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Jegou, A.

Publications and source records attributed to Jegou, A..

At least 19 recordsLinked to original sources

Intrafilament nucleotide exchange in a prokaryotic actin homolog

Polymerization and disassembly govern the cellular functions of cytoskeletal proteins. Canonical nucleotide-dependent polymers, including actin and microtubules, renew their nucleotide state through subunit subunit dissociation, nucleotide exchange in solution and repolymerization. Yet the assembly dynamics of the membrane-bound bacterial actin MreB remain unresolved. Here, using total internal reflection fluorescence microscopy and high-speed atomic force microscopy, we visualise Bacillus subtilis MreB assembly on supported lipid bilayers in real time. ATP binding drives polymerization into symmetrically elongating filaments, whereas ATP hydrolysis within filaments promotes disassembly. Unexpectedly, nucleotides continuously exchange within membrane-bound filaments without detectable subunit turnover, coupling filament stability to the surrounding nucleotide pool: ATP exchange stabilizes filaments, whereas ADP exchange triggers rapid fragmentation and disassembly. Monte-Carlo modelling and single-cell in vivo imaging support this mechanism. Thus, intrafilament nucleotide exchange enables MreB filaments to renew their nucleotide state without polymer turnover, revealing nucleotide-state rejuvenation as a new mode of biological polymer regulation.

microbiology↗

SPIN90 modulates the architecture of lamellipodial actin in an ARPC5L dependent fashion.

When stimulated by nucleation-promoting factors such as WAVE, the Arp2/3 complex generates branched actin networks. In contrast, when activated by SPIN90, the Arp2/3 complex generates linear actin filaments. The Arp2/3 complex in mammals, consists of 8 iso-complexes with dieerent properties as there are two isoforms of Arp3, ArpC1 and ArpC5. Here, using recombinant Arp2/3 iso-complexes with defined compositions, we show that SPIN90 selectively activates ArpC5L- rather than ArpC5- containing complexes to generate linear actin filaments. Consistent with this, SPIN90 at the leading edge of migrating cells enhances the recruitment of ArpC5L-, but not ArpC5- containing, Arp2/3 complexes to lamellipodia. These SPIN90-Arp2/3-ArpC5L complexes generate linear actin filaments that integrate into lamellipodia and impact protrusion eeiciency. Moreover, using polarised light microscopy, we show that loss of SPIN90 leads to an enrichment in actin filaments oriented more perpendicular to the plasma membrane. Our results demonstrate that SPIN90 regulates the architecture and dynamics of lamellipodial actin in an Arp2/3 iso-complex dependent fashion. SummarySPIN90 selectively recruits and activates ArpC5L containing Arp2/3 to shape the architecture and dynamics of lamellipodial actin.

cell biology↗

Vimentin promotes actin assembly by stabilizing ATP-actin subunits at the barbed end

Vimentin intermediate filaments play essential roles in maintaining cell integrity and regulating numerous cellular functions. In particular, vimentin cooperates with the actin cytoskeleton in key cellular processes that rely on actin dynamics, such as migration, division, and mechanosensing. While there is evidence that these two cytoskeletal components interact in cells, the underlying molecular mechanisms are only partially understood. Actin and vimentin can interact through biochemical signaling pathways or via cross-linkers, but whether they engage in a direct protein-protein interaction has remained controversial, in part because such interactions are difficult to isolate and characterize in cells. Using in vitro reconstitution coupled to theoretical modeling, and total internal reflection fluorescence microscopy to monitor the elongation of single actin filaments, we show that vimentin promotes actin elongation by stabilizing actin subunits at the barbed end in a dose-dependent manner. Strikingly, this effect depends on the nucleotide state of actin, as the acceleration is only observed for the elongation from ATP-actin, and not ADP-actin monomers. We further establish that neither the vimentin tail nor head domains are required for this effect, and both filamentous and non-filamentous vimentin enhance actin elongation. Finally, we find that vimentin promotes the nucleation of actin filaments. Consistently, magnetic pull-down assays demonstrate a direct interaction between vimentin and ATP-actin monomers. Altogether, these findings identify vimentin as an unexpected new actor in the regulation of actin dynamics at the barbed end and bring new insights into the functional role of vimentin through cytoskeletal crosstalk.

