Talin-KANK1 interaction controls the recruitment of cortical microtubule stabilizing complexes to focal adhesions

Bouchet, Benjamin Pierre; Gough, Rosemarie E.; Willige, Dieudonnée van de; Ammon, York-Christoph; Post, Harm; Jacquemet, Guillaume; Altelaar, A.F. Maarten; Heck, Albert J. R.; Goult, Benjamin T.; Akhmanova, Anna

doi:10.1101/055210

Cited by 54 publications

(121 citation statements)

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“…the area occupied by the cell on the substrate) was negatively correlated with centrosomal actin density and positively correlated with the density of microtubules at the centrosome and throughout the cell (Fig D and E). Although these results do not indicate the exact mechanism by which cell spreading modulates the amount of microtubules, and notably do not exclude the possibility that microtubules were stabilized by contact with focal adhesions (Byron et al , ; Bouchet et al , ), they support a model in which microtubule growth from the centrosome is modulated by the adhesion state of the cell via the degree to which actin filaments are prevented from forming at the centrosome.…”

Section: Resultsmentioning

confidence: 68%

Actin filaments regulate microtubule growth at the centrosome

et al. 2019

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The centrosome is the main microtubule‐organizing centre. It also organizes a local network of actin filaments. However, the precise function of the actin network at the centrosome is not well understood. Here, we show that increasing densities of actin filaments at the centrosome of lymphocytes are correlated with reduced amounts of microtubules. Furthermore, lymphocyte activation resulted in disassembly of centrosomal actin and an increase in microtubule number. To further investigate the direct crosstalk between actin and microtubules at the centrosome, we performed in vitro reconstitution assays based on (i) purified centrosomes and (ii) on the co‐micropatterning of microtubule seeds and actin filaments. These two assays demonstrated that actin filaments constitute a physical barrier blocking elongation of nascent microtubules. Finally, we showed that cell adhesion and cell spreading lead to lower densities of centrosomal actin, thus resulting in higher microtubule growth. We therefore propose a novel mechanism, by which the number of centrosomal microtubules is regulated by cell adhesion and actin‐network architecture.

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Section: Resultsmentioning

confidence: 68%

Actin filaments regulate microtubule growth at the centrosome

et al. 2019

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“…KANK family proteins also interact with liprin‐β1 and are recruited to large protein complexes that cluster around focal adhesions. This complex recruits cytoplasmic linker‐associated protein (CLASP) proteins and aids focal adhesion disassembly as well as restricts cortical microtubule growth through the recruitment of Kinesin Family Member 21A (KIF21A) [van der Vaart et al., ; Stehbens et al., ; Bouchet et al., ].…”

Section: Textmentioning

confidence: 99%

Integrin diversity brings specificity in mechanotransduction

Seetharaman

Etienne-Manneville

2018

Biology of the Cell

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Cells sense and respond to the biochemical and physical properties of the extracellular matrix (ECM) through adhesive structures that bridge the cell cytoskeleton and the surrounding environment. Integrin-mediated adhesions interact with specific ECM proteins and sense the rigidity of the substrate to trigger signalling pathways that, in turn, regulate cellular processes such as adhesion, motility, proliferation and differentiation. This process, called mechanotransduction, influenced by the involvement of different integrin subtypes and their high ECM-ligand binding specificity, contributes to the cell-type-specific mechanical responses. In this review, we describe how the expression of particular integrin subtypes affects cellular adaptation to substrate rigidity. We then explain the role of integrins and associated proteins in mechanotransduction, focusing on their specificity in mechanosensing and force transmission.

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“…focal adhesions (FAs), that was described in the late 1990s (Kaverina et al, 1998). Specialized cortical complexes that involve +TIPs were shown to modulate this interaction (Lansbergen et al, 2006;van der Vaart et al, 2013;Wu et al, 2008;Bouchet et al, 2016), and the majority of existing data suggest that microtubules promote FA turnover (Stehbens and Wittmann, 2012) (Fig. 1).…”

Section: Introductionmentioning

confidence: 99%

Microtubules in 3D cell motility

Bouchet

Akhmanova

2017

Journal of Cell Science

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101

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Three-dimensional (3D) cell motility underlies essential processes, such as embryonic development, tissue repair and immune surveillance, and is involved in cancer progression. Although the cytoskeleton is a well-studied regulator of cell migration, most of what we know about its functions originates from studies conducted in twodimensional (2D) cultures. This research established that the microtubule network mediates polarized trafficking and signaling that are crucial for cell shape and movement in 2D. In parallel, developments in light microscopy and 3D cell culture systems progressively allowed to investigate cytoskeletal functions in more physiologically relevant settings. Interestingly, several studies have demonstrated that microtubule involvement in cell morphogenesis and motility can differ in 2D and 3D environments. In this Commentary, we discuss these differences and their relevance for the understanding the role of microtubules in cell migration in vivo. We also provide an overview of microtubule functions that were shown to control cell shape and motility in 3D matrices and discuss how they can be investigated further by using physiologically relevant models.

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Talin-KANK1 interaction controls the recruitment of cortical microtubule stabilizing complexes to focal adhesions

Cited by 54 publications

References 64 publications

Actin filaments regulate microtubule growth at the centrosome

Actin filaments regulate microtubule growth at the centrosome

Integrin diversity brings specificity in mechanotransduction

Microtubules in 3D cell motility

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