Journal articles: 'Cortex actine'

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CAVALCANTI, FERNANDA F., HANS TORE RAPP, and MICHELLE KLAUTAU. "Taxonomic revision of Leucascus Dendy, 1892 (Porifera: Calcarea) with revalidation of Ascoleucetta Dendy & Frederick, 1924 and description of three new species." Zootaxa 3619, no. 3 (February 28, 2013): 275–314. http://dx.doi.org/10.11646/zootaxa.3619.3.3.

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Sponges of the genus Leucascus are frequently recognised as possessing anastomosed tubes with choanocytes, and cortical and atrial membranes with pinacocytes. In the last years, five species of other genera were transferred to Leucascus, and several other species were suggested but not formally included in this genus. In the present work, all these species accepted or suggested as Leucascus were revised. According to our results, Leucascus is now composed of nine species: L. clavatus, L. leptoraphis comb. nov., L. lobatus, L. neocaledonicus, L. protogenes comb. nov., L. roseus, L. simplex (type species), L. albus sp. nov., and L. flavus sp. nov. The presence of spines in the apical actine of the tetractines had never been observed in Leucascus, but it was found in all species with tetractines in their skeletons. Some species were transferred from Leucascus to the genus Ascoleucetta, which is revalidated here based on important differences in the cortex. Modifications are also proposed in the definition of both genera. Based on our results, the family Leucascidae is now composed of Ascaltis, Leucascus and Ascoleucetta.

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Staddon, Michael F., Edwin M. Munro, and Shiladitya Banerjee. "Pulsatile contractions and pattern formation in excitable actomyosin cortex." PLOS Computational Biology 18, no. 3 (March 30, 2022): e1009981. http://dx.doi.org/10.1371/journal.pcbi.1009981.

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The actin cortex is an active adaptive material, embedded with complex regulatory networks that can sense, generate, and transmit mechanical forces. The cortex exhibits a wide range of dynamic behaviours, from generating pulsatory contractions and travelling waves to forming organised structures. Despite the progress in characterising the biochemical and mechanical components of the actin cortex, the emergent dynamics of this mechanochemical system is poorly understood. Here we develop a reaction-diffusion model for the RhoA signalling network, the upstream regulator for actomyosin assembly and contractility, coupled to an active actomyosin gel, to investigate how the interplay between chemical signalling and mechanical forces regulates stresses and patterns in the cortex. We demonstrate that mechanochemical feedback in the cortex acts to destabilise homogeneous states and robustly generate pulsatile contractions. By tuning active stress in the system, we show that the cortex can generate propagating contraction pulses, form network structures, or exhibit topological turbulence.

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Cytrynbaum, E. N., P. Sommi, I. Brust-Mascher, J. M. Scholey, and A. Mogilner. "Early Spindle Assembly in Drosophila Embryos: Role of a Force Balance Involving Cytoskeletal Dynamics and Nuclear Mechanics." Molecular Biology of the Cell 16, no. 10 (October 2005): 4967–81. http://dx.doi.org/10.1091/mbc.e05-02-0154.

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Mitotic spindle morphogenesis depends upon the action of microtubules (MTs), motors and the cell cortex. Previously, we proposed that cortical- and MT-based motors acting alone can coordinate early spindle assembly in Drosophila embryos. Here, we tested this model using microscopy of living embryos to analyze spindle pole separation, cortical reorganization, and nuclear dynamics in interphase-prophase of cycles 11-13. We observe that actin caps remain flat as they expand and that furrows do not ingress. As centrosomes separate, they follow a linear trajectory, maintaining a constant pole-to-furrow distance while the nucleus progressively deforms along the elongating pole-pole axis. These observations are incorporated into a model in which outward forces generated by zones of active cortical dynein are balanced by inward forces produced by nuclear elasticity and during cycle 13, by Ncd, which localizes to interpolar MTs. Thus, the force-balance driving early spindle morphogenesis depends upon MT-based motors acting in concert with the cortex and nucleus.

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McCall, Patrick M., Frederick C. MacKintosh, David R. Kovar, and Margaret L. Gardel. "Cofilin drives rapid turnover and fluidization of entangled F-actin." Proceedings of the National Academy of Sciences 116, no. 26 (June 12, 2019): 12629–37. http://dx.doi.org/10.1073/pnas.1818808116.

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The shape of most animal cells is controlled by the actin cortex, a thin network of dynamic actin filaments (F-actin) situated just beneath the plasma membrane. The cortex is held far from equilibrium by both active stresses and polymer turnover: Molecular motors drive deformations required for cell morphogenesis, while actin-filament disassembly dynamics relax stress and facilitate cortical remodeling. While many aspects of actin-cortex mechanics are well characterized, a mechanistic understanding of how nonequilibrium actin turnover contributes to stress relaxation is still lacking. To address this, we developed a reconstituted in vitro system of entangled F-actin, wherein the steady-state length and turnover rate of F-actin are controlled by the actin regulatory proteins cofilin, profilin, and formin, which sever, recycle, and assemble filaments, respectively. Cofilin-mediated severing accelerates the turnover and spatial reorganization of F-actin, without significant changes to filament length. We demonstrate that cofilin-mediated severing is a single-timescale mode of stress relaxation that tunes the low-frequency viscosity over two orders of magnitude. These findings serve as the foundation for understanding the mechanics of more physiological F-actin networks with turnover and inform an updated microscopic model of single-filament turnover. They also demonstrate that polymer activity, in the form of ATP hydrolysis on F-actin coupled to nucleotide-dependent cofilin binding, is sufficient to generate a form of active matter wherein asymmetric filament disassembly preserves filament number despite sustained severing.

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Sanders, M. C., and Y. L. Wang. "Assembly of actin-containing cortex occurs at distal regions of growing neurites in PC12 cells." Journal of Cell Science 100, no. 4 (December 1, 1991): 771–80. http://dx.doi.org/10.1242/jcs.100.4.771.

