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Romet-Lemonne, G.

Publications and source records attributed to Romet-Lemonne, G..

26 records · Page 2Linked to original sources

Cryo-EM of human Arp2/3 complexes provides structural insights into actin nucleation modulation by ARPC5 isoforms

The Arp2/3 complex regulates many cellular processes by stimulating formation of branched actin filament networks. Because three of its seven subunits exist as two different isoforms, mammals produce a family of Arp2/3 complexes with different properties that may be suited to different physiological contexts. To shed light on how isoform diversification affects Arp2/3 function, we determined a 4.2 [A] resolution cryo-EM structure of the most active human Arp2/3 complex containing ARPC1B and ARPC5L, and compared it with the structure of the least active ARPC1A-ARPC5-containing complex. The architecture of each isoform-specified Arp2/3 is the same. Strikingly, however, the N-terminal half of ARPC5L is partially disordered compared to ARPC5, suggesting that this region of ARPC5/ARPC5L is an important determinant of complex activity. Confirming this idea, the nucleation activity of Arp2/3 complexes containing hybrid ARPC5/ARPC5L subunits is higher when the ARPC5L N-terminus is present, thereby explaining activity differences between the different Arp2/3 complexes.

biophysics↗

Actin filament oxidation by MICAL1 suppresses protections from cofilin-induced disassembly

Proteins of the ADF/cofilin family play a central role in the disassembly of actin filaments, and their activity must be tightly regulated in cells. Recently, the oxidation of actin filaments by the enzyme MICAL1 was found to amplify the severing action of cofilin through unclear mechanisms. Two essential factors normally prevent filament disassembly: the inactivation of cofilin by phosphorylation, and the protection of filaments by tropomyosins, but whether actin oxidation might interfere with these safeguard mechanisms is unknown. Using single filament experiments in vitro, we found that actin filament oxidation by MICAL1 increases, by several orders of magnitude, both cofilin binding and severing rates, explaining the dramatic synergy between oxidation and cofilin for filament disassembly. Remarkably, we found that actin oxidation bypasses the need for cofilin activation by dephosphorylation. Indeed, non-activated, phosphomimetic S3D-cofilin binds and severs oxidized actin filaments rapidly, in conditions where non-oxidized filaments are unaffected. Finally, tropomyosin Tpm1.8 loses its ability to protect filaments from cofilin severing activity when actin is oxidized by MICAL1. Together, our results show that MICAL1-induced oxidation of actin filaments suppresses their physiological protection from the action of cofilin. We propose that in cells, direct post-translational modification of actin filaments by oxidation is a way to trigger their severing, in spite of being decorated by tropomyosin, and without requiring the activation of cofilin.

biochemistry↗

Twinfilin uncaps filament barbed ends to promote turnover of lamellipodial actin networks

Coordinated polymerization of actin filaments provides force for cell migration, morphogenesis, and endocytosis. Capping Protein (CP) is central regulator of actin dynamics in all eukaryotes. It binds actin filament (F-actin) barbed ends with high affinity and slow dissociation kinetics to prevent filament polymerization and depolymerization. In cells, however, CP displays remarkably rapid dynamics within F-actin networks, but the underlying mechanism has remained enigmatic. We report that a conserved cytoskeletal regulator, twinfilin, is responsible for CPs rapid dynamics and specific localization in cells. Depletion of twinfilin led to stable association of CP with cellular F-actin arrays and its treadmilling throughout leading-edge lamellipodium. These were accompanied by diminished F-actin disassembly rates. In vitro single filament imaging approaches revealed that twinfilin directly promotes dissociation of CP from filament barbed ends, while allowing subsequent filament depolymerization. These results uncover an evolutionary conserved bipartite mechanism that controls how actin cytoskeleton-mediated forces are generated in cells.

cell biology↗

Geometrical constraints greatly hinder formin mDia1 activity

Formins are one of the central players in the assembly of most actin networks in cells. The sensitivity of these processive molecular machines to mechanical tension is now well established. However, how the activity of formins is affected by geometrical constraints related to network architecture, such as filament crosslinking and formin spatial confinement, remains largely unknown. Combining microfluidics and micropatterning, we reconstituted in vitro mDia1 formin-elongated filament bundles induced by fascin, with different geometrical constraints on the formins, and measured the impact of these constraints on formin elongation rates and processivity. When filaments are not bundled, formins can be anchored to static or fluid surfaces, by either end of the proteins, without affecting their activity. We show that filament bundling by fascin reduces both unanchored formin elongation rate and processivity. Strikingly, when filaments elongated by surface-anchored formins are cross-linked together, formin elongation rate immediately decreases and processivity is reduced, up to 24-fold, depending on the cumulative impact of formin rotational and translational freedoms. Our results reveal an unexpected crosstalk between the constraints at the filament and the formin levels. We anticipate that in cells, the molecular details of formin anchoring to the plasma membrane, strongly modulate formin activity at actin filament barbed ends.

