Initiation of multicellular differentiation in<i>Dictyostelium discoideum</i>is regulated by coronin A

Vinet, Adrien F.; Fiedler, Thomas M.; Studer, Vera; Froquet, Romain Bruno; Dardel, Anna; Cosson, Pierre; Pieters, Jean

doi:10.1091/mbc.e13-04-0219

Cited by 28 publications

(46 citation statements)

References 78 publications

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“…Coronin levels were therefore analyzed (Figure B). Coronin was already increased in control cells, probably because coronin is mandatory for initiation of cAMP pulsing upon starvation in a serum‐free medium . Nicotine does not seem to increase, but rather it decreases coronin levels.…”

Section: Resultsmentioning

confidence: 93%

“…Coronin was already increased in control cells, probably because coronin is mandatory for initiation of cAMP pulsing upon starvation in a serum-free medium. 45 Nicotine does not seem to increase, but rather it decreases coronin levels. Therefore, at least in our model, increase in cofilin activity in nicotine-stimulated cells does not seem to be linked to coronin or to ERK activity.…”

Section: Melatonin Counteracts Cofilin Phosphorylation and Reduces mentioning

confidence: 96%

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Increase in motility and invasiveness of MCF7 cancer cells induced by nicotine is abolished by melatonin through inhibition of ERK phosphorylation

Proietti

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Masiello

et al. 2018

Journal of Pineal Research

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Through activation of the ERK pathway, nicotine, in both normal MCF-10A and low-malignant breast cancer cells (MCF7), promotes increased motility and invasiveness. Melatonin antagonizes both these effects by inhibiting almost completely ERK phosphorylation. As melatonin has no effect on nonstimulated cells, it is likely that melatonin can counteract ERK activation only downstream of nicotine-induced activation. This finding suggests that melatonin hampers ERK phosphorylation presumably by targeting a still unknown intermediate factor that connects nicotine stimulation to ERK phosphorylation. Furthermore, downstream of ERK activation, melatonin significantly reduces fascin and calpain activation while restoring normal vinculin levels. Melatonin also counteracts nicotine effects by reshaping the overall cytoskeleton architecture and abolishing invasive membrane protrusion. In addition, melatonin decreases nicotine-dependent ROCK1/ROCK2 activation, thus further inhibiting cell contractility and motility. Melatonin actions are most likely attributable to ERK inhibition, although melatonin could display other ERK-independent effects, namely through a direct modulation of additional molecular and structural factors, including coronin, cofilin, and cytoskeleton components.

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Section: Resultsmentioning

confidence: 93%

Section: Melatonin Counteracts Cofilin Phosphorylation and Reduces mentioning

confidence: 96%

Increase in motility and invasiveness of MCF7 cancer cells induced by nicotine is abolished by melatonin through inhibition of ERK phosphorylation

Proietti

Catizone

Masiello

et al. 2018

Journal of Pineal Research

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“…However, very recently, the importance of coronins in signaling pathways has been revealed. The mammalian neural coronin 1 and the more primitive Dictyostelium coronin A play important, notably F‐actin‐independent roles in cAMP signaling (76, 77). Mouse coronin 6, which is the closest mammalian homologue to TgCOR, participates in the clustering of acetylcholine receptors at the postsynaptic membrane (78).…”

Section: Discussionmentioning

confidence: 99%

Structure of Toxoplasma gondii coronin, an actin‐binding protein that relocalizes to the posterior pole of invasive parasites and contributes to invasion and egress

et al. 2014

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Coronins are involved in the regulation of actin dynamics in a multifaceted way, participating in cell migration and vesicular trafficking. Apicomplexan parasites, which exhibit an actin-dependent gliding motility that is essential for traversal through tissues, as well as invasion of and egress from host cells, express only a single coronin, whereas higher eukaryotes possess several isoforms. We set out to characterize the 3-D structure, biochemical function, subcellular localization, and genetic ablation of Toxoplasma gondii coronin (TgCOR), to shed light on its biological role. A combination of X-ray crystallography, small-angle scattering of X-rays, and light scattering revealed the atomic structure of the conserved WD40 domain and the dimeric arrangement of the fulllength protein. TgCOR binds to F-actin and increases the rate and extent of actin polymerization. In vivo, TgCOR relocalizes transiently to the posterior pole of motile and invading parasites, independent of actin dynamics, but concomitant to microneme secretory organelle discharge. TgCOR contributes to, but is not essential for, invasion and egress. Taken together, our data point toward a role for TgCOR in stabilizing newly formed, short filaments and F-actin cross-linking, as well as functions linked to endocytosis and recycling of membranes.-Salamun, J., Kallio, J. P., Daher, W., Soldati-Favre, D., Kursula, I. Structure of Toxoplasma gondii coronin, an actin-binding protein that relocalizes to the posterior pole of invasive parasites and contributes to invasion and egress. FASEB J. 28, 4729 -4747 (2014). www.fasebj.orgKey Words: apicomplexan parasite ⅐ gliding motility ⅐ WD40 domain TOXOPLASMA GONDII is an obligate intracellular parasite of medical and veterinary significance that invades almost any nucleated cell from virtually all warmblooded animals. The invasive stages exhibit a substrate-dependent motility, driven by an actin-and myosin-based motor complex machinery termed the glideosome, which is critical for parasite dissemination (1). Gliding motility depends on an intact parasite actin cytoskeleton and requires actin polymerization (2). However, parasite actin filaments have been difficult to visualize in physiological conditions. Typically, apicomplexan actins appear to be maintained mainly in globular form (3). In vitro polymerization assays performed on purified T. gondii actin indicated that the actin filaments are very short (50 -100 nm; ref. 4). The instability of apicomplexan actin filaments seems to be a prerequisite for efficient gliding motility, since stabilization of actin filaments, either by the known stabilizing agent jasplakinolide (JAS; refs. 2, 5, 6) or by substituting key residues assumed to be involved in the intermolecular contacts between different protomers, disrupt the normal gliding motility of parasites (7).Actin dynamics and its regulation in the Apicomplexa differ significantly from higher eukaryotes. The rapid 1 These authors contributed equally to this work.

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“…Here, we describe an essential role for coronin 1 in allograft rejection via the modulation of the phosphodiesterase 4-CREB-CaMKIV pathway in T cells. We found that coronin 1 maintains appropriate levels of cAMP, similar to its role in regulating the cAMP-protein kinase A pathway in neurons and Dictyostelium (via its ortholog coronin A, Jayachandran et al, 2014;Vinet et al, 2014). Suppression was specific for alloresponses, since infection-mediated CD28 ligation through CD80 could overcome cAMP-mediated suppression of T cell responses.…”

Section: Introductionmentioning

confidence: 55%

Disruption of Coronin 1 Signaling in T Cells Promotes Allograft Tolerance while Maintaining Anti-Pathogen Immunity

et al. 2019

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Initiation of multicellular differentiation inDictyostelium discoideumis regulated by coronin A

Cited by 28 publications

References 78 publications

Increase in motility and invasiveness of MCF7 cancer cells induced by nicotine is abolished by melatonin through inhibition of ERK phosphorylation

Increase in motility and invasiveness of MCF7 cancer cells induced by nicotine is abolished by melatonin through inhibition of ERK phosphorylation

Structure of Toxoplasma gondii coronin, an actin‐binding protein that relocalizes to the posterior pole of invasive parasites and contributes to invasion and egress

Disruption of Coronin 1 Signaling in T Cells Promotes Allograft Tolerance while Maintaining Anti-Pathogen Immunity

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