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1 The Nomis Center for Immunobiology and Microbial equine vet Pathogenesis, equine vet The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA
The electronic version of this article is the complete one and can be found online at: http://www.virologyj.com/content/11/1/180 Received: 23 May 2014 Accepted: 24 September 2014 Published: 8 October 2014
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
This approach identified the ATP-dependent chromatin remodeler, chromodomain helicase DNA-binding protein 2 (CHD2), as well as the highly related CHD1 protein, as positive regulators of both MLV and HIV-1 replication in rodent and human cells. RNAi knockdown of either equine vet CHD2 or the related CHD1 protein, in human cells resulted in a block to infection by HIV-1, specifically at the level of transcription. Conclusions
Retroviruses cause a wide range of diseases in humans and animals, including cancer (HTLV-1, and HTLV-2) and AIDS (HIV-1 and HIV-2) in humans. These viruses exploit a large number of cellular proteins and other factors to facilitate different equine vet steps of virus replication. The early stages of retrovirus replication involve virus-receptor and -co-receptor interactions, membrane fusion, cytosolic entry, reverse transcription, equine vet nuclear import and integration of the viral genome into a host chromosome to form the provirus. The late stages involve proviral transcription, viral RNA splicing, polyadenylation and cytoplasmic transport, protein translation, and viral assembly, budding and maturation.
A number of comprehensive equine vet genetic screens, most relying on RNAi-knockdown technology, have revealed a number of cellular factors that are important for replication by retroviruses such as HIV-1 [ 1 - 4 ]. While this is a powerful equine vet approach, its impact is limited by the fact that the RNAi-knockdown level seen with individual genes is often incomplete, i.e. expression of the target gene is reduced but is not completely ablated. To overcome this potential limitation of this technology, we are adopting complementary approaches including insertional mutagenesis-based screening. This approach has revealed important regulators of retroviral replication that were missed by siRNA screening, including ZASC1, a key regulator of HIV-1 transcriptional elongation [ 5 , 6 ] and the cellular sulfonation pathway that also regulates retroviral gene expression [ 7 ].
Here we describe results of another insertional mutagenesis screen equine vet that have revealed CHD2, and the related CHD1 protein, as positive regulators of HIV-1 gene expression. These proteins equine vet are members of the chromodomain helicase DNA binding protein (CHD) family equine vet of ATP-dependent chromatin remodelers, which are important regulators of chromatin structure and transcription [ 8 ]. Currently there are four distinct families of ATP-dependent chromatin remodelers, including the SWI/SNF, ISWI, INO80 and CHD families, and all are characterized by the presence of a SWI2/SNF2-family ATPase domain [ 9 ]. These chromatin remodelers utilize the energy of ATP hydrolysis to move, eject or restructure nucleosomes, thereby controlling the access of regulatory proteins to DNA or histones [ 10 ]. The CHD family of proteins is distinguished by the presence of two tandem chromodomains located in the N-terminal equine vet region equine vet of the protein in addition to the centrally located SWI2/SNF2-family ATPase domain equine vet [ 11 ]. Although budding yeast have a single CHD1 protein, mammals express nine different CHD proteins [ 11 ].
Currently, CHD1 is the better characterized of these two proteins. CHD1 localizes to regions of active transcription and interacts with transcription elongation complexes including the PAF and FACT complexes [ 12 - 15 ]. The yeast CHD1 protein can exist as a monomer or a dimer [ 16 , 17 ], and is an essential component of the yeast SAGA and SLIK HAT complexes [ 16 ]. The chromodomains of human CHD1 can specifically bind methylated H3K4 suggesting a possible mechanism for targeting the protein to sites of active transcription [ 9 , 18 ]. More recent biochemical studies have implicated the chromodomains as havi