Abstract
The softening of fleshy fruits, such as tomato (Solanum lycopersicum), during ripening is generally reported to result principally from disassembly of the primary cell wall and middle lamella. However, unsuccessful attempts to prolong fruit firmness by suppressing the expression of a range of wall-modifying proteins in transgenic tomato fruits do not support such a simple model. 'Delayed Fruit Deterioration' (DFD) is a previously unreported tomato cultivar that provides a unique opportunity to assess the contribution of wall metabolism to fruit firmness, since DFD fruits exhibit minimal softening but undergo otherwise normal ripening, unlike all known nonsoftening tomato mutants reported to date. Wall disassembly, reduced intercellular adhesion, and the expression of genes associated with wall degradation were similar in DFD fruit and those of the normally softening 'Ailsa Craig'. However, ripening DFD fruit showed minimal transpirational water loss and substantially elevated cellular turgor. This allowed an evaluation of the relative contribution and timing of wall disassembly and water loss to fruit softening, which suggested that both processes have a critical influence. Biochemical and biomechanical analyses identified several unusual features of DFD cuticles and the data indicate that, as with wall metabolism, changes in cuticle composition and architecture are an integral and regulated part of the ripening program. A model is proposed in which the cuticle affects the softening of intact tomato fruit both directly, by providing a physical support, and indirectly, by regulating water status.
Highlights
Researchspanningmore than40 years has targeted the causal mechanisms of fruit softening, much of it using tomato (Solariumlycopersicumr)ipening as a modelsystem.A declinein fruitfirmnesstypicallycoincides with dissolutionof the middle lamella,resulting in a reduction in intercellularadhesion, depolymerization,and solubilizationof hemicellulosicand pectic cell wall polysaccharides and, in some cases, wall swelling (Brummelland Harpster,2001).Theseevents are accompanied by the increased expression of numerous cell wall degrading enzymes, including
Other studies have reported substantial variation among normally softening tomato cultivarsof cellwall polysaccharidedepolymerization, the abundanceof cell wall degradingproteinsand the correspondingenzyme activities(Wallnerand Bloom, 1977;Careyet al., 1995;Blumeret al.,2000;Baniket al., 2001).These results indicate that the prolonged firmness of DFD fruit is not solely a consequence of impairedmetabolismof the wall and middle lamella, althoughwe cannotexclude the possibilitythatminor differencesin wall metabolism,thatwere not detected in our analyses, contributeto some extent to the differences between DFD and Ailsa Craig' (AC) softening rates
Our results suggest that multiple coordinatedprocessesareinvolved, includingdisassembly of polysaccharidenetworks in the primary wall and middle lamella and transpirationalwater/turgor loss
Summary
Researchspanningmore than years has targeted the causal mechanisms of fruit softening, much of it using tomato (Solariumlycopersicumr)ipening as a modelsystem.A declinein fruitfirmnesstypicallycoincides with dissolutionof the middle lamella,resulting in a reduction in intercellularadhesion, depolymerization,and solubilizationof hemicellulosicand pectic cell wall polysaccharides and, in some cases, wall swelling (Brummelland Harpster,2001).Theseevents are accompanied by the increased expression of numerous cell wall degrading enzymes, including. The Tomato Fruit Cuticle, Water Relations, and Softening polysaccharidehydrolases, transglycosylases,lyases, and other wall loosening proteins, such as expansin (Harkeret al., 1997;Roseet al., 2003;Brummell,2006). An alternativeexplanation is that polysaccharidedegradationis not the sole determinantof fruit softening and that other ripening-relatedphysiological processes play criticalroles. Wehave addressed this latterhypothesis by evaluating a previously uncharacterizedtomato cultivar, referred to here as 'Delayed Fruit Deterioration' (DFD), whose fruits undergo normal ripening, but remainfirmand show no loss of integrityfor remarkably extended periods after reaching the fully ripe stage. We reportthat ripening-relateddisassembly of the cell wall and middle lamella have similar characteristicsin fruitsfromDFDand the normallysoftening 'Ailsa Craig' (AC), even though DFD fruits typically remainfirmforatleast monthsafterachievinga fully ripe stage. Our results suggest that while changes in the polysaccharidecomponentsof thecellwall areundoubtedly important for fruit texture, equivalent alterations in cuticlearchitectureare an integralelement of the ripeningprogram.The data highlight the mechanisticdistinctionbetween a reductionin firmness,or resistanceto compression,of intactfruit,and ripening-
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