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Article ; Online: Des complexes protéiques impliqués dans la surveillance de l’ARN nucléaire inhibent la transcription du VIH-1.

Salifou, Kader / Kiernan, Rosemary / Contreras, Xavier

2019 Volume 35, Issue 2, Page(s) 113–115

Title translation	Nuclear RNA surveillance complexes control HIV-1 transcription.
MeSH term(s)	Exosome Multienzyme Ribonuclease Complex/physiology ; Gene Expression Regulation, Viral ; HIV-1/genetics ; Humans ; Multiprotein Complexes/physiology ; RNA Processing, Post-Transcriptional/genetics ; RNA Stability/genetics ; RNA, Nuclear/genetics ; RNA, Nuclear/metabolism ; RNA, Viral/genetics ; RNA, Viral/metabolism ; Transcription Factors/physiology ; Transcription, Genetic/genetics ; Virus Latency/genetics
Chemical Substances	Multiprotein Complexes ; RNA, Nuclear ; RNA, Viral ; Transcription Factors ; Exosome Multienzyme Ribonuclease Complex (EC 3.1.-)
Language	French
Publishing date	2019-02-18
Publishing country	France
Document type	News
ZDB-ID	632733-3
ISSN	1958-5381 ; 0767-0974
ISSN (online)	1958-5381
ISSN	0767-0974
DOI	10.1051/medsci/2019018
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Article ; Online: PAPγ associates with PAXT nuclear exosome to control the abundance of PROMPT ncRNAs.

Contreras, Xavier / Depierre, David / Akkawi, Charbel / Srbic, Marina / Helsmoortel, Marion / Nogaret, Maguelone / LeHars, Matthieu / Salifou, Kader / Heurteau, Alexandre / Cuvier, Olivier / Kiernan, Rosemary

Nature communications

2023 Volume 14, Issue 1, Page(s) 6745

Abstract: Pervasive transcription of the human genome generates an abundance of RNAs that must be processed and degraded. The nuclear RNA exosome is the main RNA degradation machinery in the nucleus. However, nuclear exosome must be recruited to its substrates by ... ...

Abstract	Pervasive transcription of the human genome generates an abundance of RNAs that must be processed and degraded. The nuclear RNA exosome is the main RNA degradation machinery in the nucleus. However, nuclear exosome must be recruited to its substrates by targeting complexes, such as NEXT or PAXT. By proteomic analysis, we identify additional subunits of PAXT, including many orthologs of MTREC found in S. pombe. In particular, we show that polyA polymerase gamma (PAPγ) associates with PAXT. Genome-wide mapping of the binding sites of ZFC3H1, RBM27 and PAPγ shows that PAXT is recruited to the TSS of hundreds of genes. Loss of ZFC3H1 abolishes recruitment of PAXT subunits including PAPγ to TSSs and concomitantly increases the abundance of PROMPTs at the same sites. Moreover, PAPγ, as well as MTR4 and ZFC3H1, is implicated in the polyadenylation of PROMPTs. Our results thus provide key insights into the direct targeting of PROMPT ncRNAs by PAXT at their genomic sites.
MeSH term(s)	Humans ; Exosome Multienzyme Ribonuclease Complex/genetics ; Exosome Multienzyme Ribonuclease Complex/metabolism ; Exosomes/genetics ; Exosomes/metabolism ; Proteomics ; RNA/metabolism ; RNA Stability/genetics ; RNA, Untranslated/metabolism ; Polynucleotide Adenylyltransferase/metabolism
Chemical Substances	Exosome Multienzyme Ribonuclease Complex (EC 3.1.-) ; RNA (63231-63-0) ; RNA, Untranslated ; Polynucleotide Adenylyltransferase (EC 2.7.7.19)
Language	English
Publishing date	2023-10-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-42620-9
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Article ; Online: Adipose tissue is a source of regenerative cells that augment the repair of skeletal muscle after injury.

