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Plant Physiology Preview Published on February 2, 2007; 10.1104/pp.106.091413
Received October 18, 2006 Candidate Genes and QTLs Affecting Fruit Ascorbic Acid Content in Three Tomato Populations
INRA, UR1052, Unité de génétique et amélioration des fruits et légumes, Domaine St Maurice BP94, 84143 Montfavet, France; INRA, UMR A408, Sécurité et qualité des produits d'origine végétale, Domaine St Paul, Site Agroparc, 84914 Avignon cedex 9, France; INRA, UMR Physiologie et Biotechnologie Végétale, BP 81, 33883 Villenave d'Ornon, France * Corresponding author; email: stevens{at}avignon.inra.fr.
Fresh fruit and vegetables are a major source of ascorbic acid (vitamin C), an important antioxidant for the human diet and also for plants. Ascorbic acid content in fruit exhibits a quantitative inheritance. QTLs for ascorbic acid content have been mapped in three tomato populations derived from crosses between cultivated tomato varieties (Solanum lycopersicum accessions) and three related wild species or subspecies. The first population consists of a set of introgression lines derived from Solanum pennellii, each containing a unique fragment of the wild species genome. The second population is an advanced backcross population derived from a cross between a cultivated tomato and an S. habrochaites (formerly L. hirsutum) accession. The third population is a recombinant inbred line population derived from the cross between a cherry tomato line and a large fruited line. Common regions controlling ascorbic acid content have been identified on chromosomes 2, 8, 9, 10 and 12. In general the wild alleles increased ascorbic acid content, but some improvement could also be provided by S. lycopersicum. Most QTLs appeared relatively stable over years and in different environments. Mapping of candidate genes involved in the metabolism of ascorbic acid has revealed a few colocations between genes and QTLs, notably in the case of a monodehydroascorbate reductase (MDHAR) gene and a QTL present in two of the populations on chromosome 9 (bin 9-D) and a GDP-mannose epimerase (GME) mapped by Zou et al (2006) and a QTL on chromosome 9 (bin 9-J).
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