biophysics↗

Quantitative variations of ADF/cofilin’s multiple actions on actin filaments with pH

Actin Depolymerizing Factor (ADF)/cofilin is the main protein family promoting the disassembly of actin filaments, which is essential for numerous cellular functions. ADF/cofilin proteins disassemble actin filaments through different reactions, as they bind to their sides, sever them, and promote the depolymerization of the resulting ADF/cofilin-saturated filaments. Moreover, the efficiency of ADF/cofilin is known to be very sensitive to pH. ADF/cofilin thus illustrates two challenges in actin biochemistry: separating the different regulatory actions of a single protein, and characterizing them as a function of specific biochemical conditions. Here, we investigate the different reactions of ADF/cofilin on actin filaments, over four different values of pH ranging from pH 6.6 to pH 7.8, using single filament microfluidics techniques. We show that lowering pH reduces the effective filament severing rate by increasing the rate at which filaments become saturated by ADF/cofilin, thereby reducing the number of ADF/cofilin domain boundaries, where severing can occur. The severing rate per domain boundary, however, remains unchanged at different pH values. The ADF/cofilin-decorated filaments (refered to as \"cofilactin\" filaments) depolymerize from both ends. We show here that, at physiological pH (pH 7.0 to 7.4), the pointed end depolymerization of cofilactin filaments is barely faster than that of bare filaments. In contrast, cofilactin barbed ends undergo an \"unstoppable\" depolymerization (depolymerizing for minutes despite the presence of free actin monomers and capping protein in solution), throughout our range of pH. We thus show that, at physiological pH, the main contribution of ADF/cofilin to filament depolymerization is at the barbed end.\n\nA number of key cellular processes rely on the proper assembly and disassembly of actin filament networks 1. The central regulator of actin disassembly is the ADF/cofilin protein family 2, 3, which comprises three isoforms in mammals: cofilin-1 (cof1, found in nearly all cell types), cofilin-2 (cof2, found primarily in muscles) and Actin Depolymerization Factor (ADF, found mostly in neurons and epithelial cells). We refer to them collectively as \"ADF/cofilin\".\n\nOver the years, the combined efforts of several labs have led to the following understanding of actin filament disassembly by ADF/cofilin. Molecules of ADF/cofilin bind stoechiometrically 4, 5 to the sides of actin filaments, with a strong preference for ADP-actin subunits 6-10. Though ADF/cofilin molecules do not contact each other 11, they bind in a cooperative manner, leading to the formation of ADF/cofilin domains on the filaments 5, 7, 9, 12, 13. Compared to bare F-actin, the filament portions decorated by ADF/cofilin (refered to as \"cofilactin\") are more flexible 14, 15 and exhibit a shorter right-handed helical pitch, with a different subunit conformation 11, 16-19. Thermal fluctuations are then enough to sever actin filaments at (or near) domain boundaries8, 9, 13, 20, 21. Cofilactin filaments do not sever, but depolymerize from both ends 13 thereby renewing the actin monomer pool.\n\nADF/cofilin thus disassembles actin filaments through the combination of different actions. As such, it vividly illustrates a current challenge in actin biochemistry: identifying and quantifying the multiple reactions involving a single protein. This is a very difficult task for bulk solution assays, where a large number of reactions take place simultaneously, and single-filament techniques have played a key role in deciphering ADF/cofilins actions 9, 13, 20, 22-24. In particular, the microfluidics-based method that we have developed over the past years, is a powerful tool for such investigations 25. It has recently allowed us to quantify the kinetics of the aforementioned reactions, and to discover that ADF/cofilin-saturated filament (cofilactin) barbed ends can hardly stop depolymerizing, even when ATP-G-actin and capping protein are present in solution 13.\n\nIn addition, ADF/cofilin is very sensitive to pH 4, 5, 26-29. In cells, pH can be a key regulatory factor 30. It can vary between compartments, between cell types, and be specifically modulated. We can consider that a typical cytoplasmic pH would be comprised between 7.0 and 7.4. Recently, we have quantified the different reactions involving ADF/cofilin at pH 7.8 13, leaving open the question of how these reaction rates are indivdually affected by pH variations. For instance, it has been reported that ADF/cofilin is a more potent filament disassembler at higher pH values 4, 5, 26-29 but the actual impact of pH on the rate constants of individual reactions has yet to be characterized. Moreover, whether the unstoppable barbed end depolymerization that we have recently discovered for ADF/cofilin-saturated filaments at pH 7.8 13 remains significant at lower, more physiological pH values is an open question.