Triple basepair changes within and adjacent to the conserved YY1 motif upstream of the U3 enhancer repeats of SL3-3 murine leukemia virus cause a small but significant shortening of latency of T-lymphoma induction.

Shi Liang Ma; Jette Lovmand; Annette Balle Sørensen; Arne Luz; Jörg Schmidt; Finn Skou Pedersen

Triple basepair changes within and adjacent to the conserved YY1 motif upstream of the U3 enhancer repeats of SL3-3 murine leukemia virus cause a small but significant shortening of latency of T-lymphoma induction.

Shi Liang Ma, Jette Lovmand, Annette Balle Sørensen, Arne Luz, Jörg Schmidt, Finn Skou Pedersen

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

Abstrakt

Udgivelsesdato: 2003-Sep-1

Originalsprog	Engelsk
Tidsskrift	Virology
Vol/bind	313
Udgave nummer	2
Sider (fra-til)	638-44
Antal sider	6
ISSN	0042-6822
Status	Udgivet - 2003
Udgivet eksternt	Ja

Citationsformater

@article{30e65ff1ba854c27b98f5685205fe6d7,

title = "Triple basepair changes within and adjacent to the conserved YY1 motif upstream of the U3 enhancer repeats of SL3-3 murine leukemia virus cause a small but significant shortening of latency of T-lymphoma induction.",

abstract = "A highly conserved sequence upstream of the transcriptional enhancer in the U3 of murine leukemia viruses (MLVs) was reported to mediate negative regulation of their expression. In transient expression studies, negative regulation was reported to be conferred by coexpression of the transcription factor YY1, which binds to a motif in the upstream conserved region (UCR). To address the function of the UCR and its YY1-motif in an in vivo model of MLV-host interactions we introduced six consecutive triple basepair mutations into this region of the potent T-lymphomagenic SL3-3 MLV. We report that all mutants have retained their replication competence and that they all, like the SL3-3 wild type (wt), induce T-cell lymphomas when injected into newborn mice of the SWR strain. However, all mutants induced disease with slightly shorter latency periods than the wt SL3-3, suggesting that the YY1 motif as well as its immediate context in the UCR have a negative effect on the pathogenicity of the virus. This result may have implications for the design of retroviral vectors.",

author = "Ma, {Shi Liang} and Jette Lovmand and S{\o}rensen, {Annette Balle} and Arne Luz and J{\"o}rg Schmidt and Pedersen, {Finn Skou}",

year = "2003",

language = "English",

volume = "313",

pages = "638--44",

journal = "Virology",

issn = "0042-6822",

publisher = "Academic Press",

number = "2",

}

Triple basepair changes within and adjacent to the conserved YY1 motif upstream of the U3 enhancer repeats of SL3-3 murine leukemia virus cause a small but significant shortening of latency of T-lymphoma induction. / Ma, Shi Liang; Lovmand, Jette; Sørensen, Annette Balle et al.

I: Virology, Bind 313, Nr. 2, 2003, s. 638-44.

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

TY - JOUR

T1 - Triple basepair changes within and adjacent to the conserved YY1 motif upstream of the U3 enhancer repeats of SL3-3 murine leukemia virus cause a small but significant shortening of latency of T-lymphoma induction.

AU - Ma, Shi Liang

AU - Lovmand, Jette

AU - Sørensen, Annette Balle

AU - Luz, Arne

AU - Schmidt, Jörg

AU - Pedersen, Finn Skou

PY - 2003

Y1 - 2003

N2 - A highly conserved sequence upstream of the transcriptional enhancer in the U3 of murine leukemia viruses (MLVs) was reported to mediate negative regulation of their expression. In transient expression studies, negative regulation was reported to be conferred by coexpression of the transcription factor YY1, which binds to a motif in the upstream conserved region (UCR). To address the function of the UCR and its YY1-motif in an in vivo model of MLV-host interactions we introduced six consecutive triple basepair mutations into this region of the potent T-lymphomagenic SL3-3 MLV. We report that all mutants have retained their replication competence and that they all, like the SL3-3 wild type (wt), induce T-cell lymphomas when injected into newborn mice of the SWR strain. However, all mutants induced disease with slightly shorter latency periods than the wt SL3-3, suggesting that the YY1 motif as well as its immediate context in the UCR have a negative effect on the pathogenicity of the virus. This result may have implications for the design of retroviral vectors.

AB - A highly conserved sequence upstream of the transcriptional enhancer in the U3 of murine leukemia viruses (MLVs) was reported to mediate negative regulation of their expression. In transient expression studies, negative regulation was reported to be conferred by coexpression of the transcription factor YY1, which binds to a motif in the upstream conserved region (UCR). To address the function of the UCR and its YY1-motif in an in vivo model of MLV-host interactions we introduced six consecutive triple basepair mutations into this region of the potent T-lymphomagenic SL3-3 MLV. We report that all mutants have retained their replication competence and that they all, like the SL3-3 wild type (wt), induce T-cell lymphomas when injected into newborn mice of the SWR strain. However, all mutants induced disease with slightly shorter latency periods than the wt SL3-3, suggesting that the YY1 motif as well as its immediate context in the UCR have a negative effect on the pathogenicity of the virus. This result may have implications for the design of retroviral vectors.

M3 - Journal article

C2 - 12954229

VL - 313

SP - 638

EP - 644

JO - Virology

JF - Virology

SN - 0042-6822

IS - 2

ER -