Distinct roles of enhancer nuclear factor 1 (NF1) sites in plasmacytoma and osteopetrosis induction by Akv1-99 murine leukemia virus

Karina Dalsgaard Sørensen; Annette Balle Sørensen; Leticia Quintanilla-Martinez; Sandra Kunder; Jörg Schmidt; Finn Skou Pedersen

doi:10.1016/j.virol.2005.01.039

Distinct roles of enhancer nuclear factor 1 (NF1) sites in plasmacytoma and osteopetrosis induction by Akv1-99 murine leukemia virus

Karina Dalsgaard Sørensen, Annette Balle Sørensen, Leticia Quintanilla-Martinez, Sandra Kunder, Jörg Schmidt, Finn Skou Pedersen

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

Abstrakt

Udgivelsesdato: 2005-Apr-10

Originalsprog	Engelsk
Tidsskrift	Virology
Vol/bind	334
Udgave nummer	2
Sider (fra-til)	234-244
Antal sider	11
ISSN	0042-6822
DOI	https://doi.org/10.1016/j.virol.2005.01.039
Status	Udgivet - 2005
Udgivet eksternt	Ja

Adgang til dokumentet

10.1016/j.virol.2005.01.039

Citationsformater

@article{05f7bead356b478f841a51e009902700,

title = "Distinct roles of enhancer nuclear factor 1 (NF1) sites in plasmacytoma and osteopetrosis induction by Akv1-99 murine leukemia virus",

abstract = "Murine leukemia viruses (MLVs) can be lymphomagenic and bone pathogenic. In this work, the possible roles of two distinct proviral enhancer nuclear factor 1 (NF1) binding sites in osteopetrosis and tumor induction by B-lymphomagenic Akv1-99 MLV were investigated. Akv1-99 and mutants either with NF1 site 1, NF1 site 2 or both sites disrupted induced tumors (plasma cell proliferations by histopathology) with remarkably similar incidence and mean latency in inbred NMRI mice. Clonal immunoglobulin gene rearrangement detection, by Southern analysis, confirmed approximately half of the tumors induced by each virus to be plasmacytomas while the remaining lacked detectable clonally rearranged Ig genes and were considered polyclonal; a demonstration that enhancer NF1 sites are dispensable for plasmacytoma induction by Akv1-99. In contrast, X-ray analysis revealed significant differences in osteopetrosis induction by the four viruses strongly indicating that NF1 site 2 is critical for viral bone pathogenicity, whereas NF1 site 1 is neutral or moderately inhibitory. In conclusion, enhancer NF1 sites are major determinants of osteopetrosis induction by Akv1-99 without significant influence on viral oncogenicity.",

author = "S{\o}rensen, {Karina Dalsgaard} and S{\o}rensen, {Annette Balle} and Leticia Quintanilla-Martinez and Sandra Kunder and J{\"o}rg Schmidt and Pedersen, {Finn Skou}",

year = "2005",

doi = "10.1016/j.virol.2005.01.039",

language = "English",

volume = "334",

pages = "234--244",

journal = "Virology",

issn = "0042-6822",

publisher = "Academic Press",

number = "2",

}

Distinct roles of enhancer nuclear factor 1 (NF1) sites in plasmacytoma and osteopetrosis induction by Akv1-99 murine leukemia virus. / Sørensen, Karina Dalsgaard; Sørensen, Annette Balle; Quintanilla-Martinez, Leticia; Kunder, Sandra; Schmidt, Jörg; Pedersen, Finn Skou.

I: Virology, Bind 334, Nr. 2, 2005, s. 234-244.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

TY - JOUR

T1 - Distinct roles of enhancer nuclear factor 1 (NF1) sites in plasmacytoma and osteopetrosis induction by Akv1-99 murine leukemia virus

AU - Sørensen, Karina Dalsgaard

AU - Sørensen, Annette Balle

AU - Quintanilla-Martinez, Leticia

AU - Kunder, Sandra

AU - Schmidt, Jörg

AU - Pedersen, Finn Skou

PY - 2005

Y1 - 2005

N2 - Murine leukemia viruses (MLVs) can be lymphomagenic and bone pathogenic. In this work, the possible roles of two distinct proviral enhancer nuclear factor 1 (NF1) binding sites in osteopetrosis and tumor induction by B-lymphomagenic Akv1-99 MLV were investigated. Akv1-99 and mutants either with NF1 site 1, NF1 site 2 or both sites disrupted induced tumors (plasma cell proliferations by histopathology) with remarkably similar incidence and mean latency in inbred NMRI mice. Clonal immunoglobulin gene rearrangement detection, by Southern analysis, confirmed approximately half of the tumors induced by each virus to be plasmacytomas while the remaining lacked detectable clonally rearranged Ig genes and were considered polyclonal; a demonstration that enhancer NF1 sites are dispensable for plasmacytoma induction by Akv1-99. In contrast, X-ray analysis revealed significant differences in osteopetrosis induction by the four viruses strongly indicating that NF1 site 2 is critical for viral bone pathogenicity, whereas NF1 site 1 is neutral or moderately inhibitory. In conclusion, enhancer NF1 sites are major determinants of osteopetrosis induction by Akv1-99 without significant influence on viral oncogenicity.

AB - Murine leukemia viruses (MLVs) can be lymphomagenic and bone pathogenic. In this work, the possible roles of two distinct proviral enhancer nuclear factor 1 (NF1) binding sites in osteopetrosis and tumor induction by B-lymphomagenic Akv1-99 MLV were investigated. Akv1-99 and mutants either with NF1 site 1, NF1 site 2 or both sites disrupted induced tumors (plasma cell proliferations by histopathology) with remarkably similar incidence and mean latency in inbred NMRI mice. Clonal immunoglobulin gene rearrangement detection, by Southern analysis, confirmed approximately half of the tumors induced by each virus to be plasmacytomas while the remaining lacked detectable clonally rearranged Ig genes and were considered polyclonal; a demonstration that enhancer NF1 sites are dispensable for plasmacytoma induction by Akv1-99. In contrast, X-ray analysis revealed significant differences in osteopetrosis induction by the four viruses strongly indicating that NF1 site 2 is critical for viral bone pathogenicity, whereas NF1 site 1 is neutral or moderately inhibitory. In conclusion, enhancer NF1 sites are major determinants of osteopetrosis induction by Akv1-99 without significant influence on viral oncogenicity.

U2 - 10.1016/j.virol.2005.01.039

DO - 10.1016/j.virol.2005.01.039

M3 - Journal article

C2 - 15780873

VL - 334

SP - 234

EP - 244

JO - Virology

JF - Virology

SN - 0042-6822

IS - 2

ER -