Nucleic Acids Research, Vol 24, Issue 13 2528-2534, Copyright © 1996 by Oxford University Press
T Schmidt, M Zornig, R Beneke and T Moroy
Infecting mice with a mutant Moloney murine leukemia virus which contains
the bacterial suppressor tRNA supF in its LTR allows rapid cloning of
proviral integration sites from genomic tumour DNA. In a previous study Emu
pim-1/Emu L-myc bitransgenic mice had been inoculated neonatally with
MoMuLV supF virus. The retroviral infection led to acceleration of
lymphomagenesis indicating the proviral activation of further oncogenes
cooperating with myc and pim-1 in tumour development. Using a functional
supF screen for analysis of genomic mouse tumour DNA libraries which had
been constructed in the phage vector EMBL3A, a common proviral integration
site on mouse chromosome 5 was cloned and found to be identical to the
proviral integration site evi-5 which has recently been identified in an
AKXD T- cell lymphoma and which is located 18 kb upstream of the gfi-1
gene. Tumours bearing evi-5 integrations showed an enhanced gfi-1
expression level suggesting that gfi-1 is the target gene for insertions at
the evi-5 locus. Together with three other previously described Moloney
integration clusters all responsible for enhanced gfi-1 expression the
number of tumours from infected double transgenic Emu L-myc/Emu pim-1
transgenic mice with retrovirally activated gfi-1 added up to 53%
underscoring the role of GFI-1 as an effective collaborator for MYC and
PIM-1 in the process of lymphomagenesis.
ARTICLES
MoMuLV proviral integrations identified by Sup-F selection in tumors from infected myc/pim bitransgenic mice correlate with activation of the gfi-1 gene
Institut fur Zellbiologie (Tumorforschung), IFZ, Universitatsklinikum Essen, Essen, Germany.
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