Detection and cloning of unique integration sites of retrotransposon, intracisternal A‐particle element in the genome of acute myeloid leukemia cells in mice<sup>1</sup>

Ishiguro, Hiroshi; Tanaka, Izumi

doi:10.1016/s0014-5793(97)01383-5

Cited by 11 publications

(9 citation statements)

References 17 publications

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“…Active role of I⌬1-type IAP protein in trans-complementation IAP-transposition has been reported in both germ cells and somatic tissues (Ishihara and Tanaka 1997;Maksakova et al 2006). In both cases, most of the transposed elements were I⌬1 type with an internal deletion that results in in-frame fusion of gag-pol genes (Kuff and Lueders 1988).…”

Section: Resultsmentioning

confidence: 99%

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Translation from nonautonomous type IAP retrotransposon is a critical determinant of transposition activity: Implication for retrotransposon-mediated genome evolution

Saito¹,

Keng²,

Takeda³

et al. 2008

Genome Res.

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Retrotransposons constitute a major component of the genome and their proliferation significantly impacts genome evolution. Retrotransposons can propagate autonomously or nonautonomously. Nonautonomous type transposition occurs through trans-complementation by autonomous type retrotransposons. While autonomous type retrotransposons have been studied extensively, the translation products from nonautonomous type retrotransposons are not well characterized. In a previous study, we isolated both autonomous and nonautonomous type intracisternal A particle (IAP) elements from the mouse genome and established a tissue culture assay to examine trans-complementation of nonautonomous type IAP element. Using this system in the present study, we determined an active role for the translation product from nonautonomous type IAP element. Point mutations that either eliminated or truncated the IAP protein were introduced and their effects on trans-complementation were examined. Trans-complementation efficiency correlated with the expression of nonautonomous type IAP protein. The effect of nonautonomous type IAP protein was observed only when it was provided in cis, suggesting an interaction of nonautonomous type IAP protein and its transcript immediately after transcription. Interaction of autonomous and nonautonomous type IAP proteins was demonstrated by immunostaining and coimmunoprecipitation assay. Based on these findings, we propose a model in which nonautonomous type IAP protein associates with its transcript, recruits autonomous type IAP protein, and promotes the assembly of transposition competent IAP particle. The active role of the nonautonomous type IAP protein revealed in this study may provide a new insight into retrotransposon proliferation within the genome.

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Section: Resultsmentioning

confidence: 99%

“…A previous study reported frequent IAP-transposition in radiation-induced mouse acute myeloid leukemia (AML) (Ishihara and Tanaka 1997). We hypothesized that IAP-transposition in AML may provide a unique experimental system to investigate the regulatory mechanisms of retrotransposon proliferation.…”

mentioning

confidence: 99%

Translation from nonautonomous type IAP retrotransposon is a critical determinant of transposition activity: Implication for retrotransposon-mediated genome evolution

Saito¹,

Keng²,

Takeda³

et al. 2008

Genome Res.

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“…Although the full-length type constitutes 70% of the entire IAP population in the mouse genome (Kuff and Lueders 1988), mostly ID1 type were found as a causative insertion of spontaneous mutant mice (Maksakova et al 2006), consistent with the predominance of ID1 type in our analysis of AML cells. The full-length IAP element, designated as Q14 (Ishihara and Tanaka 1997), retained the open reading frames of gag, pro, and pol genes, suggesting that it is an autonomous IAP element. We therefore isolated the Q14 IAP element from the AML genome and inserted an indicator GFP cassette that contains an intron in the antisense orientation relative to the GFP gene (Ostertag et al 2000) (Figure 1A).…”

Section: Resultsmentioning

confidence: 99%

“…We have previously reported a high frequency of IAP retrotransposition in radiation-induced mouse acute myeloid leukemia (AML) in C3H/He mice (Ishihara and Tanaka 1997) and identified eight IAP elements that retrotransposed during AML formation (Ishihara et al 2004). We hypothesized that these retrotranspositioncompetent IAP elements could be useful tools for studying the direct effect of retrotransposition on the genome.…”

mentioning

confidence: 99%

Retrotransposons Influence the Mouse Transcriptome: Implication for the Divergence of Genetic Traits