biophysics↗

Sleep deprivation constrains dynamic configurations of integrated and segregated brain states impacting cognitive performance

The breakdown of cognitive control following sleep deprivation is widely recognised, but the physiological mechanisms and brain signatures that produce this vulnerability have not been resolved. Effective cognition relies on large-scale brain networks flexibly reconfiguring between states of integration and segregation. Here we combined functional magnetic resonance imaging (fMRI), electroencephalography (EEG), and electrocardiography (ECG) collected during cognitive tasks under rested wakefulness, after sleep deprivation, and following a recovery nap to test the hypothesis that sleep deprivation constrains this dynamical repertoire and disrupts its physiological regulation. Using time-resolved functional connectivity and graph theory, we show that sleep deprivation increases the distribution of connections across networks, while reducing the temporal variability of between-network connectivity. Furthermore, dynamic fluctuations between integrated and segregated modes of network topology were dampened, with brain regions spending more time in intermediate configurations and showing greater instability of mode transitions. These alterations were tightly linked to behavioural impairment: participants who exhibited greater contraction toward intermediate topologies also showed poorer task accuracy and slower responses. Under well-rested conditions, thalamic activity peaked prior to transitions into integrated states and was suppressed during transitions into segregated states, consistent with a coordinating role in cortical dynamics. Sleep deprivation weakened and delayed this thalamic coupling. Finally, global and regional fMRI fluctuations were elevated after sleep loss, becoming decoupled from cardiac physiology while more strongly coupled to EEG delta power, further linking reduced arousal to constrained network flexibility. Together, these findings show that sleep deprivation narrows the brains dynamical repertoire, due to disrupted thalamic regulation and changes to the physiological integration with cortical networks.

neuroscience↗

Inorganic phosphate in Arp2/3 complex acts as a rapid switch for the stability of actin filament branches

The rate at which actin filaments turn over modulates actin network architecture and mechanosensitivity. Actin filaments often appear as branches, nucleated by the Arp2/3 complex. Within the Arp2/3 complex, Arp2 and Arp3 are ATPases, which, similar to actin, may adopt slightly different conformations depending on their bound nucleotide. We investigate the impact of the nucleotide state of Arp2/3 complexes on branch stability, by mechanically pulling on them. Remarkably, we find that branches with mammalian ADP-Pi and ADP-Arp2/3 complexes detach with the same exponential increase as a function of force, but ADP-Pi-Arp2/3 complex branch junctions are 20 times more stable at all forces. We observe that inorganic phosphate (Pi) is in rapid equilibrium with ADP-Arp2/3 at the branch junction, and is released at a rate greater than 1 s-1. Upon branch dissociation, the surviving Arp2/3 complex, remaining attached to the mother filament, is a thousand times more stable in the ADP-Pi than in the ADP state. Surprisingly, branch regrowth from surviving ADP-Pi-Arp2/3 complex does not require reloading ATP, indicating that the Arp2/3 complex remained in an active state upon debranching. We reveal that GMF destabilizes ADP-Arp2/3 complex branch junctions by accelerating first the dissociation of the daughter filament, and then the dissociation of the surviving Arp2/3 complex from the mother filament. We also report that cortactin stabilizes branches in a force dependent manner, and enhances branch renucleation. GMF and cortactin do not bind to Arp2/3 in the ADP-Pi state. Overall, Our results give a new importance to cytoplasmic Pi, as a possible regulator of branched actin network stability.

biophysics↗

Probing protein-protein interactions with drag flow: A case study of F-actin and tropomyosin

