Phenotype of the Tomato high pigment-2 Mutant Is Caused by a Mutation in the Tomato Homolog of DEETIOLATED1

Mustilli, Anna Chiara; Fenzi, Francesca; Ciliento, Rosalia; Alfano, Flora; Bowler, Chris

doi:10.2307/3870847

Cited by 76 publications

(143 citation statements)

References 29 publications

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“…The phenotype in LeCOP1LIKE-repressed seedlings is similar to that observed for the hp1 and hp2 mutations (11,19,35) in that little, if any, phenotypic variation is observed in the dark. The data for LeHY5-and LeCOP1LIKE-repressed lines suggest that these genes represent antagonistic components of tomato light signal transduction useful in assessing the potential for manipulating this regulatory pathway for modified fruit color and nutrient quality.…”

Section: Lehy5 and Lecop1like Antagonistically Modify Hypocotyl Growthsupporting

confidence: 68%

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Manipulation of light signal transduction as a means of modifying fruit nutritional quality in tomato

Liu

Roof

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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408

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Fruit constitutes a major component of human diets, providing fiber, vitamins, and phytonutrients. Carotenoids are a major class of compounds found in many fruits, providing nutritional benefits as precursors to essential vitamins and as antioxidants. Although recent gene isolation efforts and metabolic engineering have primarily targeted genes involved in carotenoid biosynthesis, factors that regulate flux through the carotenoid pathway remain largely unknown. Characterization of the tomato high-pigment mutations (hp1 and hp2) suggests the manipulation of light signal transduction machinery may be an effective approach toward practical manipulation of plant carotenoids. We demonstrate here that hp1 alleles represent mutations in a tomato UV-DAMAGED DNA-BINDING PROTEIN 1 (DDB1) homolog. We further demonstrate that two tomato light signal transduction genes, LeHY5 and LeCOP1LIKE, are positive and negative regulators of fruit pigmentation, respectively. Down-regulated LeHY5 plants exhibit defects in light responses, including inhibited seedling photomorphogenesis, loss of thylakoid organization, and reduced carotenoid accumulation. In contrast, repression of LeCOP1LIKE expression results in plants with exaggerated photomorphogenesis, dark green leaves, and elevated fruit carotenoid levels. These results suggest genes encoding components of light signal transduction machinery also influence fruit pigmentation and represent genetic tools for manipulation of fruit quality and nutritional value.

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Section: Lehy5 and Lecop1like Antagonistically Modify Hypocotyl Growthsupporting

confidence: 68%

“…Genetic analysis of the hp2 alleles revealed mutations in a negative regulator of light signal transduction, DE-ETIOLATED1 (DET1), originally defined in Arabidopsis (19,20). Here we demonstrate that hp1 is a mutation in a tomato UV-DAMAGED DNA-BINDING PROTEIN 1 (DDB1) homolog whose Arabidopsis counterpart interacts with DET1 (21).…”

mentioning

confidence: 97%

Manipulation of light signal transduction as a means of modifying fruit nutritional quality in tomato

Liu

Roof

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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408

365

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“…From Arabidopsis mutants we have come to know of the involvement of quinones in the desaturation reactions (the pds1 mutant) [42], the necessity for an alternative oxidase (PTOX) in non-green plastids (immutans) [43,44], and the need for a carotene isomerase (CRTISO; mutant ccr2) [45]. From tomato mutants, we have learned of a fruit-specific PSY (yellow flesh) [46], a linkage between carotenogenesis and light signal transduction (high pigment) [47], the need for an alternative oxidase (ghost) [48], the existence of a second LCYb that also serves as the NSY (high-beta and old-gold crimson) [49], and the need for a carotene isomerase (tangerine) [50]. A number of other Arabidopsis and tomato carotenoid mutants are currently under study, as are some interesting mutants of cauliflower (Or) [51] and carrot (rp) [52].…”

Section: Current and Future Approachesmentioning

confidence: 99%

Regulation of carotenoid synthesis and accumulation in plants

Cunningham

2002

Pure and Applied Chemistry

117

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Although genes that encode most enzymes of the carotenoid pathway in higher plants have been identified, the regulatory mechanisms that govern the synthesis and accumulation of carotenoid pigments are still obscure. Recent findings relevant to two aspects of carotenoid pathway control are reviewed: availability of substrate and pathway branching. Experimental approaches that are likely to enhance our understanding of carotenoid pathway regulation are also described.

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“…The molecular basis of three of them has been determined: yellow-flesh (r), a loss-of-function mutation in the Psy-1 gene (15); Delta, a dominant mutation in the gene CrtL-e (11); and high-pigment-2 (hp-2), a mutation in the tomato homolog of the Arabidopsis signal transduction gene Det1 (16).…”

mentioning

confidence: 99%

An alternative pathway to β-carotene formation in plant chromoplasts discovered by map-based cloning of Beta and old-gold color mutations in tomato

Ronen

Carmel-Goren

Zamir

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

557

473

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Carotenoid pigments in plants fulfill indispensable functions in photosynthesis. Carotenoids that accumulate as secondary metabolites in chromoplasts provide distinct coloration to flowers and fruits. In this work we investigated the genetic mechanisms that regulate accumulation of carotenoids as secondary metabolites during ripening of tomato fruits. We analyzed two mutations that affect fruit pigmentation in tomato (Lycopersicon esculentum): Beta (B), a single dominant gene that increases ␤-carotene in the fruit, and old-gold (og), a recessive mutation that abolishes ␤-carotene and increases lycopene. Using a map-based cloning approach we cloned the genes B and og. Molecular analysis revealed that B encodes a novel type of lycopene ␤-cyclase, an enzyme that converts lycopene to ␤-carotene. The amino acid sequence of B is similar to capsanthin-capsorubin synthase, an enzyme that produces red xanthophylls in fruits of pepper (Capsicum annum). Our results prove that ␤-carotene is synthesized de novo during tomato fruit development by the B lycopene cyclase. In wild-type tomatoes B is expressed at low levels during the breaker stage of ripening, whereas in the Beta mutant its transcription is dramatically increased. Null mutations in the gene B are responsible for the phenotype in og, indicating that og is an allele of B. These results confirm that developmentally regulated transcription is the major mechanism that governs lycopene accumulation in ripening fruits. The cloned B genes can be used in various genetic manipulations toward altering pigmentation and enhancing nutritional value of plant foods.

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Phenotype of the Tomato high pigment-2 Mutant Is Caused by a Mutation in the Tomato Homolog of DEETIOLATED1

Cited by 76 publications

References 29 publications

Manipulation of light signal transduction as a means of modifying fruit nutritional quality in tomato

Manipulation of light signal transduction as a means of modifying fruit nutritional quality in tomato

Regulation of carotenoid synthesis and accumulation in plants

An alternative pathway to β-carotene formation in plant chromoplasts discovered by map-based cloning of Beta and old-gold color mutations in tomato

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