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Although actin filaments are known to be localized in the cortex of axons and in the growth cones of nerve cells, it is unclear how actin-containing structures are assembled during nerve growth. We have studied the formation of actin structures in growing neurites by microinjecting fluorescent phalloidin or actin into PC12 neuron-like cells to label endogenous actin filaments. Upon stimulation of neurite growth in cells microinjected with fluorescent phalloidin, little or no fluorescence was detected in nascent growth cones and adjacent neurites despite the presence of actin filaments in these regions, suggesting that actin filaments were primarily formed by de novo assembly rather than the transport and reorganization of pre-existing, phalloidin-labeled actin filaments. Time-lapse observations of the distribution of phalloidin-labeled actin filaments during neurite elongation confirmed that fluorescence associated with pre-existing neurite cortex spread out more slowly than the elongation of neurites. Furthermore, when a dark spot was photobleached with a laser microbeam along neurites of cells microinjected with either fluorescent phalloidin or actin, the spot showed no appreciable translocation during active neurite elongation. Taken together, these results suggest that de novo assembly of actin filaments plays a crucial role in the formation of growth cones and adjacent cortex in the distal region of neurites, but does not appear to require the anterograde or retrograde transport of cortical filaments, or the passive stretching of the proximal segment of the neurite cortex.

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Gilyazutdinova, Z. Sh, G. V. Sukhanova, and A. A. Kilensky. "Hormone-active adrenal cortex tumors." Kazan medical journal 66, no. 2 (April 15, 1985): 159. http://dx.doi.org/10.17816/kazmj61215.

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Gilyazutdinova, Z. Sh, G. V. Sukhanova, and A. A. Kalensky. "Hormone-active adrenal cortex tumors." Kazan medical journal 66, no. 2 (April 15, 1985): 103–5. http://dx.doi.org/10.17816/kazmj60734.

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Considering the comparative rarity of hormonally active tumors of the adrenal cortex with androgenic effect and the complexity of their diagnosis, we present our observations. From 1980 to 1983, among women with neuroendocrine pathology, 4 patients aged 23 to 27 years were diagnosed with adrenal cortex tumors.

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Koester, Darius V., Kabir Husain, Elda Iljazi, Scott Hansen, Dyche R. Mullins, Madan Rao, and Satyajit Mayor. "In Vitro Reconstitution of Remodeling Actin Asters - Steps towards a Minimal Active Actomyosin Cortex." Biophysical Journal 106, no. 2 (January 2014): 170a. http://dx.doi.org/10.1016/j.bpj.2013.11.964.

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Eda, Masatoshi, Shigenobu Yonemura, Takayuki Kato, Naoki Watanabe, Toshimasa Ishizaki, Pascal Madaule, and Shuh Narumiya. "Rho-dependent transfer of Citron-kinase to the cleavage furrow of dividing cells." Journal of Cell Science 114, no. 18 (September 15, 2001): 3273–84. http://dx.doi.org/10.1242/jcs.114.18.3273.

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Citron-kinase (Citron-K) is a Rho effector working in cytokinesis. It is enriched in cleavage furrow, but how Rho mobilizes Citron-K remains unknown. Using anti-Citron antibody and a Citron-K Green Fluorescence Protein (GFP)-fusion, we monitored its localization in cell cycle. We have found: (1) Citron-K is present as aggregates in interphase cells, disperses throughout the cytoplasm in prometaphase, translocates to cell cortex in anaphase and accumulates in cleavage furrow in telophase; (2) Rho colocalizes with Citron-K in the cortex of ana- to telophase cells and the two proteins are concentrated in the cleavage furrow and to the midbody; (3) inactivation of Rho by C3 exoenzyme does not affect the dispersion of Citron-K in prometaphase, but prevented its transfer to the cell cortex, and Citron-K stays in association with the midzone spindles of C3 exoenzyme-treated cells. To clarify further the mechanism of the Rho-mediated transfer and concentration of Citron-K in cleavage furrow, we expressed active Val14RhoA in interphase cells expressing GFP-Citron-K. Val14RhoA expression transferred Citron-K to the ventral cortex of interphase cells, where it formed band-like structures in a complex with Rho. This structure was localized at the same plane as actin stress fibers, and they exclude each other. Disruption of F-actin abolished the band and dispersed the Citron-K-Rho-containing patches throughout the cell cortex. Similarly, in dividing cells, a structure composed of Rho and Citron-K in cleavage furrow excludes cortical actin cytoskeleton, and disruption of F-actin disperses Citron-K throughout the cell cortex. These results suggest that Citron-K is a novel type of a passenger protein, which is dispersed to the cytoplasm in prometaphase and associated with midzone spindles by a Rho-independent signal. Rho is then activated, binds to Citron-K and translocates it to cell cortex, where the complex is then concentrated in the cleavage furrow by the action of actin cytoskeleton beneath the equator of dividing cells.

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Hurtley, Stella M. "Actin cortex controls cell migration." Science 368, no. 6496 (June 11, 2020): 1201.11–1203. http://dx.doi.org/10.1126/science.368.6496.1201-k.

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Haraszti, Tamás, Anabel E. M. Clemen, and Joachim P. Spatz. "Biomimetic F-Actin Cortex Models." ChemPhysChem 10, no. 16 (November 3, 2009): 2777–86. http://dx.doi.org/10.1002/cphc.200900581.

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Charras, Guillaume T., Chi-Kuo Hu, Margaret Coughlin, and Timothy J. Mitchison. "Reassembly of contractile actin cortex in cell blebs." Journal of Cell Biology 175, no. 3 (November 6, 2006): 477–90. http://dx.doi.org/10.1083/jcb.200602085.

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Contractile actin cortex is involved in cell morphogenesis, movement, and cytokinesis, but its organization and assembly are poorly understood. During blebbing, the membrane detaches from the cortex and inflates. As expansion ceases, contractile cortex reassembles under the membrane and drives bleb retraction. This cycle enabled us to measure the temporal sequence of protein recruitment to the membrane during cortex reassembly and to explore dependency relationships. Expanding blebs were devoid of actin, but proteins of the erythrocytic submembranous cytoskeleton were present. When expansion ceased, ezrin was recruited to the membrane first, followed by actin, actin-bundling proteins, and, finally, contractile proteins. Complete assembly of the contractile cortex, which was organized into a cagelike mesh of filaments, took ∼30 s. Cytochalasin D blocked recruitment of actin and α-actinin, but had no effect on membrane association of ankyrin B and ezrin. Ezrin played no role in actin nucleation, but was essential for tethering the membrane to the cortex. The Rho pathway was important for cortex assembly in blebs.

