A Novel “Petaloid” Mutant of Torenia (Torenia fournieri Lind. ex Fourn.) Bears Double Flowers through Insertion of the DNA Transposon Ttf1 into a C-class Floral Homeotic Gene
A Novel “Petaloid” Mutant of Torenia (Torenia fournieri Lind. ex Fourn.) Bears Double Flowers through Insertion of the DNA Transposon Ttf1 into a C-class Floral Homeotic Gene
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DOI：
10.2503/hortj.mi-108
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发表时间：
2016
期刊：
影响因子：
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通讯作者：
T. Nishijima;T. Niki;T. Niki
中科院分区：
文献类型：
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作者：
T. Nishijima;T. Niki;T. Niki
一种重花托伦尼亚（托伦尼亚）。（ex Fourn.）突变体“Petaloid”是从“Flecked”突变体的自生后代中获得的，其中DNA转座子Ttf1的转位是活跃的。正常的托尔尼花有一个合生的花萼，由5片萼片组成，一个合生的花冠由5片花瓣组成，4个不同的雄蕊，和一个合生的雌蕊由2个心皮组成。相比之下，“Petaloid”突变体的花有4个不同的花瓣由雄蕊转化而来，而花萼、花冠和雌蕊保持不变。“Petaloid”突变体重瓣性状不稳定；部分或全部的4瓣由雄蕊转化而来，经常恢复为雄蕊。此外，大多数体细胞逆转花自花授粉获得的S1植株只开出正常的单花。在雄蕊转化的花瓣中，c级花同源基因T. fournieri FARINELLI （TfFAR）的表达几乎完全被抑制。这种抑制作用是由Ttf1插入到TfFAR的第二个内含子中引起的，而从TfFAR中切除Ttf1引起了转化花瓣向雄蕊的逆转。TfFAR基因型与花型的明显对应表明，Ttf1插入的TfFAR等位基因纯合子导致了突变表型。相比之下，TfFAR在“Petaloid”突变体的雌蕊中表达适度，雌蕊保持不变。我们成功地通过突变型和正常型植物之间的异花授粉灭活Ttf1转座，使Ttf1转座子与激活其转座的未知因子遗传分离，从而使“Petaloid”突变更加稳定。
A double-flowered torenia (Torenia fournieri Lind. ex Fourn.) mutant, “Petaloid”, was obtained from selfed progeny of the “Flecked” mutant, in which the transposition of the DNA transposon Ttf1 is active. A normal torenia flower has a synsepalous calyx consisting of 5 sepals, a synpetalous corolla consisting of 5 petals, 4 distinct stamens, and a syncarpous pistil consisting of 2 carpels. In contrast, a flower of the “Petaloid” mutant has 4 distinct petals converted from stamens, whereas the calyx, corolla, and pistil remain unchanged. The double-flower trait of the “Petaloid” mutant was unstable; some or all of the 4 petals converted from stamens frequently reverted to stamens. Furthermore, most S1 plants obtained from self-pollination of the somatic revertant flower bore only normal single flowers. In petals converted from stamens, expression of the C-class floral homeotic gene T. fournieri FARINELLI (TfFAR) was almost completely inhibited. This inhibition was caused by insertion of Ttf1 into the 2nd intron of TfFAR, whereas reversion of converted petals to stamens was caused by excision of Ttf1 from TfFAR. The clear correspondence of the TfFAR genotype to the floral phenotype suggested that homozygous TfFAR alleles with the Ttf1 insertion caused the mutant phenotype. In contrast, TfFAR was moderately expressed in the pistil of the “Petaloid” mutant, leaving the pistil unchanged. We succeeded in inactivating Ttf1 transposition by cross-pollination between mutant and normal-type plants to genetically separate the transposon Ttf1 from the unidentified factor activating its transposition, which made the “Petaloid” mutation more stable.