\n\nHere, we investigate how the different contributions of ADF/cofilin (using unlabeled ADF, unlabeled cof1 and eGFP-cof1) to actin filament disassembly depend on pH, which we varied from 6.6 to 7.8. We first present the methods which we have used to do so, based on the observation of individual filaments, using microfluidics (Fig. 1). We measured cofilins abitility to decorate actin filament by binding to its sides (Fig. 2), and the rate at which individual cofilin domains severed actin filaments (Fig. 3). We next quantified the kinetic parameters of filament ends, for bare and ADF/cofilin-saturated (cofilactin) filaments (Fig. 4), and we specifically quantified the extent to which the barbed ends of cofilactin filaments are in a state which can hardly stop depolymerizing (Fig. 5). We finally summarize our results (Fig. 6).\n\nO_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=87 SRC=\"FIGDIR/small/422824_fig1.gif\" ALT=\"Figure 1\">\nView larger version (38K):\norg.highwire.dtl.DTLVardef@5a6fdorg.highwire.dtl.DTLVardef@1165d4borg.highwire.dtl.DTLVardef@146f0b7org.highwire.dtl.DTLVardef@658f72_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 1.C_FLOATNO Using microfluidics to monitor individual actin filaments and the binding of cofilin. (A) Experiments are performed in microfluidic chambers, sketched from above. The main channel is connected through three inlets to different protein solutions. Controlling the pressure in each inlet allows one to rapidly change the solution in the field of view.\n\n(B) Sketch of a typical experiment (side view). Filaments are elongated from coverslip-anchored spectrin-actin seeds, by flowing in with ATP-G-actin. Filaments are then aged by flowing in a solution of ATP-G-actin at the critical concentration, for at least 15 min. This results in >99% of the monomers in the ADP-state. Finally, filaments are exposed to ADF/cofilin.\n\n(C) Example of a field of view, imaged with TIRFm. ADP-F-actin labelled with Alexa-488 is exposed to mCherry-cofilin-1, which forms observable domains on the filaments.\n\nC_FIG O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=180 SRC=\"FIGDIR/small/422824_fig2.gif\" ALT=\"Figure 2\">\nView larger version (47K):\norg.highwire.dtl.DTLVardef@1aca24borg.highwire.dtl.DTLVardef@d2f404org.highwire.dtl.DTLVardef@1924892org.highwire.dtl.DTLVardef@daaaac_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 2.C_FLOATNO Cofilin binds more slowly to filaments at higher pH values. (A). Experimental configuration. Actin filaments are grown from spectrin-actin seeds with a long middle segment of unlabelled ADP-actin.\n\n(B). Time-lapse showing an unlabeled ADP-actin filament become saturated by eGFP-cof1 over time.\n\n(C-D). Mean normalized eGFP-cofilin-1 fluorescence signal, binding onto unlabelled ADP-F-actin. 150 nM (C) and 400 nM (D) eGFP-cofilin-1 was injected in the chamber from time t=0 onwards. The fluorescence signal was averaged along 20 to 35 pixels (3.5 to 6 {micro}m) for each filment. Number of filaments (C) N = 10, 10, 18, 20, for pH 6.6 Hepes, 7.0 Hepes, 7.0 Tris and 7.4 Tris, respectively, and\n\n(D) N = 10 in all conditions.\n\n(E). Number of cofilin subunits in individual domains, increasing over time. For clarity, the time origin has been shifted for each curve. Lines: linear fit. Condition: 400 nM eGFP-cofilin-1, pH 7.0 Hepes.\n\n(F). Growth rate of individual cofilin domains at different eGFP-cofilin-1 concentrations and pH. Value: median, error bars: interquartile range. N = 10 domains, except N = 9 for pH 6.6 Hepes 150 nM cof1, and for pH 7.8 Tris 400 nM cof1.\n\nC_FIG O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=41 SRC=\"FIGDIR/small/422824_fig3.gif\" ALT=\"Figure 3\">\nView larger version (18K):\norg.highwire.dtl.DTLVardef@1fb31d4org.highwire.dtl.DTLVardef@846198org.highwire.dtl.DTLVardef@12379d0org.highwire.dtl.DTLVardef@127b96_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 3.C_FLOATNO The severing rate per cofilin domain is unaffected by pH. (A). Experimental setup. Alexa-568-labelled actin filaments are polymerized from actin-spectrin seeds, and aged before being exposed to eGFP-cof1.\n\n(B). Typical kymograph. 200 nM eGFP-cof1 (green) is constantly injected, binds F-actin (red) and induces severing (lightning symbols).\n\n(C). Fraction of cofilin domains with no severing event detected near their edges, over time. Time t=0 is defined for each domain as the last frame before they become visible. The survival fraction curves are calculated using the Kaplan-Meier method over 22 to 43 filaments, 78 to 90 cofilin domains and 30 to 33 severing events, for each data set.