Tropomyosin are central regulators of the actin cytoskeleton, controlling the binding and activity of the other actin binding proteins. The interaction between tropomyosin and actin is quite unique: single tropomyosin dimers bind weakly to actin filaments but get stabilised by end-to-end attachment with neighbouring tropomyosin dimers, forming clusters which wrap around the filament. Force spectroscopy is a powerful approach for studying protein-protein interactions, but classical methods which usually pull with pN forces on a single protein pair, are not well adapted to tropomyosins. Here, we propose a method in which a hydrodynamic drag force is applied directly to the proteins of interest, by imposing a controlled fluid flow inside a microfluidic chamber. The breaking of the protein bonds is directly visualised with fluorescence microscopy. Using this approach, we reveal that very low forces from 0.01 to 0.1 pN per tropomyosin dimer trigger the detachment of entire tropomyosin clusters from actin filaments. We show that the tropomyosin cluster detachment rate depends on the cytoplasmic tropomyosin isoform (Tpm1.6, 1.7, 1.8) and increases exponentially with the applied force. These observations lead us to propose a cluster detachment model which suggests that tropomyosins dynamically explore different positions over the actin filament. Our experimental setup can be used with many other cytoskeletal proteins, and we show, as a proof-of-concept, that the velocity of myosin-X motors is reduced by an opposing fluid flow. Overall, this method expands the range of protein-protein interactions that can be studied by force spectroscopy. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=173 HEIGHT=200 SRC="FIGDIR/small/653996v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@19298b4org.highwire.dtl.DTLVardef@16766beorg.highwire.dtl.DTLVardef@18a70c6org.highwire.dtl.DTLVardef@1f1fad5_HPS_FORMAT_FIGEXP M_FIG C_FIG

biophysics↗

HIV-1 budding requires cortical actin disassembly by the oxidoreductase MICAL1

Many enveloped viruses bud from the plasma membrane that is tightly associated with a dense and thick actin cortex. This actin network represents a significant challenge for membrane deformation and scission, and how it is remodeled during the late steps of the viral cycle is largely unknown. Using super-resolution microscopy, we show that HIV-1 buds in areas of the plasma membrane with low cortical F-actin levels. We find that the cellular oxidoreductase MICAL1 locally depolymerizes actin at budding sites to promote HIV-1 budding and release. In the absence of MICAL1, F-actin abnormally remains at viral budding sites, incompletely budded viruses accumulate at the plasma membrane and viral release is impaired. Remarkably, normal viral release can be restored in MICAL1-depleted cells by inhibiting Arp2/3-dependent branched actin networks. Mechanistically, we find that MICAL1 directly disassembles branched-actin networks and controls the timely recruitment of the ESCRT scission machinery during viral budding. In addition, the MICAL1 activator Rab35 is recruited at budding sites, functions in the same pathway as MICAL1 and is also required for viral release. This work reveals a role for oxidoreduction in triggering local actin depolymerization to control HIV-1 budding, a mechanism that may be widely used by other viruses. The debranching activity of MICAL1 could be involved beyond viral budding in various other cellular functions requiring local plasma membrane deformation.

cell biology↗

EEG source imaging technique to investigate sleep oscillations for simultaneous EEG-fMRI

