Migration cues interpretation by clathrin-coated structures

Elkhatib, Nadia; Porshneva, Kesniia; Montagnac, Guillaume

doi:10.1016/j.ceb.2021.07.005

Cited by 6 publications

(6 citation statements)

References 51 publications

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“…Large clathrin plaques can serve as cell-matrix adhesions, signaling platforms and mechanosensory devices 6 , 13 , 86 , 87 . All these functions require clathrin plaques to be adaptive, and therefore regulated.…”

Section: Discussionmentioning

confidence: 99%

Actin polymerization promotes invagination of flat clathrin-coated lattices in mammalian cells by pushing at lattice edges

et al. 2022

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Clathrin-mediated endocytosis (CME) requires energy input from actin polymerization in mechanically challenging conditions. The roles of actin in CME are poorly understood due to inadequate knowledge of actin organization at clathrin-coated structures (CCSs). Using platinum replica electron microscopy of mammalian cells, we show that Arp2/3 complex-dependent branched actin networks, which often emerge from microtubule tips, assemble along the CCS perimeter, lack interaction with the apical clathrin lattice, and have barbed ends oriented toward the CCS. This structure is hardly compatible with the widely held “apical pulling” model describing actin functions in CME. Arp2/3 complex inhibition or epsin knockout produce large flat non-dynamic CCSs, which split into invaginating subdomains upon recovery from Arp2/3 inhibition. Moreover, epsin localization to CCSs depends on Arp2/3 activity. We propose an “edge pushing” model for CME, wherein branched actin polymerization promotes severing and invagination of flat CCSs in an epsin-dependent manner by pushing at the CCS boundary, thus releasing forces opposing the intrinsic curvature of clathrin lattices.

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Section: Discussionmentioning

confidence: 99%

Actin polymerization promotes invagination of flat clathrin-coated lattices in mammalian cells by pushing at lattice edges

et al. 2022

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“…Live incubation of 12G10 on ECs simultaneously hampered the clustering of active β1 integrins in fibrillar adhesions and strongly increased their endocytosis. Thus, it is possible that, unless mechanically stabilized, for example, by tensin-mediated interaction with the actomyosin network, ligand-bound active β1 integrins are promptly internalized, likely via PTB domain–containing endocytic adaptors that compete with tensin for binding the membrane proximal NPxY motif of integrin β subunit cytotails ( Mana et al, 2020 ; Elkhatib et al, 2021 ). From this perspective, active β1 integrin internalization and endosomal signaling ( Alanko et al, 2015 ; Moreno-Layseca et al, 2019 ; Mana et al, 2020 ) may represent a further strategy to mechanically probe the surrounding environment.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, ligand-bound/active integrin internalization is fostered by shifting their association from cytoskeletal to endocytic adaptors, such as Dab2 ( Yu et al, 2015 ; Cao et al, 2020 ). Because polymerization of multivalent ECM ligands impairs integrin endocytosis ( Shi & Sottile, 2011 ; Stehbens & Wittmann, 2012 ; Mana et al, 2020 ; Elkhatib et al, 2021 ), clustering may play a major role in the control of active integrin internalization and function.…”

Section: Introductionmentioning

confidence: 99%

The βI domain promotes active β1 integrin clustering into mature adhesion sites

et al. 2022

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Modulation of integrin function is required in many physiological and pathological settings, such as angiogenesis and cancer. Integrin allosteric changes, clustering, and trafficking cooperate to regulate cell adhesion and motility on extracellular matrix proteins via mechanisms that are partly defined. By exploiting four monoclonal antibodies recognizing distinct conformational epitopes, we show that in endothelial cells (ECs), the extracellular βI domain, but not the hybrid or I-EGF2 domain of active β1 integrins, promotes their FAK-regulated clustering into tensin 1–containing fibrillar adhesions and impairs their endocytosis. In this regard, the βI domain–dependent clustering of active β1 integrins is necessary to favor fibronectin-elicited directional EC motility, which cannot be effectively promoted by β1 integrin conformational activation alone.

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“…The membrane tension difference between the leading and the rear ends is believed to ensure unidirectional migration. , It is observed that there is higher accumulation and dynamics of clathrin-coated pits at the low-tension rear edge of the migrating cell than at the higher tension leading edge. ,, However, clathrin-heavy chains have an independent role to play in the formation of lamellopodia apart from membrane trafficking, aiding scar/wave complex formation for stabilizing the lamellipodia . Finally, CME affects cell adhesion during migration through internalization of integrins and their redistribution at the leading edge by recycling. , It is observed that in 3D migration clathrin plays a novel endocytosis-independent role. Clathrin/AP2 lattices pinch off the ECM and form elongated tube-like structures that in turn stabilize the protrusions and help in 3D migration .…”

Section: Endocytosis and Mechanoregulationmentioning

confidence: 99%

“… 160 Finally, CME affects cell adhesion during migration through internalization of integrins 161 and their redistribution at the leading edge by recycling. 162 , 163 It is observed that in 3D migration clathrin plays a novel endocytosis-independent role. Clathrin/AP2 lattices pinch off the ECM and form elongated tube-like structures that in turn stabilize the protrusions and help in 3D migration.…”

Section: Endocytosis and Mechanoregulationmentioning

confidence: 99%

The Plasma Membrane and Mechanoregulation in Cells

Mukhopadhyay,

Mandal,

Chakraborty

et al. 2024

ACS Omega

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Cells inhabit a mechanical microenvironment that they continuously sense and adapt to. The plasma membrane (PM), serving as the boundary of the cell, plays a pivotal role in this process of adaptation. In this Review, we begin by examining well-studied processes where mechanoregulation proves significant. Specifically, we highlight examples from the immune system and stem cells, besides discussing processes involving fibroblasts and other cell types. Subsequently, we discuss the common molecular players that facilitate the sensing of the mechanical signal and transform it into a chemical response covering integrins YAP/TAZ and Piezo. We then review how this understanding of molecular elements is leveraged in drug discovery and tissue engineering alongside a discussion of the methodologies used to measure mechanical properties. Focusing on the processes of endocytosis, we discuss how cells may respond to altered membrane mechanics using endo- and exocytosis. Through the process of depleting/adding the membrane area, these could also impact membrane mechanics. We compare pathways from studies illustrating the involvement of endocytosis in mechanoregulation, including clathrin-mediated endocytosis (CME) and the CLIC/GEEC (CG) pathway as central examples. Lastly, we review studies on cell–cell fusion during myogenesis, the mechanical integrity of muscle fibers, and the reported and anticipated roles of various molecular players and processes like endocytosis, thereby emphasizing the significance of mechanoregulation at the PM.

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Migration cues interpretation by clathrin-coated structures

Cited by 6 publications

References 51 publications

Actin polymerization promotes invagination of flat clathrin-coated lattices in mammalian cells by pushing at lattice edges

Actin polymerization promotes invagination of flat clathrin-coated lattices in mammalian cells by pushing at lattice edges

The βI domain promotes active β1 integrin clustering into mature adhesion sites

The Plasma Membrane and Mechanoregulation in Cells

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