Myosin Vb controls biogenesis of post-Golgi Rab10 carriers during axon development

Liu, Yang; Xu, Xiaohui; Chen, Qi; Wang, Tong; Deng, Cai-Yun; Song, Bao-Liang; Du, Jiulin; Luo, Zhen-Ge

doi:10.1038/ncomms3005

Cited by 69 publications

(68 citation statements)

References 61 publications

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“…Rab10 is also reported to be necessary for axonal membrane trafficking and axonal elongation (Wang et al, 2011b;Liu et al, 2013). Rab13, a Rab closely related to Rab8 and Rab10, is reported to be necessary for neurite elongation (Sakane et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Rab8a and Rab8b are essential for several apical transport pathways but insufficient for ciliogenesis

Satō¹,

Iwano²,

Kunii³

et al. 2014

Development

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The small GTP-binding protein Rab8 is known to play an essential role in intracellular transport and cilia formation. We have previously demonstrated that Rab8a is required for localising apical markers in various organisms. Rab8a has a closely related isoform, Rab8b. To determine whether Rab8b can compensate for Rab8a, we generated Rab8b-knockout mice. Although the Rab8b-knockout mice did not display an overt phenotype, Rab8a and Rab8b double-knockout mice exhibited mislocalisation of apical markers and died earlier than Rab8a-knockout mice. The apical markers accumulated in three intracellular patterns in the double-knockout mice. However, the localisation of basolateral and/or dendritic markers of the double-knockout mice seemed normal. The morphology and the length of various primary and/or motile cilia, and the frequency of ciliated cells appeared to be identical in control and double-knockout mice. However, an additional knockdown of Rab10 in double-knockout cells greatly reduced the percentage of ciliated cells. Our results highlight the compensatory effect of Rab8a and Rab8b in apical transport, and the complexity of the apical transport process. In addition, neither Rab8a nor Rab8b are required for basolateral and/or dendritic transport. However, simultaneous loss of Rab8a and Rab8b has little effect on ciliogenesis, whereas additional loss of Rab10 greatly affects ciliogenesis.

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Section: Discussionmentioning

confidence: 99%

Rab8a and Rab8b are essential for several apical transport pathways but insufficient for ciliogenesis

Satō¹,

Iwano²,

Kunii³

et al. 2014

Development

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“…Recently, we have shown that Rab10 is associated with PPVs [24], Myosin V controls biogenesis of postGolgi Rab10 carriers [27], and JIP1 mediates anterograde transport of Rab10-PPVs during axon development [56]. How do Rab10 vesicles dock and fuse with the membrane at the destination sites?…”

Section: Discussionmentioning

confidence: 99%

“…In addition to several known Rab10-binding partners, such as AS160, a GTPase-activating protein (GAP) for Rab10 [25], or Myosin V [26,27], we also identified MARCKS as one of the interesting hits. Indeed, both MARCKS and Rab10 were expressed in the rat brain at early or late developmental stages (Figure 1A).…”

Section: Rab10 Binds To Marcks Through Effector Domainmentioning

confidence: 99%

“…These phenomena could be caused by the failure in the fusion of docked vesicles. The D3-induced Rab10 tubules were much different from those caused by downregulation of Myosin Vb (MYO5B) (Supplementary information, Figure S4E), which has been shown recently to control fission of Rab10 carriers from the trans-Golgi network (TGN) [27], because MYO5B knockdown-induced tubules were distributed in peri-nuclear regions and derived from TGN and MARCKS D3-induced Rab10 tubules were associated with the PM (Supplementary information, Figure S4D and S4E). Actually, D3 itself can associate with the PM (Supplementary information, Figure S5A and S5B), and may still mediate docking of Rab10 vesicles without successful fusion.…”

Section: Marcks Mediates Docking and Fusion Of Rab10 Vesicles With Thmentioning

confidence: 99%

“…Our previous study has shown that IGFR, the receptor for insulin-like growth factor, and TrkB, the receptor for brain-derived neurotrophic factor (BDNF), were present in Rab10-positive PPVs [24,27]. Both IGFR and TrkB have been shown to be involved in axon development [43,44].…”

Section: Marcks Regulates Membrane Targeting Of Axon Growthrelated Rementioning

confidence: 99%

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MARCKS regulates membrane targeting of Rab10 vesicles to promote axon development

Deng

Liu

et al. 2014

Cell Res

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Axon development requires membrane addition from the intracellular supply, which has been shown to be mediated by Rab10-positive plasmalemmal precursor vesicles (PPVs). However, the molecular mechanisms underlying the membrane trafficking processes of PPVs remain unclear. Here, we show that myristoylated alanine-rich C-kinase substrate (MARCKS) mediates membrane targeting of Rab10-positive PPVs, and this regulation is critical for axon development. We found that the GTP-locked active form of Rab10 binds to membrane-associated MARCKS, whose affinity depends on the phosphorylation status of the MARCKS effector domain. Either genetic silencing of MARCKS or disruption of its interaction with Rab10 inhibited axon growth of cortical neurons, impaired docking and fusion of Rab10 vesicles with the plasma membrane, and consequently caused a loss of membrane insertion of axonal receptors responsive to extracellular axon growth factors. Thus, this study has identified a novel function of MARCKS in mediating membrane targeting of PPVs during axon development.

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Rab GTPase signaling in neurite outgrowth and axon specification

2016

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Neurons are highly polarized cells that contain specialized subcellular domains involved in information transmission in the nervous system. Specifically, the somatodendritic compartment receives neuronal inputs while the axons convey information through the synapse. The establishment of asymmetric domains requires a specific delivery of components, including organelles, proteins, and membrane. The Rab family of small GTPases plays an essential role in membrane trafficking. Signaling cascades triggered by extrinsic and intrinsic factors tightly regulate Rab functions in cells, with Rab protein activation depending on GDP/GTP binding to establish a binary mode of action. This review summarizes the contributions of several Rab family members involved in trans-Golgi, early/late endosomes, and recycling endosomes during neurite development and axonal outgrowth. The regulation of some Rabs by guanine exchanging factors and GTPase activating proteins will also be addressed. Finally, discussion will be provided on how specific effector-mediated Rab activation modifies several molecules essential to neuronal differentiation. V C 2016 Wiley Periodicals, Inc.

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Myosin Vb controls biogenesis of post-Golgi Rab10 carriers during axon development

Cited by 69 publications

References 61 publications

Rab8a and Rab8b are essential for several apical transport pathways but insufficient for ciliogenesis

Rab8a and Rab8b are essential for several apical transport pathways but insufficient for ciliogenesis

MARCKS regulates membrane targeting of Rab10 vesicles to promote axon development

Rab GTPase signaling in neurite outgrowth and axon specification

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