Simultaneous recording of electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) is a widely used non-invasive neuroimaging technique in sleep studies. However, EEG data are strongly influenced by two types of MRI-related artefacts: gradient artefacts (GA) and ballistocardiogram artefacts (BCG). If artefacts correction is suboptimal, the BCG obscures the EEG signals below 20Hz and could make it difficult to investigate sleep oscillations, especially sleep spindles, sleep specific oscillations occurring within 11-16Hz frequency band. We previously demonstrated the utility of beamforming spatial filtering in correcting MRI-related artefacts on EEG. Here, we investigated the use of beamforming spatial filtering for improving the detection of EEG oscillations during sleep, in particular, 1) to accurately estimate single-event spindle EEG power changes, and 2) to demonstrate the potential improvement of fMRI general linear model (GLM) analysis when involving such additional EEG information. We analysed EEG-fMRI data acquired during a recovery nap after sleep deprivation in 20 young healthy participants (12 females, 8 males, age = 21.3 {+/-} 2.5 years). Based on spindle events (onset and duration) detected by trained sleep scorers on BCG corrected EEG signals through a conventional average artefact subtraction (AAS) method, we compared four different EEG processing steps: non-BCG corrected; AAS BCG corrected; beamforming BCG corrected; beamforming+AAS BCG corrected. These processing steps consist of non-BCG corrected and AAS BCG corrected considered either at the sensor level or at the source-level (after beamformer localization) to evaluate the impact of the BCG artefact on the detection of spindle activity. Then we further investigated four different fMRI GLM approaches using 1) the spindle onset and duration (GLM1), 2) spindle onset, duration, and parametric modulation of single-spindle power change from the Cz electrode of the AAS BCG corrected data (GLM2), 3) spindle onset, duration, and parametric modulation of single-spindle power change from the beamforming+AAS BCG corrected (GLM3) and 4) spindle onset, duration, and parametric modulation of single-spindle power change from the beamforming BCG corrected data (GLM4). We found that the beamforming approach did not only attenuate the BCG artefacts, but also recovered sleep spindle activity occurring during NREM sleep. Furthermore, this beamforming approach allowed us to accurately estimate single-event power change of each spindle in the source space when compared to the channel level analysis, and therefore to further improve the specificity of fMRI GLM analysis, better localizing the recruited brain regions during spindles. Our findings show the benefit of applying beamforming source imaging technique to EEG-fMRI acquired during sleep. We demonstrate that this approach would be beneficial especially for long EEG-fMRI data acquisitions (i.e., sleep, resting-state), when the BCG correction becomes problematic due to inherent dynamic changes of heart rates. Our findings extend previous work regarding the application of the source imaging to the sleep EEG-fMRI. Combining with this advanced methodology and analysis, sleep EEG-fMRI will help us better understand the functional roles of human sleep.

neuroscience↗

NREM sleep brain networks modulate cognitive recovery from sleep deprivation

Decrease in cognitive performance after sleep deprivation and its recovery following sleep suggests the key role of sleep, especially non-rapid eye movement (NREM) sleep, in maintaining cognition. It remains unknown whether brain network reorganization in NREM sleep stages N2 and N3 can uniquely be mapped onto individual differences in cognitive performance after a recovery nap following sleep deprivation. Using resting state functional magnetic resonance imaging (fMRI), we quantified the integration and segregation of brain networks during N2 and N3 sleep in a 1-hour nap following 24-hour sleep deprivation, compared to well-rested wakefulness. Here, we introduce a new analytic framework called the hierarchical segregation index (HSI) to quantify network segregation across spatial scales, from whole-brain to the voxel level, by identifying spatio-temporally overlapping large-scale networks and the corresponding voxel-to-region hierarchy. We found that network segregation increased in the posterior cingulate cortex during both N2 and N3 sleep compared to wakefulness. In contrast, increased segregation in the visual cortex and decreased segregation in the posterior ventromedial prefrontal cortex during N2 returned to levels comparable to wakefulness during N3. More segregation during N3 sleep was associated with worse recovery of working memory, executive attention, and psychomotor vigilance after the nap. Sleep-related changes in network segregation emerged at different spatial scales, with regional- and voxel-level alterations being associated with different cognitive tasks. Finally, we demonstrated the sensitivity and reliability of voxel-level HSI to provide key insights into within-region variation, suggesting a mechanistic understanding of how NREM sleep replenishes cognition after sleep deprivation.

neuroscience↗

Regeneration of actin filament branches from the same Arp2/3 complex

Branched actin filaments are found in many key cellular structures. Branches are nucleated by the Arp2/3 complex activated by nucleation-promoting factor (NPF) proteins and bound to the side of pre-existing mother filaments. Over time, branches dissociate from their mother filament, leading to network reorganization and turnover, but this mechanism is less understood. Here, using microfluidics and purified proteins, we examined the dissociation of individual branches under controlled biochemical and mechanical conditions. We observe that Arp2/3 remains bound to the mother filament after most debranching events, even when accelerated by force. Unexpectedly, this mother-remaining Arp2/3 readily nucleates a new actin filament branch, without being activated anew by an NPF: it simply needs to exchange its nucleotide and bind an actin monomer. The protein GMF, which accelerates debranching, prevents branch re-nucleation. Our results suggest that actin filament re-nucleation can provide a self-repair mechanism, helping branched networks to sustain mechanical stress in cells over extended periods of time.

