Bury-Moné, S

Manic, G

Maurin, A

Mouscadet, JF

Subra, F

Tauc, P

Retrovirology

English

PubMed

A Maurin

G Manic

F Subra

P Tauc

S Bury-Moné

JF Mouscadet

Springer - Publisher Connector

BioMed Central
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Retrovirology
Open AccessPoster presentation
The cellular factor Ku80 modulates retroviral expression in rodent 
and human cells
A Maurin, G Manic, F Subra, P Tauc, S Bury-Moné* and JF Mouscadet
Address: LBPA, UMR8113, IFR121, ENS-CACHAN, 94230, France
* Corresponding author    
Background
DNA repair factors are putative effectors for cellular
response to foreign DNA invasion since they specifically
recognize DNA anomalies. The heterodimer Ku70/80 is
the DNA-binding component of the DNA-PK complex
required for the nonhomologous end-joining pathway
(NHEJ) of double-strand break repair. It participates in
numerous nuclear processes, including telomere and
chromatin structure maintenance, replication, and tran-
scription. We have observed a nuclear translocation of
Ku80 following retroviral transduction, suggesting that it
could correspond to an active response of the cell to infec-
tion. However, conflicting results concerning positive or
negative effects of Ku80 on retroviral cycle are reported.
Our aim was to clarify the role of Ku80 during retroviral
infection.
Materials and methods
We therefore conducted a systematic analysis of retroviral
integration and expression from a collection of gammaret-
roviral and lentiviral vectors or viruses transducing the gfp
transgene under viral (native LTR or CMV) or cellular
(hPGK) promoters. With respect to human cells, the
investigation of Ku impact on retroviral transduction is
confronted with the problem of the strict requirement of
Ku for cell survival. Here, we explore the roles of Ku80
within a new model of human cells partially depleted in
Ku80 (epithelial cell lines HCT116 WT or heterozygote
Ku80+/- derivates) in parallel to the rodent model of com-
plete depletion (hamster cells xrs6 versus their parental
line CHO and xrs6 line expressing human Ku80).
Results
The rate of integrated provirus estimated by Q-PCR does
not vary depending on Ku status in these cellular models.
While Ku80 depletion leads to an increased expression of
all vectors within rodent cells, it is associated with a
decrease of transgene expression under the only control of
HIV LTR in human cells, independently of the presence of
HIV accessory proteins. The impact of Ku80 on transgene
expression could not be observed from plasmidic con-
structs, suggesting that its action requires its recruitment
during retroviral transduction.
Conclusion
These results highlight the importance of Ku80 in the con-
trol of the retroviral expression, and the complexity of its
action associated to real differences between the models.
We propose that differences on the proviral environment
depending on Ku status could have opposite conse-
quences on transgene expression in rodent or human
cells. Our study confirms that Ku80 promotes HIV multi-
plication in human cells.
from Frontiers of Retrovirology: Complex retroviruses, retroelements and their hosts
Montpellier, France. 21-23 September 2009
Published: 24 September 2009
Retrovirology 2009, 6(Suppl 2):P18 doi:10.1186/1742-4690-6-S2-P18
<supplement> <title> <p>Frontiers of Retrovirology: Complex retroviruses, retroelements and their hosts</p> </title> <note>Meeting abstracts - A single PDF containing all abstracts in this Supplement is available <a href="http://www.biomedcentral.com/content/files/pdf/1742-4690-6-S2-full.pdf">here</a>.</note> <url>http://www.biomedcentral.com/content/pdf/1742-4690-6-S2-info.pdf</url> </supplement>
This abstract is available from: http://www.retrovirology.com/content/6/S2/P18
© 2009 Maurin et al; licensee BioMed Central Ltd. 


The cellular factor Ku80 modulates retroviral expression in rodent and human cells

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The cellular factor Ku80 modulates retroviral expression in rodent and human cells

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