Analysis of transposition mechanisms of the active transposon firstly identified in rice

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A mutable slender mutant (line : IM294) was induced with gamma-ray irradiation to seeds of the rice variety Gimbozu. This mutant character is governed by a recessive mutant gene and has never been fixed in spite of repeated self-propagation. Our previous study suggested that the mutability is caused by the precise excision of a MITE (Miniature Invereted-repeat Transposable Element mPing) that was inserted in the wild type allele at the Rurm1(Rice ubiquitin related modifier 1) locus. The present study confirmed this point, and also indicated that mPing, which lacks coding region, is a deletion derivative of a 5.2-kb element named Ping. There was a related element of Ping named Pong in the rice genom. Both elements contained two open reading frames(ORFs). The function of ORF1 is unknown, while the ORF2 is assumed to encode the transposase. The excision frequencies of mPing at six mPing insertion sites were compared among two varieties and IM294. No excision was found in Gimbozu and Nipponbare, while in IM294 six excision events were observed at the two sites. This indicates that the inactivation of Rurm1 might affect the transposition activity of mPing. We investigated transcription activities of Rurm1 alleles and the two ORFs of Ping and Pong by real time quantitative PCR and found that the activities of Ping ORFs and Pong ORF1 showed a significant increase in IM294. This suggests that Rurm1^+ inhibits the transcription and amplification of Ping and mPing occurred simultaneously in the Gimbozu genome. A gamma-ray irradiation significantly increased the copy number of Ping in the Gimbozu genome. These results indicate that Gimbozu genetic background and the rare mutation at the Rurm1 locus will provide a basic model for the amplification of MITE in several organisms.