TBC1D5-Catalyzed Cycling of Rab7 Is Required for Retromer-Mediated Human Papillomavirus Trafficking during Virus Entry

Xie, Jierui; Heim, Erin N.; Crite, Mac; DiMaio, Daniel

doi:10.1016/j.celrep.2020.107750

Cited by 34 publications

(82 citation statements)

References 62 publications

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“…How Rab7a mediates HPV trafficking remained unclear until recently. Using a protein interference screen, Xie et al (2020) identified that TBC1D5 was essential to HPV entry. The recruitment of TBC1D5 to the retromer–L2 protein complexes likely leads to the disassembly of the retromer–HPV complex through inactivation of Rab7a-GTP, thereby promoting the recycling of retromer.…”

Section: Hpv L2 and Tbc1d5mentioning

confidence: 99%

“…Notably, Xie et al demonstrated that the cycling of Rab7a-GTP and Rab7a-GDP is required for HPV trafficking. In contrast, the cellular trafficking of CI-MPR and DMT1-II requires only Rab7-GTP ( Xie et al, 2020 ). These findings greatly expand our understanding the mechanisms by which HPV manipulates host cellular activity, and suggest that TBC1D5 inhibitors could suppress HPV infection.…”

Section: Hpv L2 and Tbc1d5mentioning

confidence: 99%

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Targeting Endosomal Recycling Pathways by Bacterial and Viral Pathogens

Xin

Mao

Shen

et al. 2021

Front. Cell Dev. Biol.

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Endosomes are essential cellular stations where endocytic and secretory trafficking routes converge. Proteins transiting at endosomes can be degraded via lysosome, or recycled to the plasma membrane, trans-Golgi network (TGN), or other cellular destinations. Pathways regulating endosomal recycling are tightly regulated in order to preserve organelle identity, to maintain lipid homeostasis, and to support other essential cellular functions. Recent studies have revealed that both pathogenic bacteria and viruses subvert host endosomal recycling pathways for their survival and replication. Several host factors that are frequently targeted by pathogens are being identified, including retromer, TBC1D5, SNX-BARs, and the WASH complex. In this review, we will focus on the recent advances in understanding how intracellular bacteria, human papillomavirus (HPV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) hijack host endosomal recycling pathways. This exciting work not only reveals distinct mechanisms employed by pathogens to manipulate host signaling pathways, but also deepens our understanding of the molecular intricacies regulating endosomal receptor trafficking.

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Section: Hpv L2 and Tbc1d5mentioning

confidence: 99%

Section: Hpv L2 and Tbc1d5mentioning

confidence: 99%

Targeting Endosomal Recycling Pathways by Bacterial and Viral Pathogens

Xin

Mao

Shen

et al. 2021

Front. Cell Dev. Biol.

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“…Traptamer genes were recovered from the DNA of proliferating cells and tested individually for their ability to inhibit expression of a reporter gene expressed from a different HPV16 virus. Details of library construction, selection, and traptamer recovery are described in [22].…”

Section: Traptamers That Inhibit Human Papillomavirus Entrymentioning

confidence: 99%

“…The ability of individual cloned traptamers to inhibit HPV infection is tested to confirm activity. Figure reproduced from Xie et al [22]. intracellular localizations, and inhibit HPV entry at different steps [23].…”

Section: Traptamers That Inhibit Human Papillomavirus Entrymentioning

confidence: 99%

Traptamer screening: a new functional genomics approach to study virus entry and other cellular processes

Xie

DiMaio

2021

The FEBS Journal

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Historically, the genetic analysis of mammalian cells entailed the isolation of randomly arising mutant cell lines with altered properties, followed by laborious genetic mapping experiments to identify the mutant gene responsible for the phenotype. In recent years, somatic cell genetics has been revolutionized by functional genomics screens, in which expression of every protein-coding gene is systematically perturbed, and the phenotype of the perturbed cells is determined. We outline here a novel functional genomics screening strategy that differs fundamentally from commonly used approaches. In this strategy, we express libraries of artificial transmembrane proteins named traptamers and select rare cells with the desired phenotype because, by chance, a traptamer specifically perturbs the expression or activity of a target protein. Active traptamers are then recovered from the selected cells and can be used as tools to dissect the biological process under study. We also briefly describe how we have used this new strategy to provide insights into the complex process by which human papillomaviruses enter cells.

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“…Retromer is also a prominent target hijacked by intracellular pathogens to facilitate their transport and replication. This includes viruses such as SARS-CoV-2, human immunodeficiency virus (HIV), hepatitis C virus (HCV), and human papilloma virus (HPV) [58][59][60][61][62][63][64][65][66][67][68][69][70] , and intracellular bacteria such as Coxiella burnetii and Legionella pneumophila [71][72][73][74][75][76][77] . Mechanistic studies have shown that the secreted effector protein RidL from L. pneumophila binds directly to Vps29, competing with endogenous regulators TBC1D5 and VARP, inhibiting…”

Section: Introductionmentioning

confidence: 99%

De novomacrocyclic peptides for inhibiting, stabilising and probing the function of the Retromer endosomal trafficking complex

Chen

Guo

Cui

et al. 2020

Preprint

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The Retromer complex (Vps35-Vps26-Vps29) is essential for endosomal membrane trafficking and signalling. Mutations in Retromer cause late-onset Parkinson’s disease, while viral and bacterial pathogens can hijack the complex during cellular infection. To modulate and probe its function we have created a novel series of macrocyclic peptides that bind Retromer with high affinity and specificity. Crystal structures show the majority of cyclic peptides bind to Vps29 via a Pro-Leu-containing sequence, structurally mimicking known interactors such as TBC1D5, and blocking their interaction with Retromer in vitro and in cells. By contrast, macrocyclic peptide RT-L4 binds Retromer at the Vps35-Vps26 interface and is a more effective molecular chaperone than reported small molecules, suggesting a new therapeutic avenue for targeting Retromer. Finally, tagged peptides can be used to probe the cellular localisation of Retromer and its functional interactions in cells, providing novel tools for studying Retromer function.

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TBC1D5-Catalyzed Cycling of Rab7 Is Required for Retromer-Mediated Human Papillomavirus Trafficking during Virus Entry

Cited by 34 publications

References 62 publications

Targeting Endosomal Recycling Pathways by Bacterial and Viral Pathogens

Targeting Endosomal Recycling Pathways by Bacterial and Viral Pathogens

Traptamer screening: a new functional genomics approach to study virus entry and other cellular processes

De novomacrocyclic peptides for inhibiting, stabilising and probing the function of the Retromer endosomal trafficking complex

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