Substitution of Feline Leukemia Virus Long Terminal Repeat Sequences into Murine Leukemia Virus Alters the Pattern of Insertional Activation and Identifies New Common Insertion Sites

Johnson, Chassidy; Lobelle‐Rich, Patricia; Puetter, Adriane; Lévy, Laurence

doi:10.1128/jvi.79.1.57-66.2005

Cited by 18 publications

(16 citation statements)

References 46 publications

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“…This is exemplified by the tropism of Moloney MLV for T-and B-cells and the induction of predominantly myeloid leukaemia by the Graffi-type murine leukaemia viruses (Erkeland et al, 2003(Erkeland et al, , 2004. Substitution of MLV U3 enhancer sequences with Feline leukaemia Virus U3 sequences induces a different spectrum of insertion sites in lymphoma than wild-type MLV virus, indicating that enhancer sequences not only regulate cell-type specificity of viral replication but also determine the pattern of insertional activation by the provirus (Starkey et al, 1998;Johnson et al, 2005;Nielsen et al, 2005).…”

Section: Ltrs Regulate Viral Transcriptionmentioning

confidence: 99%

Retroviral insertional mutagenesis: past, present and future

et al. 2005

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Retroviral insertion mutagenesis screens in mice are powerful tools for efficient identification of oncogenic mutations in an in vivo setting. Many oncogenes identified in these screens have also been shown to play a causal role in the development of human cancers. Sequencing and annotation of the mouse genome, along with recent improvements in insertion site cloning has greatly facilitated identification of oncogenic events in retrovirus-induced tumours. In this review, we discuss the features of retroviral insertion mutagenesis screens, covering the mechanisms by which retroviral insertions mutate cellular genes, the practical aspects of insertion site cloning, the identification and analysis of common insertion sites, and finally we address the potential for use of somatic insertional mutagens in the study of nonhaematopoietic and nonmammary tumour types.

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Section: Ltrs Regulate Viral Transcriptionmentioning

confidence: 99%

Retroviral insertional mutagenesis: past, present and future

et al. 2005

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“…A response of a given promoter to a specific enhancer could also be involved so that different enhancers would affect gene expression differently. Indeed, long terminal repeat sequences have a great influence on the insertional activation, as recently shown by Johnson et al (29). In light of this, it would be interesting to know if Moloney murine leukemia virus or SL3-3 enhancers do affect the expression of Kis2 and Phf6 when integrated at the Kis2 locus.…”

mentioning

confidence: 90%

Radiation Leukemia Virus Common Integration at the Kis2 Locus: Simultaneous Overexpression of a Novel Noncoding RNA and of the Proximal Phf6 Gene

Landais

Quantin

Rassart

2005

J Virol

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Retroviral tagging has been used extensively and successfully to identify genes implicated in cancer pathways. In order to find oncogenes implicated in T-cell leukemia, we used the highly leukemogenic radiation leukemia retrovirus VL3 (RadLV/VL3). We applied the inverted PCR technique to isolate and analyze sequences flanking proviral integrations in RadLV/VL3-induced T lymphomas. We found retroviral integrations in c-myc and Pim1 as already reported but we also identified for the first time Notch1 as a RadLV common integration site. More interestingly, we found a new RadLV common integration site that is situated on mouse chromosome X (XA4 region, bp 45091000). This site has also been reported as an SL3-3 and Moloney murine leukemia virus integration site, which strengthens its implication in murine leukemia virus-induced T lymphomas. This locus, named Kis2 (Kaplan Integration Site 2), was found rearranged in 11% of the tumors analyzed. In this article, we report not only the alteration of the Kis2 gene located nearby in response to RadLV integration but also the induction of the expression of Phf6, situated about 250 kbp from the integration site. The Kis2 gene encodes five different alternatively spliced noncoding RNAs and the Phf6 gene codes for a 365-amino-acid protein which contains two plant homology domain fingers, recently implicated in the Börje-son-Forssman-Lehmann syndrome in humans. With the recent release of the mouse genome sequence, highthroughput retroviral tagging emerges as a powerful tool in the quest for oncogenes. It also allows the analysis of large DNA regions surrounding the integration locus.

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“…Identification of the p101 gene as a target for common integration in a retroviral tagging study suggested that p101 overexpression may play a role in the induction of T-cell malignancy (Johnson et al, 2005). It is noteworthy that p101 had not previously been identified as a common integration site in any other model of retrovirus-induced lymphoma.…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, the p101 gene was recently identified as a common site of retroviral integration in T-cell lymphomas induced in mice by MoFe2-MuLV, a unique recombinant gammaretrovirus (Johnson et al, 2005). Identification of the p101 gene as a common integration site suggests that it encodes an oncogene capable of inducing T-cell lymphoma, and with malignant potential activated by insertion of adjacent retroviral transcriptional regulatory signals (Johnson et al, 2005). The current studies explore the possible effects of p101 expression and PI3Kg signaling on T-cell malignancy by examining the influence of p101 on T-cell growth and survival.…”

Section: Introductionmentioning

confidence: 99%