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Blain-Brière, Bénédicte, Caroline Bouchard, Nathalie Bigras, and Geneviève Cadoret. "Development of active control within working memory." International Journal of Behavioral Development 38, no. 3 (November 26, 2013): 239–46. http://dx.doi.org/10.1177/0165025413513202.

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This study aimed to compare children’s performance on two mnemonic functions that engage the lateral prefrontal cortex. Brain imaging studies in adults have shown that the mid-ventrolateral prefrontal cortex is specifically involved in active controlled retrieval, and the mid-dorsolateral prefrontal cortex is specifically involved in monitoring mnemonic information (Petrides, 2005). Eighty-two children aged from 6 years, 8 months to 8 years, 7 months were tested. They showed equivalent success rates in active retrieval and monitoring with color and shape information. However, children were slower in monitoring than in active retrieval in color trials. The results demonstrate that the specialized contributions of the lateral prefrontal cortex emerge conjointly during childhood giving children multiple tools to exert an active control within memory.

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Zhang, Xiaoli, Luis R. Flores, Michael C. Keeling, Kristina Sliogeryte, and Núria Gavara. "Ezrin Phosphorylation at T567 Modulates Cell Migration, Mechanical Properties, and Cytoskeletal Organization." International Journal of Molecular Sciences 21, no. 2 (January 9, 2020): 435. http://dx.doi.org/10.3390/ijms21020435.

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Ezrin, a member of the ERM (ezrin/radixin/moesin) family of proteins, serves as a crosslinker between the plasma membrane and the actin cytoskeleton. By doing so, it provides structural links to strengthen the connection between the cell cortex and the plasma membrane, acting also as a signal transducer in multiple pathways during migration, proliferation, and endocytosis. In this study, we investigated the role of ezrin phosphorylation and its intracellular localization on cell motility, cytoskeleton organization, and cell stiffness, using fluorescence live-cell imaging, image quantification, and atomic force microscopy (AFM). Our results show that cells expressing constitutively active ezrin T567D (phosphomimetic) migrate faster and in a more directional manner, especially when ezrin accumulates at the cell rear. Similarly, image quantification results reveal that transfection with ezrin T567D alters the cell’s gross morphology and decreases cortical stiffness. In contrast, constitutively inactive ezrin T567A accumulates around the nucleus, and although it does not impair cell migration, it leads to a significant buildup of actin fibers, a decrease in nuclear volume, and an increase in cytoskeletal stiffness. Finally, cell transfection with the dominant negative ezrin FERM domain induces significant morphological and nuclear changes and affects actin, microtubules, and the intermediate filament vimentin, resulting in cytoskeletal fibers that are longer, thicker, and more aligned. Collectively, our results suggest that ezrin’s phosphorylation state and its intracellular localization plays a pivotal role in cell migration, modulating also biophysical properties, such as membrane–cortex linkage, cytoskeletal and nuclear organization, and the mechanical properties of cells.

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Lechler, Terry, and Rong Li. "In Vitro Reconstitution of Cortical Actin Assembly Sites in Budding Yeast." Journal of Cell Biology 138, no. 1 (July 14, 1997): 95–103. http://dx.doi.org/10.1083/jcb.138.1.95.

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We have developed a biochemical approach for identifying the components of cortical actin assembly sites in polarized yeast cells, based on a permeabilized cell assay that we established for actin assembly in vitro. Previous analysis indicated that an activity associated with the cell cortex promotes actin polymerization in the bud. After inactivation by a chemical treatment, this activity can be reconstituted back to the permeabilized cells from a cytoplasmic extract. Fractionation of the extract revealed that the reconstitution depends on two sequentially acting protein factors. Bee1, a cortical actin cytoskeletal protein with sequence homology to Wiskott-Aldrich syndrome protein, is required for the first step of the reconstitution. This finding, together with the severe defects in actin organization associated with the bee1 null mutation, indicates that Bee1 protein plays a direct role in controlling actin polymerization at the cell cortex. The factor that acts in the second step of the reconstitution has been identified by conventional chromatography. It is composed of a novel protein, Pca1. Sequence analysis suggests that Pca1 has the potential to interact with SH3 domain-containing proteins and phospholipids.

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Payne, Helen E., and Harriet A. Allen. "Active Ignoring in Early Visual Cortex." Journal of Cognitive Neuroscience 23, no. 8 (August 2011): 2046–58. http://dx.doi.org/10.1162/jocn.2010.21562.

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Selective attention is critical for controlling the input to mental processes. Attentional mechanisms act not only to select relevant stimuli but also to exclude irrelevant stimuli. There is evidence that we can actively ignore irrelevant information. We measured neural activity relating to successfully ignoring distracters (using preview search) and found increases in both the precuneus and primary visual cortex during preparation to ignore distracters. We also found reductions in activity in fronto-parietal regions while previewing distracters and a reduction in activity in early visual cortex during search when a subset of items was successfully excluded from search, both associated with precuneus activity. These results are consistent with the proposal that actively excluding distractions has two components: an initial stage where distracters are encoded, and a subsequent stage where further processing of these items is inhibited. Our findings suggest that it is the precuneus that controls this process and can modulate activity in visual cortex as early as V1.

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Payne, H., and H. Allen. "Active ignoring in early visual cortex." Journal of Vision 9, no. 8 (September 3, 2010): 88. http://dx.doi.org/10.1167/9.8.88.

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Shi, Yu, Christopher L. Porter, John C. Crocker, and Daniel H. Reich. "Dissecting fat-tailed fluctuations in the cytoskeleton with active micropost arrays." Proceedings of the National Academy of Sciences 116, no. 28 (June 25, 2019): 13839–46. http://dx.doi.org/10.1073/pnas.1900963116.