\n\nC_FIG O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=146 SRC=\"FIGDIR/small/422824_fig4.gif\" ALT=\"Figure 4\">\nView larger version (32K):\norg.highwire.dtl.DTLVardef@16fdad8org.highwire.dtl.DTLVardef@889caborg.highwire.dtl.DTLVardef@e5b14aorg.highwire.dtl.DTLVardef@1da73c9_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 4.C_FLOATNO Higher pH slows down polymerization and depolymerization of bare F-actin but accelerates depolymerization of ADF/cofilin-saturated filaments at both ends. (A-C) Polymerization from the barbed-end.\n\n(A) Sketch of the experimental configuration, where filaments were grown from actin-spectrin seeds with G-ATP-actin and profilin.\n\n(B) Kymograph of a typical elongating filament.\n\n(C) Polymerization rate at different pH. N = 20 filaments for each condition.\n\n(D-E) Depolymerization from the barbed-end.\n\n(D) Sketch of the experimental configuration. ADP-F-actin is exposed either to buffer only, or to 1-2{micro}M unlabelled ADF or cofilin-1 in order to fully saturate the filament in less than a minute.\n\n(E) Depolymerization rate for different pH values. Right: zoom into the 0-5 sub/s range. From left to right, N = 20, 32, 22, 32, 31 (buffer only); N=9, 14, 23, 33, 34 (ADF-saturated); N=17, 18, 16 (cofilin-1-saturated).\n\n(F-H) Depolymerization from the pointed-end.\n\n(F) Sketch of the experimental configuration. ADP-F-actin was bound to the surface by gelsolin. Filaments were exposed to buffer only (supplemented with 0.4 mM CaCl2 to ensure gelsolin-actin tight binding), containing 1 to 2 {micro}M unlabelled ADF or cofilin-1 to rapidly saturate filaments.\n\n(G) Typical kymograph of a depolymerizing filament saturated with ADF.\n\n(H) Pointed-end depolymerization rate at different pH. N = 14, 20, 15, 20, 20 (buffer); N=20, 20, 16, 20, 20 (ADF-saturated); N= 20, 20, 20 (cofilin-1-saturated).\n\n(C, E, H) Symbol: median, error bars: interquartile range.\n\nC_FIG O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=94 SRC=\"FIGDIR/small/422824_fig5.gif\" ALT=\"Figure 5\">\nView larger version (22K):\norg.highwire.dtl.DTLVardef@e79318org.highwire.dtl.DTLVardef@16a4bb1org.highwire.dtl.DTLVardef@18f8fbdorg.highwire.dtl.DTLVardef@25dab6_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 5.C_FLOATNO The \"unstoppable\" depolymerization of cofilactin barbed ends is observed throughout our pH range. (A-C) Synergy of CP and ADF/cofilin to saturate filaments and initiate barbed end depolymerization.\n\n(A) Sketch of experimental configuration and events. Filaments grow until they are capped with CP. ADF/cofilin can then saturate the filaments, up to their BE which thus uncaps and depolymerizes.\n\n(B) Kymograph of a filament continuously exposed to the same solution containing 0.8 {micro}M G-ATP-actin, 1 {micro}M ADF and 2 nM CP. The filament polymerizes, pauses as it is capped by CP, and eventually depolymerizes.\n\n(C) Fraction of barbed ends that transitioned from a pause to depolymerization. Time t = 0 corresponds to the beginning of the pause (as shown on B). N = 24, 32, 32 filaments for pH 7.0 Hepes, pH 7.0 Tris, pH 7.4 Tris, respectively.\n\n(D-F) Cofilactin barbed ends sustain depolymerization in the presence of ATP-G-actin.\n\n(D) Sketch of the experimental configuration and events. Filaments are polymerized from spectrin-actin seeds and saturated with ADF. Depolymerizing cofilactin filaments are then constantly exposed to a solution of ATP-G-actin.\n\n(E) Fraction of barbed ends that transitioned from depolymerization to polymerization over time, when exposed to 1 {micro}M ATP-G-actin and 0.5 {micro}M ADF (to keep filaments saturated). N = 25, 16, 25, 24, 31 for pH 6.6 Hepes, 7.0 Hepes, 7.0 Tris, 7.4 Tris, 7.8 Tris, respectively.\n\n(F) Same as (E), with 1 {micro}M profilin added to the solution. N= 21, 27, 30 for pH 6.6 Hepes, 7.4 Tris, 7.8 Tris, respectively.\n\nC_FIG O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=178 SRC=\"FIGDIR/small/422824_fig6.gif\" ALT=\"Figure 6\">\nView larger version (34K):\norg.highwire.dtl.DTLVardef@13a07bborg.highwire.dtl.DTLVardef@d19d2forg.highwire.dtl.DTLVardef@1a697daorg.highwire.dtl.DTLVardef@3b9d59_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 6.C_FLOATNO Summary of results: barbed end depolymerization is an important contribution of cofilin disassembly at physiological pH. Within the range of pH that we have explored (pH 6.6 to 7.8) we have made the following observations (from top to bottom, on this sketch). A lower pH favors the rapid decoration of filaments by ADF/cofilin, but the severing rate per cofilin domain does not vary with pH. As a consequence, at a higher pH, domain boundaries persist longer (before domains merge) and severing is more efficient. The acceleration of pointed end depolymerization for cofilactin filaments is mostly observed at high pH. The \"unstoppable\" depolymerization of cofilactin barbed ends is observed at all pH, and is more pronounced at lower pH values.\n\nC_FIG