Nature communications

2023 Volume 14, Issue 1, Page(s) 80

Abstract: Fibro-adipogenic progenitors (FAPs) play a crucial role in skeletal muscle regeneration, as they generate a favorable niche that allows satellite cells to perform efficient muscle regeneration. After muscle injury, FAP content increases rapidly within ... ...

Abstract	Fibro-adipogenic progenitors (FAPs) play a crucial role in skeletal muscle regeneration, as they generate a favorable niche that allows satellite cells to perform efficient muscle regeneration. After muscle injury, FAP content increases rapidly within the injured muscle, the origin of which has been attributed to their proliferation within the muscle itself. However, recent single-cell RNAseq approaches have revealed phenotype and functional heterogeneity in FAPs, raising the question of how this differentiation of regenerative subtypes occurs. Here we report that FAP-like cells residing in subcutaneous adipose tissue (ScAT), the adipose stromal cells (ASCs), are rapidly released from ScAT in response to muscle injury. Additionally, we find that released ASCs infiltrate the damaged muscle, via a platelet-dependent mechanism and thus contribute to the FAP heterogeneity. Moreover, we show that either blocking ASCs infiltration or removing ASCs tissue source impair muscle regeneration. Collectively, our data reveal that ScAT is an unsuspected physiological reservoir of regenerative cells that support skeletal muscle regeneration, underlining a beneficial relationship between muscle and fat.
MeSH term(s)	Humans ; Muscle, Skeletal ; Adipose Tissue ; Cell Differentiation/genetics ; Adipogenesis/genetics ; Muscular Diseases
Language	English
Publishing date	2023-01-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-35524-7
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Article ; Online: Chromatin-associated MRN complex protects highly transcribing genes from genomic instability.

Salifou, Kader / Burnard, Callum / Basavarajaiah, Poornima / Grasso, Giuseppa / Helsmoortel, Marion / Mac, Victor / Depierre, David / Franckhauser, Céline / Beyne, Emmanuelle / Contreras, Xavier / Dejardin, Jérôme / Rouquier, Sylvie / Cuvier, Olivier / Kiernan, Rosemary

Science advances

2021 Volume 7, Issue 21

Abstract: MRN-MDC1 plays a central role in the DNA damage response (DDR) and repair. Using proteomics of isolated chromatin fragments, we identified DDR factors, such as MDC1, among those highly associating with a genomic locus upon transcriptional activation. ... ...

Abstract	MRN-MDC1 plays a central role in the DNA damage response (DDR) and repair. Using proteomics of isolated chromatin fragments, we identified DDR factors, such as MDC1, among those highly associating with a genomic locus upon transcriptional activation. Purification of MDC1 in the absence of exogenous DNA damage revealed interactions with factors involved in gene expression and RNA processing, in addition to DDR factors. ChIP-seq showed that MRN subunits, MRE11 and NBS1, colocalized throughout the genome, notably at TSSs and bodies of actively transcribing genes, which was dependent on the RNAPII transcriptional complex rather than transcription per se. Depletion of MRN increased RNAPII abundance at MRE11/NBS1-bound genes. Prolonged MRE11 or NBS1 depletion induced single-nucleotide polymorphisms across actively transcribing MRN target genes. These data suggest that association of MRN with the transcriptional machinery constitutively scans active genes for transcription-induced DNA damage to preserve the integrity of the coding genome.
MeSH term(s)	Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Chromatin/genetics ; DNA Damage ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Genomic Instability ; Humans ; MRE11 Homologue Protein/genetics ; MRE11 Homologue Protein/metabolism ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism
Chemical Substances	Cell Cycle Proteins ; Chromatin ; DNA-Binding Proteins ; Nuclear Proteins ; MRE11 Homologue Protein (EC 3.1.-)
Language	English
Publishing date	2021-05-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abb2947
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Article ; Online: Premature termination of transcription by RNAP II: the beginning of the end.