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The ability of animal cells to crawl, change their shape, and respond to applied force is due to their cytoskeleton: A dynamic, cross-linked network of actin protein filaments and myosin motors. How these building blocks assemble to give rise to cells’ mechanics and behavior remains poorly understood. Using active micropost array detectors containing magnetic actuators, we have characterized the mechanics and fluctuations of cells’ actomyosin cortex and stress fiber network in detail. Here, we find that both structures display remarkably consistent power law viscoelastic behavior along with highly intermittent fluctuations with fat-tailed distributions of amplitudes. Notably, this motion in the cortex is dominated by occasional large, step-like displacement events, with a spatial extent of several micrometers. Overall, our findings for the cortex appear contrary to the predictions of a recent active gel model, while suggesting that different actomyosin contractile units act in a highly collective and cooperative manner. We hypothesize that cells’ actomyosin components robustly self-organize into marginally stable, plastic networks that give cells’ their unique biomechanical properties.

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Chatonnet, Fabrice, Frédéric Picou, Teddy Fauquier, and Frédéric Flamant. "Thyroid Hormone Action in Cerebellum and Cerebral Cortex Development." Journal of Thyroid Research 2011 (2011): 1–8. http://dx.doi.org/10.4061/2011/145762.

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Thyroid hormones (TH, including the prohormone thyroxine (T4) and its active deiodinated derivative 3,,5-triiodo-L-thyronine (T3)) are important regulators of vertebrates neurodevelopment. Specific transporters and deiodinases are required to ensure T3 access to the developing brain. T3 activates a number of differentiation processes in neuronal and glial cell types by binding to nuclear receptors, acting directly on transcription. Only few T3 target genes are currently known. Deeper investigations are urgently needed, considering that some chemicals present in food are believed to interfere with T3 signaling with putative neurotoxic consequences.

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Chugh, Priyamvada, and Ewa K. Paluch. "The actin cortex at a glance." Journal of Cell Science 131, no. 14 (July 15, 2018): jcs186254. http://dx.doi.org/10.1242/jcs.186254.

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Salbreux, Guillaume, Guillaume Charras, and Ewa Paluch. "Actin cortex mechanics and cellular morphogenesis." Trends in Cell Biology 22, no. 10 (October 2012): 536–45. http://dx.doi.org/10.1016/j.tcb.2012.07.001.

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HARASZTI, TAMÁS, SIMON SCHULZ, KAI UHRIG, RAINER KURRE, WOUTER ROOS, CHRISTIAN H. J. SCHMITZ, JENNIFER E. CURTIS, TIMO MAIER, ANABEL E. M. CLEMEN, and JOACHIM P. SPATZ. "BIOMIMETIC MODELS OF THE ACTIN CORTEX." Biophysical Reviews and Letters 04, no. 01n02 (April 2009): 17–32. http://dx.doi.org/10.1142/s1793048009001009.

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The cytoskeleton is an actively regulated complex network in the cell. One of the most researched components is actin. In our work we developed and tested two microfluidic systems both being applicable to construct quasi 2-dimensional biomimetic actin networks. The first system uses polydimethylsiloxane micropillars, the other polystyrene microparticles held by holographic optical tweezers as anchoring points. Our devices provide actin networks with mesh sizes from a few micrometers up to the order of 10 micrometers. Qualitative analysis shows similar network formation in both systems. Crosslinking was tested using filamin, α-actinin, Ca and Mg ions. The crosslinking process is characterized by a zipping like event, which is limited only by the high stretching modulus of the actin filaments.

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Fritzsche, Marco, Christoph Erlenkämper, Guillaume T. Charras, Karsten Kruse, and Christian Eggeling. "Homeostasis of the Cellular Actin Cortex." Biophysical Journal 106, no. 2 (January 2014): 735a. http://dx.doi.org/10.1016/j.bpj.2013.11.4051.

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Santos, Alicia, Eugenia Resmini, Iris Crespo, Patricia Pires, Yolanda Vives-Gilabert, Esther Granell, Elena Valassi, et al. "Small cerebellar cortex volume in patients with active Cushing's syndrome." European Journal of Endocrinology 171, no. 4 (October 2014): 461–69. http://dx.doi.org/10.1530/eje-14-0371.

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ObjectiveCushing's syndrome (CS) is associated with neuropsychological deficits. As the cerebellum plays a key role in neuropsychological functions it may be affected in CS. The aim of this study was to investigate whether patients with CS have a smaller cerebellar volume than healthy controls, and to analyse whether cerebellar volume is associated with neuropsychological performance and clinical parameters.DesignA cross-sectional study was performed.MethodsThirty-six CS patients (15 with active CS and 21 with CS in remission) and 36 controls matched for age, sex, and education underwent neuropsychological testing, quality of life assessment, clinical evaluation, and magnetic resonance imaging brain scan. Cerebellar volumes (white matter and cortex, bilateral) were calculated using FreeSurfer Software.ResultsPatients with active CS showed smaller bilateral cerebellar cortex volumes than controls (left,P=0.035 and right,P=0.034), as well as a trend toward smaller right cerebellar cortex volumes than patients in remission CS (P=0.051). No differences were observed in the volume of cerebellar white matter between the three groups. Both right and left cerebellar cortex volumes correlated negatively with triglyceride levels (right:r=−0.358,P=0.002 and left:r=−0.317,P=0.005) and age at diagnosis (right:r=−0.433,P=0.008 and left:r=−0.457,P=0.005). Left cerebellar cortex volume also correlated positively with visual memory performance (r=0.245,P=0.038). Right cerebellar cortex volume positively correlated with quality-of-life scores (r=0.468,P=0.004).ConclusionsThe cerebellar cortex volume is smaller in active CS patients than in controls. This finding is associated with poor visual memory and quality of life and is mostly pronounced in patients with higher triglyceride levels and older age at diagnosis.

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Middelkoop, Teije C., Júlia Garcia-Baucells, Porfirio Quintero-Cadena, Lokesh G. Pimpale, Shahrzad Yazdi, Paul W. Sternberg, Peter Gross, and Stephan W. Grill. "CYK-1/Formin activation in cortical RhoA signaling centers promotes organismal left–right symmetry breaking." Proceedings of the National Academy of Sciences 118, no. 20 (May 10, 2021): e2021814118. http://dx.doi.org/10.1073/pnas.2021814118.

