Abstract
Elemental sulfur is an effective, inexpensive fungicide for many foliar pathogens, but severe phytotoxicity prohibits its use on many melon varieties. Sulfur phytotoxicity causes chlorosis and necrosis of leaf tissue, leading to plant death in the most sensitive lines, while other varieties have little to no damage. A high-density, genotyping-by-sequencing (GBS)-based genetic map of a recombinant inbred line (RIL) population segregating for sulfur tolerance was used for a quantitative trait loci (QTL) mapping study of sulfur phytotoxicity in melon. One major (qSulf-1) and two minor (qSulf-8 and qSulf-12) QTL were associated with sulfur tolerance in the population. The development of Kompetitive Allele-Specific PCR (KASP) markers developed across qSulf-1 decreased the QTL interval from 239 kb (cotyledons) and 157 kb (leaves) to 97 kb (both tissues). The markers were validated for linkage to sulfur tolerance in a set of melon cultivars. These KASP markers can be incorporated into melon breeding programs for introgression of sulfur tolerance into elite melon germplasm.
Highlights
Elemental sulfur is widely used as an organic fungicide in fruit and vegetable crops for control of powdery mildew and rusts (Williams and Cooper, 2004)
A previously described recombinant inbred line (RIL) population (Branham et al, 2018) consisting of 170 lines generated from a cross of MR-1 and Ananas Yok’neum (AY) was evaluated for elemental sulfur tolerance
The strong skew towards tolerance in the response of the RIL population to vaporized elemental sulfur can be explained by the epistatic interactions of the genes contributing to its polygenic inheritance
Summary
Elemental sulfur is widely used as an organic fungicide in fruit and vegetable crops for control of powdery mildew and rusts (Williams and Cooper, 2004). Sulfur is an inexpensive and effective method for controlling powdery mildew (Podosphaera xanthii) (Koller, 2010; Keinath and Dubose, 2012). Sulfur can be applied to plants by direct contact, diffusion through water, or as a vapor (Bent, 1967). The underlying fungicide mechanism of sulfur is not known, but the current hypothesis is that it permeates into the fungus and interferes with mitochondrial respiration (Cooper and Williams, 2004), resulting in the inhibition of conidial germination (Gogoi et al, 2013). The Fungicide Resistance Action Committee defines sulfur’s mode of action as multi-site contact activity and is considered a low risk for pathogen resistance development.
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