Contreras, Xavier / Benkirane, Monsef / Kiernan, Rosemary

Transcription

2013 Volume 4, Issue 2, Page(s) 72–76

Abstract: Transcription elongation is now recognized as an important mechanism of gene regulation in eukaryotes. A large number of genes undergo an early step in transcription that is rate limiting for expression. Genome-wide studies showing that RNA polymerase II ...

Abstract	Transcription elongation is now recognized as an important mechanism of gene regulation in eukaryotes. A large number of genes undergo an early step in transcription that is rate limiting for expression. Genome-wide studies showing that RNA polymerase II accumulates to high densities near the promoters of many genes has led to the idea that promoter-proximal pausing of transcription is a widespread, rate-limiting step in early elongation. Recent evidence suggests that much of this paused RNA polymerase II is competent for transcription elongation. Here, we discuss recent studies suggesting that RNA polymerase II that accumulates nearby the promoter of a subset of genes is undergoing premature termination of transcription.
MeSH term(s)	Endoribonucleases/metabolism ; Exoribonucleases/genetics ; Exoribonucleases/metabolism ; HIV-1/metabolism ; Humans ; Models, Molecular ; Promoter Regions, Genetic ; RNA Polymerase II/genetics ; RNA Polymerase II/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Transcription, Genetic
Chemical Substances	RNA-Binding Proteins ; mRNA decapping enzymes ; trans-activation responsive RNA-binding protein (136628-24-5) ; RNA Polymerase II (EC 2.7.7.-) ; Endoribonucleases (EC 3.1.-) ; Exoribonucleases (EC 3.1.-) ; XRN2 protein, human (EC 3.1.13.1)
Language	English
Publishing date	2013-05-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2646974-1
ISSN	2154-1272 ; 2154-1264
ISSN (online)	2154-1272
ISSN	2154-1264
DOI	10.4161/trns.24148
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Article ; Online: Nuclear RNA surveillance complexes silence HIV-1 transcription.

Contreras, Xavier / Salifou, Kader / Sanchez, Gabriel / Helsmoortel, Marion / Beyne, Emmanuelle / Bluy, Lisa / Pelletier, Stéphane / Rousset, Emilie / Rouquier, Sylvie / Kiernan, Rosemary

PLoS pathogens

2018 Volume 14, Issue 3, Page(s) e1006950

Abstract: Expression from the HIV-1 LTR can be repressed in a small population of cells, which contributes to the latent reservoir. The factors mediating this repression have not been clearly elucidated. We have identified a network of nuclear RNA surveillance ... ...

Abstract	Expression from the HIV-1 LTR can be repressed in a small population of cells, which contributes to the latent reservoir. The factors mediating this repression have not been clearly elucidated. We have identified a network of nuclear RNA surveillance factors that act as effectors of HIV-1 silencing. RRP6, MTR4, ZCCHC8 and ZFC3H1 physically associate with the HIV-1 TAR region and repress transcriptional output and recruitment of RNAPII to the LTR. Knock-down of these factors in J-Lat cells increased the number of GFP-positive cells, with a concomitant increase in histone marks associated with transcriptional activation. Loss of these factors increased HIV-1 expression from infected PBMCs and led to reactivation of HIV-1 from latently infected PBMCs. These findings identify a network of novel transcriptional repressors that control HIV-1 expression and which could open new avenues for therapeutic intervention.
MeSH term(s)	Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Exoribonucleases/genetics ; Exoribonucleases/metabolism ; Exosome Multienzyme Ribonuclease Complex/genetics ; Exosome Multienzyme Ribonuclease Complex/metabolism ; Gene Expression Regulation, Viral ; HIV Infections/genetics ; HIV Infections/metabolism ; HIV Infections/virology ; HIV Long Terminal Repeat/genetics ; HIV-1/genetics ; HIV-1/pathogenicity ; HeLa Cells ; Humans ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; RNA Helicases/genetics ; RNA Helicases/metabolism ; RNA, Nuclear/genetics ; RNA, Nuclear/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic ; Transcriptional Activation ; Virus Activation ; Virus Latency
Chemical Substances	Carrier Proteins ; Nuclear Proteins ; RNA, Nuclear ; Repressor Proteins ; Transcription Factors ; ZCCHC8 protein, human ; ZFC3H1 protein, human ; Exoribonucleases (EC 3.1.-) ; Exosome Multienzyme Ribonuclease Complex (EC 3.1.-) ; EXOSC10 protein, human (EC 3.1.13.-) ; MTREX protein, human (EC 3.6.1.-) ; RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2018-03-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7366
ISSN (online)	1553-7374
ISSN	1553-7366
DOI	10.1371/journal.ppat.1006950
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Article ; Online: P bodies inhibit retrotransposition of endogenous intracisternal a particles.