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Proper left–right symmetry breaking is essential for animal development, and in many cases, this process is actomyosin-dependent. In Caenorhabditis elegans embryos active torque generation in the actomyosin layer promotes left–right symmetry breaking by driving chiral counterrotating cortical flows. While both Formins and Myosins have been implicated in left–right symmetry breaking and both can rotate actin filaments in vitro, it remains unclear whether active torques in the actomyosin cortex are generated by Formins, Myosins, or both. We combined the strength of C. elegans genetics with quantitative imaging and thin film, chiral active fluid theory to show that, while Non-Muscle Myosin II activity drives cortical actomyosin flows, it is permissive for chiral counterrotation and dispensable for chiral symmetry breaking of cortical flows. Instead, we find that CYK-1/Formin activation in RhoA foci is instructive for chiral counterrotation and promotes in-plane, active torque generation in the actomyosin cortex. Notably, we observe that artificially generated large active RhoA patches undergo rotations with consistent handedness in a CYK-1/Formin–dependent manner. Altogether, we conclude that CYK-1/Formin–dependent active torque generation facilitates chiral symmetry breaking of actomyosin flows and drives organismal left–right symmetry breaking in the nematode worm.

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Parr, Thomas, Rajeev Vijay Rikhye, Michael M. Halassa, and Karl J. Friston. "Prefrontal Computation as Active Inference." Cerebral Cortex 30, no. 2 (July 10, 2019): 682–95. http://dx.doi.org/10.1093/cercor/bhz118.

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Abstract The prefrontal cortex is vital for a range of cognitive processes, including working memory, attention, and decision-making. Notably, its absence impairs the performance of tasks requiring the maintenance of information through a delay period. In this paper, we formulate a rodent task—which requires maintenance of delay-period activity—as a Markov decision process and treat optimal task performance as an (active) inference problem. We simulate the behavior of a Bayes optimal mouse presented with 1 of 2 cues that instructs the selection of concurrent visual and auditory targets on a trial-by-trial basis. Formulating inference as message passing, we reproduce features of neuronal coupling within and between prefrontal regions engaged by this task. We focus on the micro-circuitry that underwrites delay-period activity and relate it to functional specialization within the prefrontal cortex in primates. Finally, we simulate the electrophysiological correlates of inference and demonstrate the consequences of lesions to each part of our in silico prefrontal cortex. In brief, this formulation suggests that recurrent excitatory connections—which support persistent neuronal activity—encode beliefs about transition probabilities over time. We argue that attentional modulation can be understood as the contextualization of sensory input by these persistent beliefs.

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Daou, Pascale, Salma Hasan, Dennis Breitsprecher, Emilie Baudelet, Luc Camoin, Stéphane Audebert, Bruce L. Goode, and Ali Badache. "Essential and nonredundant roles for Diaphanous formins in cortical microtubule capture and directed cell migration." Molecular Biology of the Cell 25, no. 5 (March 2014): 658–68. http://dx.doi.org/10.1091/mbc.e13-08-0482.

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Formins constitute a large family of proteins that regulate the dynamics and organization of both the actin and microtubule cytoskeletons. Previously we showed that the formin mDia1 helps tether microtubules at the cell cortex, acting downstream of the ErbB2 receptor tyrosine kinase. Here we further study the contributions of mDia1 and its two most closely related formins, mDia2 and mDia3, to cortical microtubule capture and ErbB2-dependent breast carcinoma cell migration. We find that depletion of each of these three formins strongly disrupts chemotaxis without significantly affecting actin-based structures. Further, all three formins are required for formation of cortical microtubules in a nonredundant manner, and formin proteins defective in actin polymerization remain active for microtubule capture. Using affinity purification and mass spectrometry analysis, we identify differential binding partners of the formin-homology domain 2 (FH2) of mDia1, mDia2, and mDia3, which may explain their nonredundant roles in microtubule capture. The FH2 domain of mDia1 specifically interacts with Rab6-interacting protein 2 (Rab6IP2). Further, mDia1 is required for cortical localization of Rab6IP2, and concomitant depletion of Rab6IP2 and IQGAP1 severely disrupts cortical capture of microtubules, demonstrating the coinvolvement of mDia1, IQGAP1, and Rab6IP2 in microtubule tethering at the leading edge.

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Merriam, Elisha P., and Carol L. Colby. "Active Vision in Parietal and Extrastriate Cortex." Neuroscientist 11, no. 5 (October 2005): 484–93. http://dx.doi.org/10.1177/1073858405276871.

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Wang, Zhen-Bo, Zong-Zhe Jiang, Qing-Hua Zhang, Meng-Wen Hu, Lin Huang, Xiang-Hong Ou, Lei Guo, et al. "Specific deletion of Cdc42 does not affect meiotic spindle organization/migration and homologous chromosome segregation but disrupts polarity establishment and cytokinesis in mouse oocytes." Molecular Biology of the Cell 24, no. 24 (December 15, 2013): 3832–41. http://dx.doi.org/10.1091/mbc.e13-03-0123.

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Mammalian oocyte maturation is distinguished by highly asymmetric meiotic divisions during which a haploid female gamete is produced and almost all the cytoplasm is maintained in the egg for embryo development. Actin-dependent meiosis I spindle positioning to the cortex induces the formation of a polarized actin cap and oocyte polarity, and it determines asymmetric divisions resulting in two polar bodies. Here we investigate the functions of Cdc42 in oocyte meiotic maturation by oocyte-specific deletion of Cdc42 through Cre-loxP conditional knockout technology. We find that Cdc42 deletion causes female infertility in mice. Cdc42 deletion has little effect on meiotic spindle organization and migration to the cortex but inhibits polar body emission, although homologous chromosome segregation occurs. The failure of cytokinesis is due to the loss of polarized Arp2/3 accumulation and actin cap formation; thus the defective contract ring. In addition, we correlate active Cdc42 dynamics with its function during polar body emission and find a relationship between Cdc42 and polarity, as well as polar body emission, in mouse oocytes.

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Taneja, Nilay, Sophie M. Baillargeon, and Dylan T. Burnette. "Myosin light chain kinase-driven myosin II turnover regulates actin cortex contractility during mitosis." Molecular Biology of the Cell 32, no. 20 (October 1, 2021): br3. http://dx.doi.org/10.1091/mbc.e20-09-0608.

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Svitkina, Tatyana M. "Actin Cell Cortex: Structure and Molecular Organization." Trends in Cell Biology 30, no. 7 (July 2020): 556–65. http://dx.doi.org/10.1016/j.tcb.2020.03.005.

