealy fruit and was not associated with flesh bleeding. Breeding for CI resistance is thus a viable long-term strategy to reduce losses in the fresh and processed peach and nectarine industries. This study is an important first step to understanding genetic control of CI symptoms in peach.

Influence of antioxidant compounds, total sugars and genetic background on the chilling injury susceptibility of a non‐melting peach (Prunus persica (L.) Batsch) progeny

“…These authors reported that mealiness was almost non‐existent in the CNMF progeny, while bleeding incidence was higher in the CNMF progeny after 2–3 weeks of cold storage . Similarly, Martínez‐García et al reported that flesh bleeding occurs primarily in non‐melting‐flesh fruit, particularly when the fruit is white‐fleshed. Interestingly, the results of this work showed at least 17 genotypes (20, 22, 33, 44, 58, 68, 70, 72, 76, 80, 81, 96, 106, 118, 120, 124 and 129) with low susceptibility to CI symptoms and with several good organoleptic traits (values for fruit weight, vitamin C, RAC, total phenolics, flavonoids or sugars over the average).…”

In Pursuit of the Perfect Peach: Consumer-assisted Selection of Peach Fruit Traits

“…In peaches, this mealy texture is most often caused by internal tissue breakdown due to chilling injury (CI) (Lurie and Crisosto, 2005), and can significantly lower the consumer acceptability of fruit with above-average peach flavor metrics (Crisosto, 2002). In peach, mealy texture is partly determined by texture type (melting) and genetic tests have been developed to screen for susceptible varieties in breeding programs (Martínez-García et al, 2012).…”

Differential Metabolic Rearrangements after Cold Storage Are Correlated with Chilling Injury Resistance of Peach Fruits

“…Transcriptomic studies after cold storage using single genotypes (González-Agüero et al, 2008 ; Ogundiwin et al, 2008 ; Vizoso et al, 2009 ; Pavez et al, 2013 ) or contrasting genotypes with differential susceptibility to cold (Falara et al, 2011 ; Dagar et al, 2013 ; Pons et al, 2014 , 2015 ) have been powerful approaches in order to dissect the molecular mechanisms involved in peach cold tolerance. In addition, proteomic studies have also identified key proteins involved in the protection to cold or in the development of CI (Lara et al, 2009 ; Dagar et al, 2010 ; Nilo et al, 2010 ; Zhang et al, 2010 ; Almeida et al, 2016 ); while genomic studies have allowed the mapping of a number of quantitative trait loci (QTL) for CI in the peach genome (Ogundiwin et al, 2009 ; Cantín et al, 2010 ; Dhanapal et al, 2012 ; Martinez-Garcia et al, 2012 ; Nuñez-Lillo et al, 2015 ). These studies have indicated that CI is a multigenic quantitative trait, and thus, genetic engineering of CI tolerance is a very difficult challenge.…”