A fresh look at the function of Rabaptin5 on endosomes

Kälin, Simone; Buser, Dominik P; Spiess, Martin

doi:10.1080/21541248.2016.1140616

Cited by 7 publications

(11 citation statements)

References 23 publications

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“…In these cells, KIF3A does not interact with RAB5 and is not required for GLUT4 endocytosis [ 28 ]. However, RAB4 and RAB5 are concomitantly present on endosomes in distinct membrane microdomains that are connected by common RAB4/RAB5 effectors [ 29 , 30 , 31 ]. These divalent RAB effectors control RAB activation and coordinate protein sorting and recycling [ 29 , 31 ].…”

Section: Discussionmentioning

confidence: 99%

“…However, RAB4 and RAB5 are concomitantly present on endosomes in distinct membrane microdomains that are connected by common RAB4/RAB5 effectors [ 29 , 30 , 31 ]. These divalent RAB effectors control RAB activation and coordinate protein sorting and recycling [ 29 , 31 ]. It is therefore tempting to speculate that Kinesin-2 moves the RAB5 endosome for maturation or conversion into the recycling pathway, without interacting directly with this GTPase.…”

Section: Discussionmentioning

confidence: 99%

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Kinesin-2 Controls the Motility of RAB5 Endosomes and Their Association with the Spindle in Mitosis

Pupo

Avanzato

Scianna

et al. 2018

IJMS

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RAB5 is a small GTPase that belongs to the wide family of Rab proteins and localizes on early endosomes. In its active GTP-bound form, RAB5 recruits downstream effectors that, in turn, are responsible for distinct aspects of early endosome function, including their movement along microtubules. We previously reported that, at the onset of mitosis, RAB5positive vesicles cluster around the spindle poles and, during metaphase, move along spindle microtubules. RNAi-mediated depletion of the three RAB5 isoforms delays nuclear envelope breakdown at prophase and severely affects chromosome alignment and segregation. Here we show that depletion of the Kinesin-2 motor complex impairs long-range movement of RAB5 endosomes in interphase cells and prevents localization of these vesicles at the spindle during metaphase. Similarly to the effect caused by RAB5 depletion, functional ablation of Kinesin-2 delays nuclear envelope breakdown resulting in prolonged prophase. Altogether these findings suggest that endosomal transport at the onset of mitosis is required to control timing of nuclear envelope breakdown.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Kinesin-2 Controls the Motility of RAB5 Endosomes and Their Association with the Spindle in Mitosis

Pupo

Avanzato

Scianna

et al. 2018

IJMS

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“…EE Rab5 recruits Rabaptin5, which is complexed with the Rab5 exchange factor, Rabex5. These complexes are thought to interact with Rab4-GTP orchestrating a GTPase cascade resulting in recruitment of endosomal sorting domains and machinery (D’Souza et al, 2014; Kälin et al, 2016). Additionally, Rab5 plays an important role in EE fusion events by generating phosphatidylinositol 3-phosphate and recruiting EE antigen-1 (EEA1) (Simonsen et al, 1998).…”

Section: Rab-gtpases In Hpv Infectious Entrymentioning

confidence: 99%

“…Cargo sorting is generally mediated by Rab interactions, particularly Rab4, Rab5, Rab7a, and Rab11. Post-EE acidification Rab5 is replaced by Rab7a (Figure 1 step 5ii), which promotes the conversion from EE to LE (Kälin et al, 2016). The absence of Rab7a prevents the fusion of LE to lysosomes, ablating function, whereas Rab7a overexpression results in formation of large endocytic structures suggesting enhancement of cargo degradation (Bucci et al, 2000).…”

Section: Rab-gtpases In Hpv Infectious Entrymentioning

confidence: 99%

The Known and Potential Intersections of Rab-GTPases in Human Papillomavirus Infections

Young

Abidine

Gómez-Martínez

et al. 2019

Front. Cell Dev. Biol.