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Clark, Andrew G., Kai Dierkes, and Ewa K. Paluch. "Monitoring Actin Cortex Thickness in Live Cells." Biophysical Journal 105, no. 3 (August 2013): 570–80. http://dx.doi.org/10.1016/j.bpj.2013.05.057.

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Chugh, Priyamvada, Andrew G. Clark, Matthew B. Smith, Davide A. D. Cassani, Kai Dierkes, Anan Ragab, Philippe P. Roux, Guillaume Charras, Guillaume Salbreux, and Ewa K. Paluch. "Actin cortex architecture regulates cell surface tension." Nature Cell Biology 19, no. 6 (May 22, 2017): 689–97. http://dx.doi.org/10.1038/ncb3525.

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Tada, Hirobumi, Tomoyuki Miyazaki, Kiwamu Takemoto, Kenkichi Takase, Susumu Jitsuki, Waki Nakajima, Mayu Koide, et al. "Neonatal isolation augments social dominance by altering actin dynamics in the medial prefrontal cortex." Proceedings of the National Academy of Sciences 113, no. 45 (October 25, 2016): E7097—E7105. http://dx.doi.org/10.1073/pnas.1606351113.

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Social separation early in life can lead to the development of impaired interpersonal relationships and profound social disorders. However, the underlying cellular and molecular mechanisms involved are largely unknown. Here, we found that isolation of neonatal rats induced glucocorticoid-dependent social dominance over nonisolated control rats in juveniles from the same litter. Furthermore, neonatal isolation inactivated the actin-depolymerizing factor (ADF)/cofilin in the juvenile medial prefrontal cortex (mPFC). Isolation-induced inactivation of ADF/cofilin increased stable actin fractions at dendritic spines in the juvenile mPFC, decreasing glutamate synaptic AMPA receptors. Expression of constitutively active ADF/cofilin in the mPFC rescued the effect of isolation on social dominance. Thus, neonatal isolation affects spines in the mPFC by reducing actin dynamics, leading to altered social behavior later in life.

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Carvalho, Kevin, Joël Lemière, Fahima Faqir, John Manzi, Laurent Blanchoin, Julie Plastino, Timo Betz, and Cécile Sykes. "Actin polymerization or myosin contraction: two ways to build up cortical tension for symmetry breaking." Philosophical Transactions of the Royal Society B: Biological Sciences 368, no. 1629 (November 5, 2013): 20130005. http://dx.doi.org/10.1098/rstb.2013.0005.

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Cells use complex biochemical pathways to drive shape changes for polarization and movement. One of these pathways is the self-assembly of actin filaments and myosin motors that together produce the forces and tensions that drive cell shape changes. Whereas the role of actin and myosin motors in cell polarization is clear, the exact mechanism of how the cortex, a thin shell of actin that is underneath the plasma membrane, can drive cell shape changes is still an open question. Here, we address this issue using biomimetic systems: the actin cortex is reconstituted on liposome membranes, in an ‘outside geometry’. The actin shell is either grown from an activator of actin polymerization immobilized at the membrane by a biotin–streptavidin link, or built by simple adsorption of biotinylated actin filaments to the membrane, in the presence or absence of myosin motors. We show that tension in the actin network can be induced either by active actin polymerization on the membrane via the Arp2/3 complex or by myosin II filament pulling activity. Symmetry breaking and spontaneous polarization occur above a critical tension that opens up a crack in the actin shell. We show that this critical tension is reached by growing branched networks, nucleated by the Arp2/3 complex, in a concentration window of capping protein that limits actin filament growth and by a sufficient number of motors that pull on actin filaments. Our study provides the groundwork to understanding the physical mechanisms at work during polarization prior to cell shape modifications.

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Paluch, Ewa, Jasper van der Gucht, and Cécile Sykes. "Cracking up: symmetry breaking in cellular systems." Journal of Cell Biology 175, no. 5 (December 4, 2006): 687–92. http://dx.doi.org/10.1083/jcb.200607159.

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The shape of animal cells is, to a large extent, determined by the cortical actin network that underlies the cell membrane. Because of the presence of myosin motors, the actin cortex is under tension, and local relaxation of this tension can result in cortical flows that lead to deformation and polarization of the cell. Cortex relaxation is often regulated by polarizing signals, but the cortex can also rupture and relax spontaneously. A similar tension-induced polarization is observed in actin gels growing around beads, and we propose that a common mechanism governs actin gel rupture in both systems.

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Small, Lawrence E., and Adriana T. Dawes. "PAR proteins regulate maintenance-phase myosin dynamics duringCaenorhabditis eleganszygote polarization." Molecular Biology of the Cell 28, no. 16 (August 2017): 2220–31. http://dx.doi.org/10.1091/mbc.e16-04-0263.

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Establishment of anterior–posterior polarity in the Caenorhabditis elegans zygote requires two different processes: mechanical activity of the actin–myosin cortex and biochemical activity of partitioning-defective (PAR) proteins. Here we analyze how PARs regulate the behavior of the cortical motor protein nonmuscle myosin (NMY-2) to complement recent efforts that investigate how PARs regulate the Rho GTPase CDC-42, which in turn regulates the actin-myosin cortex. We find that PAR-3 and PAR-6 concentrate CDC-42–dependent NMY-2 in the anterior cortex, whereas PAR-2 inhibits CDC-42–dependent NMY-2 in the posterior domain by inhibiting PAR-3 and PAR-6. In addition, we find that PAR-1 and PAR-3 are necessary for inhibiting movement of NMY-2 across the cortex. PAR-1 protects NMY-2 from being moved across the cortex by forces likely originating in the cytoplasm. Meanwhile, PAR-3 stabilizes NMY-2 against PAR-2 and PAR-6 dynamics on the cortex. We find that PAR signaling fulfills two roles: localizing NMY-2 to the anterior cortex and preventing displacement of the polarized cortical actin–myosin network.

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Mackintosh, F. C. "Theoretical Models of Viscoelasticity of Actin Solutions and the Actin Cortex." Biological Bulletin 194, no. 3 (June 1998): 351–53. http://dx.doi.org/10.2307/1543110.

