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Plant and Cell Physiology, 2003, Vol. 44, No. 10 990-1001
© 2003 Oxford University Press

Spontaneous Mutations of the Flavonoid 3'-hydroxylase Gene Conferring Reddish Flowers in the Three Morning Glory Species

Atsushi Hoshino1,5, Yasumasa Morita1,5, Jeong-Doo Choi1,5, Norio Saito2, Kenjiro Toki3, Yoshikazu Tanaka4 and Shigeru Iida1,6

1 National Institute for Basic Biology, Okazaki, 444-8585 Japan
2 Chemical Laboratory, Meiji-Gakuin University, Yokohama, 244-8539 Japan
3 Laboratory of Floriculture, Minami Kyusyu University, Takanabe, 884-0003 Japan
4 Institute for Advanced Technology, Suntory Ltd., Shimamoto, Mishima, Osaka, 618-8503 Japan

Among the Ipomoea plants, both Ipomoea nil and Ipomoea tricolor display bright blue flowers, and Ipomoea purpurea exhibits dark purple flowers. While all of these flowers contain cyanidin-based anthocyanin pigments, the mutants of I. nil, I. purpurea, and I. tricolor carrying the magenta, pink, and fuchsia alleles, respectively, produce reddish flowers containing pelargonidin derivatives, and all of them are deficient in the gene for flavonoid 3'-hydroxylase (F3'H). The magenta allele in I. nil is a nonsense mutation caused by a single C to T base transition generating the stop codon TGA, and the cultivar Violet carries the same mutation. Several tested pink mutants in I. purpurea carry inserts of the 0.55-kb DNA transposable element Tip201 belonging to the Ac/Ds superfamily at the identical site. No excision of Tip201 from the F3'H gene could be detected, and both splicing and polyadenylation patterns of the F3'H transcripts were affected by the Tip201 integration. The fuchsia allele in I. tricolor is a single T insertion generating the stop codon TAG, and the accumulation of the F3'H transcripts was drastically reduced by the nonsense-mediated RNA decay. Spontaneous mutations in Ipomoea, including a possible founder mutation in the pink allele, are also discussed.

5 These authors contributed equally to this work.

6 Corresponding author: E-mail, shigiida{at}nibb.ac.jp; Fax, +81-564-55-7685.


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