TY - JOUR
T1 - Ini1/hSNF5 is dispensable for retrovirus-induced cytoplasmic accumulation of PML and does not interfere with integration
AU - Boese, Annette
AU - Sommer, Peter
AU - Gaussin, Armelle
AU - Reimann, Andreas
AU - Nehrbass, Ulf
N1 - Funding Information:
We thank J. Seeler, A. Dejean, C. Muchardt, M. Yaniv and P. Charneau for the kind gift of reagents, M.-C. Wagner for tireless help with FACS analysis and F. Feuerbach for critical comments (all Institut Pasteur, Paris, France). This research has been supported by a Marie Curie Fellowship of the European Community programme IHP under contract number HPMF-CT-2000-00750 and by a fellowship of the Agence Nationale de Recherches sur le SIDA (A.N.R.S.) to A.B.; P.S. acknowledges fellowships from the A.N.R.S. and Sidaction. U.N. was supported by the A.N.R.S. and the Pasteur Institute.
PY - 2004/12/17
Y1 - 2004/12/17
N2 - Retroviral infection triggers the cytoplasmic translocation of two Crm1-dependent shuttle factors, namely the Ini1 (integrase interactor 1, hSNF5) and the promyelocytic leukemia (PML) protein. Blocking nuclear export of shuttle factors by leptomycin B increases the efficiency of retroviral integration, suggesting that some may mediate antiviral activity. While PML was shown to counteract proviral establishment, it remained unclear whether Ini1, a protein implicated in various processes during human immunodeficiency virus replication, has the same potential. Employing RNA interference-mediated knock-down of Ini1, we show here that the simultaneous accumulation of both proteins in the cytoplasm likely reflects two non-interdependent phenomena. Furthermore, Ini1 does not interfere with retroviral integration, as cells lacking Ini1 show no increased infection susceptibility.
AB - Retroviral infection triggers the cytoplasmic translocation of two Crm1-dependent shuttle factors, namely the Ini1 (integrase interactor 1, hSNF5) and the promyelocytic leukemia (PML) protein. Blocking nuclear export of shuttle factors by leptomycin B increases the efficiency of retroviral integration, suggesting that some may mediate antiviral activity. While PML was shown to counteract proviral establishment, it remained unclear whether Ini1, a protein implicated in various processes during human immunodeficiency virus replication, has the same potential. Employing RNA interference-mediated knock-down of Ini1, we show here that the simultaneous accumulation of both proteins in the cytoplasm likely reflects two non-interdependent phenomena. Furthermore, Ini1 does not interfere with retroviral integration, as cells lacking Ini1 show no increased infection susceptibility.
KW - Integrase interactor 1/hSNF5
KW - Promyelocytic leukemia protein
KW - Retroviral integration
UR - http://www.scopus.com/inward/record.url?scp=10044285996&partnerID=8YFLogxK
U2 - 10.1016/j.febslet.2004.11.016
DO - 10.1016/j.febslet.2004.11.016
M3 - Article
C2 - 15589835
AN - SCOPUS:10044285996
SN - 0014-5793
VL - 578
SP - 291
EP - 296
JO - FEBS Letters
JF - FEBS Letters
IS - 3
ER -