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Fritzsche, Marco, Alexandre Lewalle, Tom Duke, Karsten Kruse, and Guillaume Charras. "Analysis of turnover dynamics of the submembranous actin cortex." Molecular Biology of the Cell 24, no. 6 (March 15, 2013): 757–67. http://dx.doi.org/10.1091/mbc.e12-06-0485.

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The cell cortex is a thin network of actin, myosin motors, and associated proteins that underlies the plasma membrane in most eukaryotic cells. It enables cells to resist extracellular stresses, perform mechanical work, and change shape. Cortical structural and mechanical properties depend strongly on the relative turnover rates of its constituents, but quantitative data on these rates remain elusive. Using photobleaching experiments, we analyzed the dynamics of three classes of proteins within the cortex of living cells: a scaffold protein (actin), a cross-linker (α-actinin), and a motor (myosin). We found that two filament subpopulations with very different turnover rates composed the actin cortex: one with fast turnover dynamics and polymerization resulting from addition of monomers to free barbed ends, and one with slow turnover dynamics with polymerization resulting from formin-mediated filament growth. Our data suggest that filaments in the second subpopulation are on average longer than those in the first and that cofilin-mediated severing of formin-capped filaments contributes to replenishing the filament subpopulation with free barbed ends. Furthermore, α-actinin and myosin minifilaments turned over significantly faster than F-actin. Surprisingly, only one-fourth of α-actinin dimers were bound to two actin filaments. Taken together, our results provide a quantitative characterization of essential mechanisms underlying actin cortex homeostasis.

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Stecker, G. Christopher. "Auditory cortex: Representing sound locations during active sensing." Current Biology 31, no. 17 (September 2021): R1042—R1044. http://dx.doi.org/10.1016/j.cub.2021.07.007.

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Bohec, P., J. Tailleur, F. van Wijland, A. Richert, and F. Gallet. "Distribution of active forces in the cell cortex." Soft Matter 15, no. 35 (2019): 6952–66. http://dx.doi.org/10.1039/c9sm00441f.

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We study the out-of-equilibrium distribution of stochastic forces generated by molecular motors activity, exerted on a probe attached to the actin cortex of premuscular cells, as a function of ligand density, temperature and biological inhibitors.

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Davatzikos, C. A., and J. L. Prince. "An active contour model for mapping the cortex." IEEE Transactions on Medical Imaging 14, no. 1 (March 1995): 65–80. http://dx.doi.org/10.1109/42.370403.

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WALTON, M. E., P. H. RUDEBECK, D. M. BANNERMAN, and M. F. S. RUSHWORTH. "Calculating the Cost of Acting in Frontal Cortex." Annals of the New York Academy of Sciences 1104, no. 1 (April 13, 2007): 340–56. http://dx.doi.org/10.1196/annals.1390.009.

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Fischer-Friedrich, Elisabeth, Yusuke Toyoda, Cedric J. Cattin, Daniel J. Müller, Anthony A. Hyman, and Frank Jülicher. "Rheology of the Active Cell Cortex in Mitosis." Biophysical Journal 111, no. 3 (August 2016): 589–600. http://dx.doi.org/10.1016/j.bpj.2016.06.008.

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Hui, Justin, Viktor Stjepić, Mitsutoshi Nakamura, and Susan M. Parkhurst. "Wrangling Actin Assemblies: Actin Ring Dynamics during Cell Wound Repair." Cells 11, no. 18 (September 6, 2022): 2777. http://dx.doi.org/10.3390/cells11182777.

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To cope with continuous physiological and environmental stresses, cells of all sizes require an effective wound repair process to seal breaches to their cortex. Once a wound is recognized, the cell must rapidly plug the injury site, reorganize the cytoskeleton and the membrane to pull the wound closed, and finally remodel the cortex to return to homeostasis. Complementary studies using various model organisms have demonstrated the importance and complexity behind the formation and translocation of an actin ring at the wound periphery during the repair process. Proteins such as actin nucleators, actin bundling factors, actin-plasma membrane anchors, and disassembly factors are needed to regulate actin ring dynamics spatially and temporally. Notably, Rho family GTPases have been implicated throughout the repair process, whereas other proteins are required during specific phases. Interestingly, although different models share a similar set of recruited proteins, the way in which they use them to pull the wound closed can differ. Here, we describe what is currently known about the formation, translocation, and remodeling of the actin ring during the cell wound repair process in model organisms, as well as the overall impact of cell wound repair on daily events and its importance to our understanding of certain diseases and the development of therapeutic delivery modalities.

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Praddaude, Françoise, Tuan Tran-Van, and Jean-Louis Ader. "Renal kallikrein activity in rats developing spontaneous hypertension." Clinical Science 76, no. 3 (March 1, 1989): 311–15. http://dx.doi.org/10.1042/cs0760311.

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1. Spontaneously hypertensive rats (SHR) excrete less kallikrein in urine than Wistar–Kyoto rats (WKY) during the developmental phase of hypertension. The present study was designed to examine whether the urinary defect is related to abnormalities in the renal kallikrein content in this hypertensive model. 2. Active and total kallikrein were measured (amidolytic assay) in the renal cortex of newborn and 4-, 8- and 12-week-old SHR and age-matched WKY. Active and total kallikrein were also measured in urine at the same ages, except at birth. 3. Tissue active kallikrein was significantly lower in SHR at birth, representing on average 53% of the values in WKY expressed as content per total cortex weight. Tissue total kallikrein did not differ between newborn SHR and WKY. 4. SHR at 4, 8 and 12 weeks of age had lower urinary active and total kallikrein excretion. Tissue active kallikrein, but not total kallikrein, was higher than in age-matched WKY per g of cortex weight or per mg of protein, whereas both tissue active and total kallikrein were lower in SHR when expressed as content per total cortex weight. At these three ages, active kallikrein represented, on average 86%, while total kallikrein represented 77%, of the values in age-matched WKY. 5. Our results indicate a defect in prokallikrein activation rather than in kallikrein synthesis in the renal cortex of SHR at birth. The reduction in urinary kallikrein excretion during the developmental phase of hypertension in young SHR is similar to the reduction observed in the renal tissue.