Lu, Chunye / Contreras, Xavier / Peterlin, B Matija

Journal of virology

2011 Volume 85, Issue 13, Page(s) 6244–6251

Abstract: mRNA-processing bodies (P bodies) are cytoplasmic foci that contain translationally repressed mRNA. Since they are important for the retrotransposition of Ty elements and brome mosaic virus in yeast cells, we assessed the role of P bodies in the movement ...

Abstract	mRNA-processing bodies (P bodies) are cytoplasmic foci that contain translationally repressed mRNA. Since they are important for the retrotransposition of Ty elements and brome mosaic virus in yeast cells, we assessed the role of P bodies in the movement of endogenous intracisternal A particles (IAPs) in mammalian cells. In contrast to the case for these other systems, their disruption via knockdown of RCK or eukaryotic initiation factor E transporter (eIF4E-T) increased IAP retrotransposition as well as levels of IAP transcripts, Gag proteins, and reverse transcription products. This increase was not mediated by impairing the microRNA pathway. Rather, the removal of P bodies shifted IAP mRNA from nonpolysomal to polysomal fractions. Although IAP mRNA localized to P bodies, Gag was targeted to the endoplasmic reticulum (ER), from which IAP buds. Thus, by sequestering IAP mRNA away from Gag, P bodies inhibit rather than promote IAP retrotransposition.
MeSH term(s)	Animals ; Cell Line ; Cytoplasmic Granules/metabolism ; Endoplasmic Reticulum ; Gene Expression Regulation ; Gene Products, gag/genetics ; Gene Products, gag/metabolism ; Genes, Intracisternal A-Particle/genetics ; Genes, Intracisternal A-Particle/physiology ; Humans ; Mice ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Recombination, Genetic ; Retroelements/genetics
Chemical Substances	Gene Products, gag ; RNA, Messenger ; Retroelements
Language	English
Publishing date	2011-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.02517-10
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Article: HIV latency: present knowledge, future directions.

Contreras, Xavier / Lenasi, Tina / Peterlin, B Matija

Future virology

2009 Volume 1, Issue 6, Page(s) 733–745

Abstract: Current therapies do not eradicate HIV from infected patients. Indeed, HIV hides in a latent form insensitive to these therapies. Thus, one priority is to purge these latent reservoirs. But what mechanisms are responsible for latency and what are the ... ...

Abstract	Current therapies do not eradicate HIV from infected patients. Indeed, HIV hides in a latent form insensitive to these therapies. Thus, one priority is to purge these latent reservoirs. But what mechanisms are responsible for latency and what are the reservoirs of latently infected cells? The present knowledge in terms of HIV latency is still incomplete and current therapeutic strategies fail to eradicate completely latently infected cells. What could the future bring?
Language	English
Publishing date	2009-05-18
Publishing country	England
Document type	Journal Article
ISSN	1746-0794
ISSN	1746-0794
DOI	10.2217/17460794.1.6.733
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Article ; Online: Protein kinase C-delta regulates HIV-1 replication at an early post-entry step in macrophages

Contreras Xavier / Mzoughi Olfa / Gaston Fabrice / Peterlin Matija B / Bahraoui Elmostafa

Retrovirology, Vol 9, Iss 1, p

2012 Volume 37

Abstract: Abstract Background Macrophages, which are CD4 and CCR5 positive, can sustain HIV-1 replication for long periods of time. Thus, these cells play critical roles in the transmission, dissemination and persistence of viral infection. Of note, current ... ...