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Papillomaviruses (PVs) were the first viruses recognized to cause tumors and cancers in mammalian hosts by Shope, nearly a century ago ( Shope and Hurst, 1933 ). Over 40 years ago, zur Hausen (1976) first proposed that human papillomaviruses (HPVs) played a role in cervical cancer; in 2008, he shared the Nobel Prize in Medicine for his abundant contributions demonstrating the etiology of HPVs in genital cancers. Despite effective vaccines and screening, HPV infection and morbidity remain a significant worldwide burden, with HPV infections and HPV-related cancers expected increase through 2040. Although HPVs have long-recognized roles in tumorigenesis and cancers, our understanding of the molecular mechanisms by which these viruses interact with cells and usurp cellular processes to initiate infections and produce progeny virions is limited. This is due to longstanding challenges in both obtaining well-characterized infectious virus stocks and modeling tissue-based infection and the replicative cycles in vitro . In the last 20 years, the development of methods to produce virus-like particles (VLPs) and pseudovirions (PsV) along with more physiologically relevant cell- and tissue-based models has facilitated progress in this area. However, many questions regarding HPV infection remain difficult to address experimentally and are, thus, unanswered. Although an obligatory cellular uptake receptor has yet to be identified for any PV species, Rab-GTPases contribute to HPV uptake and transport of viral genomes toward the nucleus. Here, we provide a general overview of the current HPV infection paradigm, the epithelial differentiation-dependent HPV replicative cycle, and review the specifics of how HPVs usurp Rab-related functions during infectious entry. We also suggest other potential interactions based on how HPVs alter cellular activities to complete their replicative-cycle in differentiating epithelium. Understanding how HPVs interface with Rab functions during their complex replicative cycle may provide insight for the development of therapeutic interventions, as current viral counter-measures are solely prophylactic and therapies for HPV-positive individuals remain archaic and limited.

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“…Besides the mechanisms of autophagy described above where a double-membrane phagophore is produced to engulf the target for subsequent fusion to lysosomes, noncanonical autophagy or LC3-associated phagocytosis (LAP) as well as LC3-associated endocytosis (LANDO) of b-amyloid have been described as a process in which the LC3 conjugation system including the ATG16L1-ATG5-ATG12 complex is recruited directly to a single-recruitment. This suggests that the Rabaptin5-Rabex5 complex is recruited mainly by Rab4 and (mono-)ubiquitinated cargo to activate Rab5 in a feed-forward manner (Kälin et al, 2016;.…”

Section: Introductionmentioning

confidence: 99%

Rabaptin5 targets autophagy to damaged endosomes and SCVs by interaction with FIP200 and ATG16L1

Millarte

Schlienger

Kälin

et al. 2020

Preprint

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SummarySelective autophagy of damaged organelles is an important process for cellular homeostasis. The mechanisms how autophagy selects specific targets is often poorly understood. Rabaptin5 was previously known as a major regulator of early endosome identity and maturation. Here we identified two novel Rabaptin5 interactors: FIP200, a subunit of the ULK1 autophagy initiator complex, and ATG16L1, a central component of the E3-like enzyme in LC3 lipidation. Indeed, autophagy of early endosomes damaged by chloroquine or monensin treatment was found to require Rabaptin5 and particularly a specific short sequence motif binding to the WD domain of ATG16L1. Rabaptin5 and this interaction with ATG16L1 is further required for much of autophagic elimination of Salmonella enterica in phagosomes with early endosomal characteristics early after infection. Our results demonstrate a novel function of Rabaptin5 in quality control of early endosomes as a selective receptor to recruit autophagy to damaged early endosomes and phagosomes.

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A fresh look at the function of Rabaptin5 on endosomes

Cited by 7 publications

References 23 publications

Kinesin-2 Controls the Motility of RAB5 Endosomes and Their Association with the Spindle in Mitosis

Kinesin-2 Controls the Motility of RAB5 Endosomes and Their Association with the Spindle in Mitosis

The Known and Potential Intersections of Rab-GTPases in Human Papillomavirus Infections

Rabaptin5 targets autophagy to damaged endosomes and SCVs by interaction with FIP200 and ATG16L1

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