biophysics↗

Fascin-induced bundling protects actin filaments from disassembly by cofilin

Actin filament turnover plays a central role in shaping actin networks, yet the feedback mechanism between network architecture and filament assembly dynamics remains unclear. The activity of ADF/cofilin, the main protein family responsible for filament disassembly, has been mainly studied at the single filament level. Here, we report that fascin, by crosslinking filaments into bundles, strongly slows down filament disassembly by cofilin. We show that this is mainly due to a slower nucleation of the first cofilin clusters, which occurs up to 100-fold slower on large bundles compared to single filaments. In contrast, severing at cofilin cluster boundaries is unaffected by fascin bundling. After the nucleation of an initial cofilin cluster on a filament of a bundle, we observe the local removal of fascin. Surprisingly, the nucleation of cofilin clusters on adjacent filaments is highly enhanced, locally. We propose that this inter-filament cooperativity in cofilin binding arises from the local propagation of the cofilin-induced change in helicity from one filament to the other filaments of the bundle. Taken together, these observations reveal the molecular events explaining why, despite inter-filament cooperativity, fascin crosslinking protects actin filaments from cofilin-induced disassembly. These findings highlight the important role played by crosslinkers in organizing actin networks and modulating the activity of other regulatory proteins.

biochemistry↗

Nucleation and stability of branched versus linear Arp2/3-generated actin filaments

Activation of the Arp2/3 complex by VCA-domain-bearing NPFs results in the formation of daughter actin filaments branching off the sides of pre-existing mother filaments. Alternatively, when stimulated by SPIN90, Arp2/3 directly nucleates linear actin filaments. Uncovering the similarities and differences of these two activation mechanisms is fundamental to understanding the regulation and function of Arp2/3. Analysis of individual filaments reveals that the catalytic VCA domain of WASP, N-WASP and WASH, accelerate the Arp2/3-mediated nucleation of linear filaments by SPIN90, in addition to their known branch-promoting activity. Unexpectedly, these VCA domains also destabilize existing branches, as well as SPIN90-Arp2/3 at filament pointed ends. Furthermore, cortactin and GMF, which respectively stabilize and destabilize Arp2/3 at branch junctions, have a similar impact on SPIN90-activated Arp2/3. However, unlike branch junctions, SPIN90-Arp2/3 at the pointed end of linear filaments is not destabilized by piconewton forces, and does not become less stable with time. It thus appears that linear and branched Arp2/3-generated filaments respond similarly to regulatory proteins, albeit with quantitative differences, and that they differ greatly in their responses to aging and to mechanical stress. These results indicate that SPIN90- and VCA-activated Arp2/3 complexes adopt similar yet non-identical conformations, and that their turnover in cells may be regulated differently.

biochemistry↗

Focal Non-invasive Deep-brain Stimulation with Temporal Interference for the Suppression of Epileptic Biomarkers

Neurostimulation applied from deep brain stimulation (DBS) electrodes is an effective therapeutic intervention in patients suffering from intractable drug-resistant epilepsy when resective surgery is contraindicated or failed. Inhibitory DBS to suppress seizures and associated epileptogenic biomarkers could be performed with high-frequency stimulation (HFS), typically between 100 -165Hz, to various deep-seated targets such as for instance the Mesio-temporal lobe (MTL) which leads to changes in brain rhythms, specifically in the hippocampus. The most prominent alterations concern high-frequency oscillations (HFOs), namely increase in ripples, a reduction in pathological Fast Ripples (FRs), and a decrease in pathological interictal epileptiform discharges (IEDs). In the current study, we use Temporal Interference stimulation to provide a non-invasive focal DBS (130 Hz) of the MTL, specifically the hippocampus, which increases physiological ripples, and decreases the number of FRs and IEDs in a mouse model of epilepsy. Similarly, we show the inability of 130 Hz transcranial current stimulation (TCS) to achieve similar results. The method could potentially revolutionize how DBS, certainly in epilepsy, is performed, and we therefore further demonstrate the translatability to human subjects via measurements of the TI stimulation vs TCS in human cadavers. Results show the better penetration of TI fields into the human hippocampus as compared with TCS. Finally, we provide evidence of the efficacy of the specific form of Pulse-width Modulated TI (PWM-TI), implemented with square waves, which is used in this study. One Sentence SummaryA non-invasive deep brain stimulation applied via temporal interference achieves the suppression of biomarkers of epilepsy in mice and is scaled to humans.

