Epigenetic floral homeotic mutation in pD991-AP3-derived T-DNA-tagged lines for CTP:Phosphorylcholine cytidylyltransferase (CCT) Genes: The homeotic mutation of the cct1-1 allele is enhanced by the cct2 allele and alleviated by CCT1 overexpression

Yoshinori Hayakawa, Zhongrui Duan, Miki Yadake, Jun Tsukano, Yasuyo Yamaoka, Rie Inatsugi, Yuki Fujiki, Akira Oikawa, Kazuki Saito, Ikuo Nishida

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The apetala3 (ap3)-like homeotic mutation (ap3-HM) is recognized among pD991-AP3-derived Arabidopsis thaliana T-DNA-tagged lines carrying the -448 to +47 region of AP3 in their T-DNA. In the corresponding mutant lines for CTP:phosphorylcholine cytidylyltransferase genes, cct1-1 and cct2 (Inatsugi et al. 2009), some flowers of cct1-1 (F4) and many flowers of cct1-1 cct2 (F3) showed ap3-HM, and all flowers of cct1-1 (F5) and cct1-1 cct2 (F4) became increasingly homeotic. In contrast, cct2 flowers were normal for all generations tested. These results demonstrated that ap3-HM is linked to the cct1-1 allele and is enhanced by the cct2 allele. The ap3-HM in cct mutants was inversely correlated with AP3 transcript levels in enriched flower buds. Bisulfite sequencing revealed severe methylation within endogenous AP3 promoter regions in cct1-1 (F3; -317 to -2) and cct1-1 cct2 (F3; -473 to -2), but wild-type (Wassilevskaja) and cct2 plants showed no corresponding methylation. The ap3-HM in cct1-1 cct2 mutants was fully rescued by expressing a PISTILLATA promoter–AP3 construct, and was better alleviated in the F1 offspring of a cross with the CCT1-overexpressing mutant cct1-2 (Columbia) than with the wild type. We discuss possible links between expression of CCT and suppression of ap3-HM.

Original languageEnglish
Pages (from-to)183-192
Number of pages10
JournalJournal of Plant Biology
Issue number3
Publication statusPublished - 2015 Jun 29
Externally publishedYes



  • CTP:phosphorylcholine cytidylyltransferase
  • DNA methylation
  • Floral homeotic mutation
  • Homology-dependent gene silencing

ASJC Scopus subject areas

  • Plant Science

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