Firmness is an important trait for fruit quality. It is related to shelf-life and to fruit texture, and thus has been frequently measured in genetic studies. Several long shelf-life mutants have contributed to the understanding of fruit maturation (Giovannoni 2001, 2004; Seymour et al. 2002). The first to be described, Never ripe (Nr, Rick 1956) was the first cloned (Wilkinson etal. 1995). The Nr gene encodes a protein homologous to ETR1 in Arabidopsis. ETR1 is an ethylene receptor, explaining the phenotype of the Nr mutant, which is insensitive to ethylene. The mutants ripening-inhibitor (rin, Robinson and Tomes 1968) and non-ripening (nor, Tigchelaar et al. 1973) are defective in ethylene biosynthesis. The corresponding genes encode MADS-box transcription factors (Vre-balov et al. 2002). The Colourless nonripening (Cnr) mutation, modified in cell-to-cell adhesion, is an epi-genetic mutation in a SQUAMOSA promoter binding protein box (SBP-box) transcription factor (Manning et al. 2006).
Firmness has also been used in quantitative genetic studies. Figure 8 presents a summary of QTLs controlling fruit firmness in nine populations (Tanksley et al. 1996; Fulton et al. 1997,2000; Bernacchi et al. 1998b; Causse et al. 2002; Doganlar et al. 2002c; Frary et al. 2003b, 2004; Walley and Seymour 2006). Forty-six QTLs controlling firmness were mapped using seven different populations. Firmness was measured by touching (30 QTLs), by mechanical instrumentation (11 QTLs), or by taste (5 QTLs). In some cases the QTLs obtained by these three different methods co-localized. More than half of the QTLs were grouped in clusters of three to four QTLs. These clusters were localized on chromosomes 1, 2, 4, 5, and 9-11. On chromosomes 2, 5, and 10, the genes rin, nor, and Cnr co-localized with firmness QTLs. It would be interesting to discover whether these QTLs are controlled by rin, nor and Cnr.
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