Florence Margottin-Goguet
Institut Cochin
Retrovirus, Infection, Latence
Website: https://institutcochin.fr/equipes/retrovirus-infection-latence
ORCID: 0000-0002-3124-6690
Twitter: @Margottin11
Our team is composed of three groups working on HIV and HTLV-1 human pathogenic retroviruses. Notably, in the case of HIV, we attempt to understand how the virus persists into cells despite antiretroviral therapy and constitute HIV reservoirs, which are the main obstacle to HIV eradication.
My group is interested in the molecular conflicts beween HIV (HIV-1 and HIV-2) and host antiviral proteins, the so-called restriction factors (previously SAMHD1, at the present time mostly the HUSH complex). On the one hand, we aim to identify new restriction factors and to determine their mechanism of action and, on the other hand, to study how the virus escapes their action. In several cases, HIV uses its auxiliary proteins to counteract host restriction factors (Vpx or Vpr for instance).
Our recent studies have focused on the Human Silencing Hub (HUSH) epigenetic complex. We recently unraveled a new mechanism of expression silencing in human cells, in which the deposition of repressive epigenetic marks on a human immunodeficiency virus (HIV)-derived transgene is connected to the recognition of the nascent transcript (Matkovic et al, Nature Com). HUSH plays a critical role in this mechanism, in association with RNA degradation pathways. Furthermore, we and others found that specific lentiviral proteins from HIV or SIV (Simian virus) antagonize HUSH, highlighting the molecular battle between the virus and its host. We are currently studying how HUSH represses viral expression and how viral proteins antagonize HUSH.
Top 5 publications
1. TASOR epigenetic repressor cooperates with a CNOT1 RNA degradation pathway to repress HIV. Matkovic R, Morel M, Lanciano S, Larrous P, Martin B, Bejjani F, Vauthier V, Hansen MMK, Emiliani S, Cristofari G, Gallois-Montbrun S, Margottin-Goguet F. Nat Commun. 2022 Jan 10;13(1):66.
2. Binding to DCAF1 distinguishes TASOR and SAMHD1 degradation by HIV-2 Vpx. Martin MM, Matkovic R, Larrous P, Morel M, Lasserre A, Vauthier V, Margottin-Goguet F. PLoS Pathogens 2021 Oct 26;17(10):e1009609.
3. HUSH, a Link Between Intrinsic Immunity and HIV Latency. Chougui G, Margottin-Goguet F. Front Microbiol. 2019 Feb 12;10:224. Review
4. [Noise from Vpx: “HUSH”!] Chougui G, Martin M, Matkovic R, Etienne L, Margottin-Goguet F. Med Sci (Paris). 2019 Jan;35(1):9-12. Review
5. HIV-2/SIV viral protein X counteracts HUSH repressor complex. Chougui G, Munir-Matloob S, Matkovic R, Martin MM, Morel M, Lahouassa H, Leduc M, Ramirez BC, Etienne L, Margottin-Goguet F. Nature Microbiol. 2018 Aug;3(8):891-897.
Dernières publications sur HAL :
- [inserm-03981630] HUSH-mediated HIV silencing is independent of TASOR phosphorylation on threonine 819by ano.nymous@ccsd.cnrs.fr.invalid (Virginie Vauthier) on 9 February 2023 at 21h56
Background: TASOR, a component of the HUSH repressor epigenetic complex, and SAMHD1, a cellular triphosphohydrolase (dNTPase), are both anti-HIV […]
- [hal-02970136] Vpx n’a pas dit son dernier mot « HUSH » !by ano.nymous@ccsd.cnrs.fr.invalid (Ghina Chougui) on 17 October 2020 at 13h19
No abstract available
- [hal-02122381] HIV-1 Vpr Induces the Degradation of ZIP and sZIP, Adaptors of the NuRD Chromatin Remodeling Complex, by Hijacking...by ano.nymous@ccsd.cnrs.fr.invalid (Claire Maudet) on 7 May 2019 at 12h04
The Vpr protein from type 1 and type 2 Human Immunodeficiency Viruses (HIV-1 and HIV-2) is thought to inactivate several host proteins through the […]
- [pasteur-01372385] HIV-1 Vpr degrades the HLTF DNA translocase in T cells and macrophages.by ano.nymous@ccsd.cnrs.fr.invalid (Hichem Lahouassa) on 27 September 2016 at 11h11
Viruses often interfere with the DNA damage response to better replicate in their hosts. The human immunodeficiency virus 1 (HIV-1) viral protein R […]