Horie¹,

Saito²,

Keng

et al. 2007

Genetics

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Massive accumulation of retrotransposons, comprising .40% of human and mouse genomes, is one of the major events in the evolution of the genome. However, most retrotransposons have lost retrotransposition competency, which makes studying their role in genome evolution elusive. Intracisternal A-particle (IAP) elements are long terminal repeat (LTR)-type mouse retrotransposons consisting of fulllength and internally deleted types. Some are retrotransposition competent and their upregulated activity has been reported in mutant mice deficient in genome defense systems, suggesting that IAP elements provide a unique platform for studying the interaction between retrotransposons and mammalian genomes. Using the IAP element as a model case, here we show that mobilization of retrotransposons alters the mouse transcriptome. Retrotransposition assay in cultured cells demonstrated that a subset of internally deleted IAP elements, called ID1 type, retrotranspose efficiently when supplied with functional IAP proteins. Furthermore, the ID1 type IAP element exhibited substantial transcription-inducing activity in the flanking region. Genomewide transcript analysis of embryonic stem (ES) cells identified IAPinduced transcripts, including fusion transcripts between IAP sequence and endogenous genes. Unexpectedly, nearly half of these IAP elements obtained from ES cells derived from 129 mouse strain were absent in the C57BL/6 genome, suggesting that IAP-driven transcription contributes to the unique trait of the individual mouse strain. On the basis of these data, we propose that retrotransposons are one of the drivers that shape the mammalian transcriptome.

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“…30,39,40,50 IAP insertions have been observed during cultivation of mouse hematopoietic stem cell lines and in mouse tumor cells. [51][52][53][54] Engineered L1 elements can retrotranspose when introduced into human ES cells, human and rat neural progenitor cells, human oocytes, primary human fibroblasts, a variety of cancer cell lines, and retrotranspose at higher levels in response to oxidative stress and ionizing radiation. [29][30][31]36,[55][56][57][58][59] The extent of ongoing retrotransposition in mammals…”

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confidence: 99%

Consequences of ongoing retrotransposition in mammalian genomes

Maxwell

2014

AGG

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Abstract:Retrotransposons can have significant influences on gene expression and genome stability through their ability to integrate reverse-transcript copies of their sequences at new genomic locations by retrotransposition. These elements have been long known to retrotranspose in mammalian germ cells to give rise to inherited insertion alleles, but more recent work has also shown that retrotransposition can occur in mammalian somatic cells, particularly in brain tissue and tumors. Retrotransposition makes appreciable contributions to spontaneous diseasecausing alleles in humans and a more significant contribution to spontaneous mutations in mice. Genome-wide studies have found high levels of polymorphic retrotransposon insertions in human populations that are consistent with ongoing retrotransposition. Many insertions do not disrupt exons, but insertions into introns or flanking genes can alter gene expression patterns, generate truncated or antisense gene transcripts, alter splicing patterns, or result in premature polyadenylation of gene transcripts. Furthermore, the very high genomic copy numbers of these elements can lead to nonallelic homologous recombination events that produce gene deletions/ duplications and genome rearrangements, and can also lead to evolution of particular insertions or types of elements to have cellular functions through exaptation. Mobility of these elements occurs despite multiple epigenetic mechanisms to restrict their expression. While the potential for retrotransposons to significantly influence mammalian health and cellular functions is clear, substantial research efforts will be needed to fully elucidate the actual contributions of natural levels of mobility of endogenous elements to the health and development of humans and other mammals.

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Detection and cloning of unique integration sites of retrotransposon, intracisternal A‐particle element in the genome of acute myeloid leukemia cells in mice¹

Abstract: We previously found retrotransposition of the intra-

Cited by 11 publications

References 17 publications

Translation from nonautonomous type IAP retrotransposon is a critical determinant of transposition activity: Implication for retrotransposon-mediated genome evolution

Translation from nonautonomous type IAP retrotransposon is a critical determinant of transposition activity: Implication for retrotransposon-mediated genome evolution

Retrotransposons Influence the Mouse Transcriptome: Implication for the Divergence of Genetic Traits

Consequences of ongoing retrotransposition in mammalian genomes

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Detection and cloning of unique integration sites of retrotransposon, intracisternal A‐particle element in the genome of acute myeloid leukemia cells in mice1

Abstract: We previously found retrotransposition of the intra-

Cited by 11 publications

References 17 publications

Translation from nonautonomous type IAP retrotransposon is a critical determinant of transposition activity: Implication for retrotransposon-mediated genome evolution

Translation from nonautonomous type IAP retrotransposon is a critical determinant of transposition activity: Implication for retrotransposon-mediated genome evolution

Retrotransposons Influence the Mouse Transcriptome: Implication for the Divergence of Genetic Traits

Consequences of ongoing retrotransposition in mammalian genomes

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Detection and cloning of unique integration sites of retrotransposon, intracisternal A‐particle element in the genome of acute myeloid leukemia cells in mice¹