論文

査読有り
2005年9月

Transgene-triggered, epigenetically regulated ectopic expression of a flower homeotic gene pMADS3 in Petunia

PLANT JOURNAL
  • M Kapoor
  • ,
  • A Baba
  • ,
  • K Kubo
  • ,
  • K Shibuya
  • ,
  • K Matsui
  • ,
  • Y Tanaka
  • ,
  • H Takatsuji

43
5
開始ページ
649
終了ページ
661
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1111/j.1365-313X.2005.02481.x
出版者・発行元
BLACKWELL PUBLISHING

pMADS3 is a class C floral homeotic gene of Petunia that is specifically expressed in stamens and carpels of developing flowers. We previously reported that introduction of a part of the pMADS3 genomic sequence silenced endogenous pMADS3 (sil-pMADS3) in transgenic Petunia hybrida. Here we report that introduction of the same sequence triggers ectopic expression of endogenous pMADS3 in sepals, petals and leaves (ect-pMADS3), accompanied by homeotic conversion of the floral organs and altered leaf morphology similar to that of an Arabidopsis curly leaf mutant. The occurrence of the ect-pMADS3 phenotype depended on the presence of pMADS3 intron 2 in the transgenes. Occasionally, sil-pMADS3 and ect-pMADS3 phenotypes somatically interconverted. Some T-1 progeny inherited their parent's pMADS3 expression pattern, while others switched from sil-pMADS3 to ect-pMADS3 and vice versa. Both phenotypes occasionally occurred even after the transgenes were segregated away. RT-PCR analyses of ectopically expressed pMADS3 transcripts indicated that two pMADS3 alleles were often differently regulated. Furthermore, reciprocal crosses with untransformed Petunia indicated that pMADS3 alleles other than the one ectopically expressed in T-0 plants were sometimes expressed ectopically in T-1 plants: the paramutation-like transmission of epigenetic regulation between alleles. We detected in the transformants aberrant transcripts, including sense and antisense pMADS3 intron 2 sequences of heterogeneous molecular sizes, irrespective of the pMADS3 phenotypes. We speculate on possible molecular mechanisms underlying these epigenetic phenomena.

リンク情報
DOI
https://doi.org/10.1111/j.1365-313X.2005.02481.x
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/16115063
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000231284100003&DestApp=WOS_CPL
ID情報
  • DOI : 10.1111/j.1365-313X.2005.02481.x
  • ISSN : 0960-7412
  • PubMed ID : 16115063
  • Web of Science ID : WOS:000231284100003

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