biochemistry↗

Torsional stress generated by ADF/cofilin on cross-linked actin filaments boosts their severing

Proteins of the Actin Depolymerizing Factor (ADF)/cofilin family are the central regulators of actin filament disassembly. A key function of ADF/cofilin is to sever actin filaments. However, how it does so in a physiological context, where filaments are interconnected and under mechanical stress, remains unclear. Here, we monitor and quantify the action of ADF/cofilin in different mechanical situations by using single molecule, single filament, and filament network techniques, coupled to microfluidics. We find that local curvature favors severing, while tension surprisingly has no effect on either cofilin binding or severing. Remarkably, we observe that filament segments that are held between two anchoring points, thereby constraining their twist, experience a mechanical torque upon cofilin binding. We find that this ADF/cofilin-induced torque does not hinder ADF/cofilin binding, but dramatically enhances severing. A simple model, which faithfully recapitulates our experimental observations, indicates that the ADF/cofilin-induced torque increases the severing rate constant 100-fold. A consequence of this mechanism, which we verify experimentally, is that cross-linked filament networks are severed by cofilin far more efficiently than non-connected filaments. We propose that this mechano-chemical mechanism is critical to boost ADF/cofilins ability to sever highly connected filament networks in cells.

biophysics↗

Modulation of formin processivity by profilin and mechanical tension

Formins are major regulators of actin networks. They enhance actin filament dynamics by remaining processively bound to filament barbed ends. How biochemical and mechanical factors affect formin processivity are open questions. Monitoring individual actin filaments in a microfluidic flow, we report that formin mDia1 dissociates faster under higher ionic strength and when actin concentration is increased. Profilin, known to increase the elongation rate of formin-associated filaments, surprisingly decreases the formin dissociation rate, by bringing formin FH1 domains in transient contact with the barbed end. In contrast, piconewton tensile forces applied to actin filaments accelerate formin dissociation by orders of magnitude, largely overcoming profilin-mediated stabilization. We developed a model of formin conformations and its confrontation to our data indicates the existence of two different dissociation pathways, with force favoring one over the other. How cells limit formin dissociation under tension is now a key question for future studies.

biophysics↗

Force dependence of filopodia adhesion: involvement of myosin II and formins

Filopodia are dynamic membrane protrusions driven by polymerization of an actin filament core, mediated by formin molecules at the filopodia tips. Filopodia can adhere to the extracellular matrix and experience both external and cell generated pulling forces. The role of such forces in filopodia adhesion is however insufficiently understood. Here, we induced sustained growth of filopodia by applying pulling force to their tips via attached fibronectin-coated beads trapped by optical tweezers. Strikingly, pharmacological inhibition or knockdown of myosin IIA, which localized to the base of filopodia, resulted in weakening of filopodia adherence strength. Inhibition of formins, which caused detachment of actin filaments from formin molecules, produced similar effect. Thus, myosin IIA-generated centripetal force transmitted to the filopodia tips through interactions between formins and actin filaments are required for filopodia adhesion. Force-dependent adhesion led to preferential attachment of filopodia to rigid versus fluid substrates, which may underlie cell orientation and polarization.

cell biology↗