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Doreian, Bryan W., Tiberiu G. Fulop, Robert L. Meklemburg, and Corey B. Smith. "Cortical F-Actin, the Exocytic Mode, and Neuropeptide Release in Mouse Chromaffin Cells Is Regulated by Myristoylated Alanine-rich C-Kinase Substrate and Myosin II." Molecular Biology of the Cell 20, no. 13 (July 2009): 3142–54. http://dx.doi.org/10.1091/mbc.e09-03-0197.

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Adrenal medullary chromaffin cells are innervated by the sympathetic splanchnic nerve and translate graded sympathetic firing into a differential hormonal exocytosis. Basal sympathetic firing elicits a transient kiss-and-run mode of exocytosis and modest catecholamine release, whereas elevated firing under the sympathetic stress response results in full granule collapse to release catecholamine and peptide transmitters into the circulation. Previous studies have shown that rearrangement of the cell actin cortex regulates the mode of exocytosis. An intact cortex favors kiss-and-run exocytosis, whereas disrupting the cortex favors the full granule collapse mode. Here, we investigate the specific roles of two actin-associated proteins, myosin II and myristoylated alanine-rich C-kinase substrate (MARCKS) in this process. Our data demonstrate that MARCKS phosphorylation under elevated cell firing is required for cortical actin disruption but is not sufficient to elicit peptide transmitter exocytosis. Our data also demonstrate that myosin II is phospho-activated under high stimulation conditions. Inhibiting myosin II activity prevented disruption of the actin cortex, full granule collapse, and peptide transmitter release. These results suggest that phosphorylation of both MARCKS and myosin II lead to disruption of the actin cortex. However, myosin II, but not MARCKS, is required for the activity-dependent exocytosis of the peptide transmitters.

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Vaillancourt, David E., Mary A. Mayka, and Daniel M. Corcos. "Intermittent Visuomotor Processing in the Human Cerebellum, Parietal Cortex, and Premotor Cortex." Journal of Neurophysiology 95, no. 2 (February 2006): 922–31. http://dx.doi.org/10.1152/jn.00718.2005.

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The cerebellum, parietal cortex, and premotor cortex are integral to visuomotor processing. The parameters of visual information that modulate their role in visuomotor control are less clear. From motor psychophysics, the relation between the frequency of visual feedback and force variability has been identified as nonlinear. Thus we hypothesized that visual feedback frequency will differentially modulate the neural activation in the cerebellum, parietal cortex, and premotor cortex related to visuomotor processing. We used functional magnetic resonance imaging at 3 Tesla to examine visually guided grip force control under frequent and infrequent visual feedback conditions. Control conditions with intermittent visual feedback alone and a control force condition without visual feedback were examined. As expected, force variability was reduced in the frequent compared with the infrequent condition. Three novel findings were identified. First, infrequent (0.4 Hz) visual feedback did not result in visuomotor activation in lateral cerebellum (lobule VI/Crus I), whereas frequent (25 Hz) intermittent visual feedback did. This is in contrast to the anterior intermediate cerebellum (lobule V/VI), which was consistently active across all force conditions compared with rest. Second, confirming previous observations, the parietal and premotor cortices were active during grip force with frequent visual feedback. The novel finding was that the parietal and premotor cortex were also active during grip force with infrequent visual feedback. Third, right inferior parietal lobule, dorsal premotor cortex, and ventral premotor cortex had greater activation in the frequent compared with the infrequent grip force condition. These findings demonstrate that the frequency of visual information reduces motor error and differentially modulates the neural activation related to visuomotor processing in the cerebellum, parietal cortex, and premotor cortex.

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Roeder, Amy D., and David L. Gard. "Confocal microscopy of F-actin distribution in Xenopus oocytes." Zygote 2, no. 2 (May 1994): 111–24. http://dx.doi.org/10.1017/s0967199400001866.

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SummaryWe have used rhodamine-conjugated phalloidin and confocal microscopy to examine the organisation of filamentous actin (F-actin) during oogenesis in Xenopus laevis. F-actin was restricted to a thin shell in the cortex of oogonia and post-mitotic oocytes less than 35 μm in diameter. In oocytes with diameters of 35–50 μm F-actin was observed in three cellular domains: in the cortex, in the germinal vesicle (GV) and in a network of cytoplasmic cables. Initially, actin cables were sparsely distributed in the cytoplasm, with no evidence of discrete organising centres. In larger stage I oocytes, a dense network of actin cables extended throughout the cytoplasm, linking the GV and mitochondrial mass to the cortical actin shell. Apart from the F-actin associated with the mitochondrial mass, no evidence of a polarised distribution of F-actin was apparent in stage I oocytes. F-actin was observed also in the cortex and the GV of stage VI oocytes, and a network of cytoplasmic cables surrounded the GV. Cytoplasmic actin cables extended from the GV to the animal cortex, and formed a three-dimensional network surrounding clusters of yolk platelets in the vegetal cytoplasm. Finally, disruption of F-actin in stage VI oocytes with cytochalasin resulted in distortion and apparent rotation of the GV in the animal hemisphere, suggesting that actin plays a role in maintaining the polarised organisation of amphibian oocytes.

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Bezdudnaya, Tatiana, and Manuel A. Castro-Alamancos. "Superior colliculus cells sensitive to active touch and texture during whisking." Journal of Neurophysiology 106, no. 1 (July 2011): 332–46. http://dx.doi.org/10.1152/jn.00072.2011.

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Rats sense the environment through rhythmic vibrissa protractions, called active whisking, which can be simulated in anesthetized rats by electrically stimulating the facial motor nerve. Using this method, we investigated barrel cortex field potential and superior colliculus single-unit responses during passive touch, whisking movement, active touch, and texture discrimination. Similar to passive touch, whisking movement is signaled during the onset of the whisker protraction by short-latency responses in barrel cortex that drive corticotectal responses in superior colliculus, and all these responses show robust adaptation with increases in whisking frequency. Active touch and texture are signaled by longer latency responses, first in superior colliculus during the rising phase of the protraction, likely driven by trigeminotectal inputs, and later in barrel cortex by the falling phase of the protraction. Thus, superior colliculus is part of a broader vibrissa neural network that can decode whisking movement, active touch, and texture.

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Journal articles on the topic 'Cortex actine'

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