Structural Polymers And Molecular Pathways That Influence Tomato Fruit Integrity And Surface Quality Traits

Abstract

Plant cuticles are protective, hydrophobic, waxy coverings produced by the epidermal cells of aerial organs of land plant. The variation in fruit cuticle structure or composition may influence many commercially important fruit traits, such as storability/shelf life, surface glossiness, and resistance to desiccation, microbial infection or cracking. Despite the fundamental importance of the fruit cuticle, current knowledge of its synthesis and metabolism is relatively limited. This work describes the cloning and characterization of four tomato fruit cuticle-related mutants, including three cutin-deficient mutants (cd1, cd2 and cd3) and one early fruit cracking mutant (hcr1), each of which provides new insights into fruit cuticles and associated structural polymers. In the first part of this thesis, the different aspects of plant cuticle biology, such as cuticle structure, functions, monomer biosynthesis and assembly are briefly reviewed, summarizing present knowledge of the cutin biosynthesis pathway. The second part of this research focuses on the mapbased cloning of three cutin-deficient mutants. The cd1 mutant was identified as having a lesion in a gene in the GDSL-motif lipase/hydrolase family. Further research has demonstrated that the CD1 enzyme catalyzes extracellular cutin polymerization at the cuticle formation site. The cd2 gene was identified as a putative transcription factor in the IV group of the homeodomain-leucine zipper family (HD-Zip IV). The cd3 gene was identified as a member of CYP86A group in cytochrome P450 family, with possible catalytic activity of [omega]-hydroxylation to C16 and C18 fatty acids in the cutin biosynthesis pathway. The last part of this research focuses on the detailed characterization of hypercracking 1 (hcr1) mutant, which exhibits early fruit cracking and subsequent massive suberin deposition on the fruit surface. The HCR1 gene encodes a 3-hydroxysteroid dehydrogenase/C-4 decarboxylase (3[beta]-HSD/D1), which is a key enzyme in the sterol biosynthesis pathway. Sterol profiling showed that the mutation results in 11~16% reduction of sterol compositions in hcr1 mutant fruits. Phenotypic and biochemical analysis of the hcr1 mutant suggests that early fruit cracking probably results from the severe inhibition of cell division/expansion in pericarp. The possible physiological and molecular mechanisms underlying the abnormal cell expansion/division in hcr1 fruit are discussed.