Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 286, Issue 42, Pages 36427-36437Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M111.251058
Keywords
-
Categories
Funding
- National Institutes of Health [GM082970, GM060518]
- California Institute for Regenerative Medicine (CIRM) [RS1-00210-1, TRI-01227, TG2/01160]
- German Academy of Sciences [BMBF-LPD 9901/8-144]
- Instituto de Salud Carlos III-Consejeria de Salud Junta de Andalucia [FEDER/EMER07/056]
- Marie Curie IRG action [FP7-PEOPLE-2007-4-3-IRG]
- Miguel Servet [FEDER/CP07/00065]
- ISCIII
- Innovacion y Ciencia [P09-CTS-4980]
- Junta de Andalucia (Spain) [PI-002]
- Spanish Ministry of Health [PI08171]
- Consejeria de Economia
Ask authors/readers for more resources
Members of the APOBEC3 (A3) family of cytidine deaminase enzymes act as host defense mechanisms limiting both infections by exogenous retroviruses and mobilization of endogenous retrotransposons. Previous studies revealed that the overexpression of some A3 proteins could restrict engineered human Long INterspersed Element-1 (LINE-1 or L1) retrotransposition in HeLa cells. However, whether endogenous A3 proteins play a role in restricting L1 retrotransposition remains largely unexplored. Here, we show that HeLa cells express endogenous A3B and A3C, whereas human embryonic stem cells (hESCs) express A3B, A3C, A3DE, A3F, and A3G. To study the relative contribution of endogenous A3 proteins in restricting L1 retrotransposition, we first generated small hairpin RNAs (shRNAs) to suppress endogenous A3 mRNA expression, and then assessed L1 mobility using a cell-based L1 retrotransposition assay. We demonstrate that in both HeLa and hESCs, shRNA-based knockdown of A3B promotes a similar to 2-3.7-fold increase in the retrotransposition efficiency of an engineered human L1. Knockdown of the other A3s produced no significant increase in L1 activity. Thus, A3B appears to restrict engineered L1 retrotransposition in a broad range of cell types, including pluripotent cells.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available