Interruption of two immunoglobulin heavy-chain switch regions in murine plasmacytoma P3.26Bu4 by insertion of retroviruslike element ETn.

Shell, Briton E.; Szurek, Paul F.; Dunnick, Wesley A.

doi:10.1128/mcb.7.4.1364

Cited by 26 publications

(17 citation statements)

References 47 publications

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“…The reported sequence of the ETn long terminal repeat upstream of that present in the RARa' mRNA is CCTAG (60), which closely resembles the consensus sequence of the splice acceptor site. ETn has a structure suggestive of a retrotransposon (60), and it has appeared in new mutations of murine T (29) and immunoglobulin (58) genes. It is possible, therefore, that the rearrangement in RAC65 cells occurred as a result of insertion of an ETn retrotransposon into intron 6 of the RARa gene.…”

Section: Discussionmentioning

confidence: 99%

A dominant negative mutation of the alpha retinoic acid receptor gene in a retinoic acid-nonresponsive embryonal carcinoma cell.

1990

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Pluripotential embryonal carcinoma cells such as those of the P19 line differentiate when exposed to retinoic acid (RA). The RAC65 cell line is a mutant clone of P19 cells selected to be RA nonresponsive. RAC65 cells carry a rearrangement affecting one of the genes encoding a nuclear retinoic acid receptor (RAR alpha). The mutant gene encodes a protein, RAR alpha', that has lost its 70 C-terminal amino acids, thus truncating the RA-binding domain. The RAR alpha' was found to be a dominant repressor of transcription from an RA-responsive target gene; however, expression of RAR alpha' was insufficient to confer RA nonresponsiveness, suggesting that RAC65 cells carry an additional mutation(s) affecting RA-induced genes.

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Section: Discussionmentioning

confidence: 99%

A dominant negative mutation of the alpha retinoic acid receptor gene in a retinoic acid-nonresponsive embryonal carcinoma cell.

1990

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“…The ETn family comprises 5.7-kb elements that can be classified into two groups differing by the 3Ј-half of the LTR and the 5Ј-internal region (Shell et al 1990): ETn I with 200 copies per haploid genome of C57BL/ 6J mice, and ETn II with 40 copies (Baust et al 2003). Their expression is limited to embryos, peaking between embryonic days 3.5 (E3.5) and E7.5 , as well as to a few cell lines (Brûlet et al 1983;Shell et al 1987;Tanaka and Ishihara 2001). ETn elements are related to MusD elements, another murine LTR-retrotransposon family (Mager and Freeman 2000).…”

mentioning

confidence: 99%

An active murine transposon family pair: Retrotransposition of “master” MusD copies and ETn trans-mobilization

Ribet¹,

Dewannieux²,

Heidmann³

2004

Genome Res.

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The ETn (Early Transposon) elements are among the most active murine mobile sequences, being responsible for a series of mutations by insertion in vivo. Yet they are noncoding, and it had long been suspected that ETn are mobilized in trans by coding-competent elements, most probably from the closely related MusD family of LTR-retrotransposons. A genome-wide in silico search for coding-competent MusD elements identified a total of nine such copies, which we cloned and marked to test their transpositional activity, using an ex vivo assay in heterologous cells. Three copies were found to be autonomous for transposition, with each gag, pro, and pol MusD gene absolutely required for mobility. These active MusD copies specifically trigger retrotransposition of marked ETn elements with high efficiency, by complementation in trans. Characterization of the structures of de novo transposed MusD and ETn marked elements, as well as of their integration sites, disclosed canonical retroviral-like retrotransposition, with 6-bp target site duplications common to both elements. These results highlight the parasitic molecular strategies that are used by the ETn elements for their mobility, and unambiguously identify their "master genes."

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“…However, little is known about the expression levels or copy numbers of MusD and the different ETn groups. ETn transcripts were found in plasmacytoma and embryonic carcinoma cells, as well as in normal cells of the early embryo, where the expression peaks between day 3.5 and 7.5 (3,35). Tanaka and Ishihara (40) described high levels of RNA in acute myeloid leukemia cells from C3H/He inbred mice but only a small amount in hepatomas, lymphomas, and normal cells (liver, thymus, and spleen cells).…”

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confidence: 99%

Structure and Expression of Mobile ETnII Retroelements and Their Coding-Competent MusD Relatives in the Mouse

Baust

Gagnier

Baillie

et al. 2003

J Virol

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ETnII elements are mobile members of the repetitive early transposon family of mouse long terminal repeat (LTR) retroelements and have caused a number of mutations by inserting into genes. ETnII sequences lack retroviral genes, but the recent discovery of related MusD retroviral elements with regions similar to gag, pro, and pol suggests that MusD provides the proteins necessary for ETnII transposition in trans. For this study, we analyzed all ETnII elements in the draft sequence of the C57BL/6J genome and classified them into three subtypes (␣, ␤, and ␥) based on structural differences. We then used database searches and quantitative real-time PCR to determine the copy number and expression of ETnII and MusD elements in various mouse strains. In 7.5-day-old embryos of a mouse strain in which two mutations due to ETnII-␤ insertions have been identified (SELH/Bc), we detected a three-to sixfold higher level of ETnII-␤ and MusD transcripts than in control strains (C57BL/6J and LM/Bc). The increased ETnII transcription level can in part be attributed to a higher number of ETnII-␤ elements, but 70% of the MusD transcripts appear to have been derived from one or a few MusD elements that are not detectable in C57BL/6J mice. This element belongs to a young MusD subgroup with intact open reading frames and identical LTRs, suggesting that the overexpressed element(s) in SELH/Bc mice might provide the proteins for the retrotransposition of ETnII and MusD elements. We also show that ETnII is expressed up to 30-fold more than MusD, which could explain why only ETnII, but not MusD, elements have been positively identified as new insertions.

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Interruption of two immunoglobulin heavy-chain switch regions in murine plasmacytoma P3.26Bu4 by insertion of retroviruslike element ETn.

Cited by 26 publications

References 47 publications

A dominant negative mutation of the alpha retinoic acid receptor gene in a retinoic acid-nonresponsive embryonal carcinoma cell.

A dominant negative mutation of the alpha retinoic acid receptor gene in a retinoic acid-nonresponsive embryonal carcinoma cell.

An active murine transposon family pair: Retrotransposition of “master” MusD copies and ETn trans-mobilization

Structure and Expression of Mobile ETnII Retroelements and Their Coding-Competent MusD Relatives in the Mouse

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