neuroscience↗

Altered functional integration of brain activity is a marker of impaired cognitive performance following sleep deprivation

Sleep deprivation (SD) leads to impairments in cognitive function. Here, we tested the hypothesis that cognitive changes in the sleep-deprived brain can be explained by information processing within and between large-scale cortical networks. We acquired functional magnetic resonance imaging (fMRI) scans of 20 healthy volunteers during attention and executive tasks following a regular night of sleep, a night of sleep deprivation, and a recovery nap containing non-rapid eye movement (NREM) sleep. Overall, sleep deprivation was associated with increased cortex-wide functional integration, driven by a rise of integration within cortical networks. The ratio of within vs between network integration in the cortex increased further in the recovery nap, suggesting that prolonged wakefulness drives the cortex toward a state resembling sleep. This balance of integration and segregation in the sleep-deprived state was tightly associated with deficits in cognitive performance. This was a distinct and better marker of cognitive impairment than conventional indicators of homeostatic sleep pressure, as well as the pronounced thalamo-cortical connectivity changes that occurs towards falling asleep. Importantly, restoration of the balance between segregation and integration of cortical activity was also related to performance recovery after the nap, demonstrating a bi-directional effect. These results demonstrate that intra- and inter-individual differences in cortical network integration and segregation during task performance may play a critical role in vulnerability to cognitive impairment in the sleep deprived state. Significance StatementSleep deprivation has significant negative consequences for cognitive function. Understanding how changes in brain activity underpin changes in cognition is important not only to discover why performance declines following extended periods of wakefulness, but also for answering the fundamental question of why we require regular and recurrent sleep for optimal performance. Finding neural correlates that predict performance following sleep deprivation also has the potential to understand which individuals are particularly vulnerable to sleep deprivation, and what aspects of brain function may protect them from these negative consequences on performance. Finally, understanding how perturbations to regular (well-rested) brain functioning affect cognitive performance, will provide important insight into how underlying principles of information processing in the brain may support cognition generally.

neuroscience↗

IN VITRO RECONSTITUTION OF DYNEIN FORCE EXERTION IN BULK CYTOPLASM

The forces generated by Microtubules (MTs) and their associated motors orchestrate essential cellular processes ranging from vesicular trafficking to centrosome positioning [1, 2]. To date, most studies have focused on force exertion from motors anchored on a static surface, such as the cell cortex in vivo or glass surfaces in vitro [2-4]. However, motors also transport large cargos and endomembrane networks, whose hydrodynamic interactions with the viscous cytoplasm should generate sizable forces in bulk. Such forces may contribute to MT aster centration, organization and orientation [5-14], but have yet to be evidenced and studied in a minimal reconstituted system. By developing a bulk motility assay, based on stabilized MTs and dynein-coated beads freely floating in a viscous medium away from any surface, we demonstrate that the motion of a cargo exerts a pulling force on the MT and propels it in opposite direction. Quantification of resulting MT movements for different motors, motor velocities, over a range of cargo size and medium viscosities, shows that the efficiency of this mechanism is primarily determined by cargo size and MT length. Forces exerted by cargos are additive, allowing us to recapitulate tug-of-war situations, or bi-dimensional motions of minimal asters. These data also reveal unappreciated effects of the nature of viscous crowders and hydrodynamic interactions between cargos and MTs, likely relevant to understand this mode of force exertion in living cells. This study places endomembrane transport as a significant mode of MT force exertion with far-reaching consequences for cellular organization.

biophysics↗

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

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