Abstract	Abstract Background Macrophages, which are CD4 and CCR5 positive, can sustain HIV-1 replication for long periods of time. Thus, these cells play critical roles in the transmission, dissemination and persistence of viral infection. Of note, current antiviral therapies do not target macrophages efficiently. Previously, it was demonstrated that interactions between CCR5 and gp120 stimulate PKC. However, the PKC isozymes involved were not identified. Results In this study, we identified PKC-delta as a major cellular cofactor for HIV-1 replication in macrophages. Indeed, PKC-delta was stimulated following the interaction between the virus and its target cell. Moreover, inhibition of PKC-delta blocked the replication of R5-tropic viruses in primary human macrophages. However, this inhibition did not have significant effects on receptor and co-receptor expression or fusion. Additionally, it did not affect the formation of the early reverse transcription product containing R/U5 sequences, but did inhibit the synthesis of subsequent cDNAs. Importantly, the inhibition of PKC-delta altered the redistribution of actin, a cellular cofactor whose requirement for the completion of reverse transcription was previously established. It also prevented the association of the reverse transcription complex with the cytoskeleton. Conclusion This work highlights the importance of PKC-delta during early steps of the replicative cycle of HIV-1 in human macrophages.
Keywords	Medicine (General) ; R5-920 ; Medicine ; R ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Immunologic diseases. Allergy ; RC581-607
Subject code	570
Language	English
Publishing date	2012-05-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
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Article ; Online: Transcriptional interference antagonizes proviral gene expression to promote HIV latency.

Lenasi, Tina / Contreras, Xavier / Peterlin, B Matija

Cell host & microbe

2008 Volume 4, Issue 2, Page(s) 123–133

Abstract: Eradication of the latent HIV reservoir remains a major barrier to curing AIDS. However, the mechanisms that direct viral persistence in the host are not well understood. Studying a model system of postintegration latency, we found that viral integration ...

Abstract	Eradication of the latent HIV reservoir remains a major barrier to curing AIDS. However, the mechanisms that direct viral persistence in the host are not well understood. Studying a model system of postintegration latency, we found that viral integration into the actively transcribed host genes led to transcriptional interference (TI) caused by the elongating RNA polymerase II (RNAPII) transcribing through the viral promoter. The resulting physical exclusion of preinitiation complex formation on the 5' long terminal repeat (LTR) promoted the silencing of HIV transcription. This block could be counteracted by inhibiting the upstream transcription or cooperatively activating viral transcription initiation and elongation. Importantly, PCR-based analysis, which detects host transcription through the 5'LTR independently of the viral integration site, revealed substantial levels of this transcription in HIV-infected primary CD4(+) T cells. Collectively, our findings suggest that TI contributes significantly to HIV latency and should be considered when attempting to purge the latent reservoir.
MeSH term(s)	CD4-Positive T-Lymphocytes/virology ; Gene Expression Regulation, Viral ; Genome, Viral ; Glycoproteins/genetics ; Glycoproteins/metabolism ; HIV/genetics ; HIV/physiology ; HIV Infections/genetics ; HIV Infections/virology ; HIV Long Terminal Repeat ; Host-Pathogen Interactions ; Humans ; Jurkat Cells ; Proviruses/genetics ; Proviruses/physiology ; RNA Polymerase II/genetics ; RNA Polymerase II/metabolism ; Transcription, Genetic ; Virus Latency
Chemical Substances	Glycoproteins ; tissue-factor-pathway inhibitor 2 ; RNA Polymerase II (EC 2.7.7.-)
Language	English
Publishing date	2008-07-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2008.05.016
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