Microtubule remodeling mediates the inhibition of store-operated calcium entry (SOCE) during mitosis in COS-7 cells

Russa, Afadhali Denis; Ishikita, Naoyuki; Masu, Kazuki; Akutsu, Hitomi; Saino, Tomoyuki; Satoh, Yuichi

doi:10.1679/aohc.71.249

Cited by 18 publications

(19 citation statements)

References 51 publications

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“…More recent studies confirmed that SOCE is inactivated during mitosis in HeLa, RBL-2H3, HEK293 and Cos-7 cells (Russa et al, 2008;Smyth et al, 2009;Tani et al, 2007). Investigating SOCE levels throughout the cell cycle showed that there is a slight enhancement of SOCE during the G1 and S phases, and dramatic downregulation during M phase (Tani et al, 2007).…”

Section: Soce Inactivates During Mitosismentioning

confidence: 87%

Section: Soce Inactivates During Mitosismentioning

confidence: 99%

“…The incentive to investigate Ca 2+ dynamics during mitosis was to determine whether changes in intracellular signaling might underlie the observed inhibition of vesicular trafficking during cell division (Volpi and Berlin, 1988). In an interesting twist of events, recent data indicate that vesicular trafficking is involved in inhibiting SOCE during M phase, as discussed in more detail below (Yu et al, 2009).More recent studies confirmed that SOCE is inactivated during mitosis in HeLa, RBL-2H3, HEK293 and Cos-7 cells (Russa et al, 2008;Smyth et al, 2009;Tani et al, 2007). Investigating SOCE levels throughout the cell cycle showed that there is a slight enhancement of SOCE during the G1 and S phases, and dramatic downregulation during M phase (Tani et al, 2007).…”

mentioning

confidence: 99%

“…Investigating SOCE levels throughout the cell cycle showed that there is a slight enhancement of SOCE during the G1 and S phases, and dramatic downregulation during M phase (Tani et al, 2007). It has also been argued that SOCE inhibition during mitosis in Cos-7 cells is the result of the microtubule-network remodeling that accompanies mitosis (Russa et al, 2008).What is the physiological significance of SOCE inactivation during mitosis? The most likely answer to this question is that tight regulation of Ca 2+ signaling is required during mitosis because of its important functional role at multiple steps throughout the process.…”

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confidence: 99%

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Regulation of store-operated Ca2+ entry during the cell cycle

Arredouani

Sun

et al. 2010

Journal of Cell Science

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Summary Cytoplasmic Ca2+ signals are central to numerous cell physiological processes, including cellular proliferation. Historically, much of the research effort in this area has focused on the role of Ca 2+ signals in cell-cycle progression. It is becoming clear, however, that the relationship between Ca 2+ signaling and the cell cycle is a 'two-way street'. Specifically, Ca 2+ -signaling pathways are remodeled during M phase, leading to altered Ca 2+ dynamics. Such remodeling probably better serves the large variety of functions that cells must perform during cell division compared with during interphase. This is clearly the case during oocyte meiosis, because remodeling of Ca 2+ signals partially defines the competence of the egg to activate at fertilization. Store-operated Ca 2+ entry (SOCE) is a ubiquitous Ca 2+ -signaling pathway that is regulated during M phase. In this Commentary, we discuss the latest advances in our understanding of how SOCE is regulated during cell division.Key words: Calcium signaling, Cell division, Store-operated Ca 2+ entry Journal of Cell Sciencesweeping Ca 2+ wave, or multiple Ca 2+ oscillations, depending on the species (Stricker, 1999). In vertebrates, the Ca 2+ transient that occurs at fertilization activates CaMKII (Lorca et al., 1993), which mediates resumption of meiosis by inactivating cytostatic factor (CSF), a protein whose activity maintains metaphase II arrest (Knott et al., 2006;Lorca et al., 1993;Morin et al., 1994;Tunquist and Maller, 2003). CaMKII phosphorylates the anaphase-promoting complex (APC) inhibitor Emi2 (Hansen et al., 2006;Liu and Maller, 2005;Rauh et al., 2005), which primes it for additional phosphorylation by polo-like kinase. The dually phosphorylated Emi2 is targeted for degradation, thereby activating APC and releasing CSF-mediated arrest. This provides an elegant example of how a Ca 2+ signal triggers a cascade of events that controls cellcycle progression -in this case, completion of meiosis II.Given the well-established role of Ca 2+ signals in cell-cycle progression, an emerging area of interest is to understand how Ca 2+ -signaling pathways themselves are regulated during the cell cycle, particularly during the cell-division phase. It is becoming evident that Ca 2+ signaling is remodeled during M phase of the cell cycle. For example, inositol (1,4,5)-trisphosphate [Ins(1,4,5)P 3 ]-dependent Ca 2+ release is sensitized during both meiosis (Fujiwara et al., 1993;Machaca, 2004) and mitosis (Malathi et al., 2003), and this sensitization depends on the cell-cycle kinase cascade (Lee et al., 2006;Lim et al., 2003;Sun et al., 2009). In addition, during the maturation of Xenopus oocytes, the number of functional Ins(1,4,5)P 3 receptors increases following their release from annulate lamellae, vesicular compartments in oocytes in which Ins(1,4,5)P 3 receptor function is suppressed (Boulware and Marchant, 2005;Boulware and Marchant, 2008). Furthermore, SOCE is inhibited both during Xenopus oocyte meiosis and during mammalian cell mitosis (Machaca and...

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Section: Soce Inactivates During Mitosismentioning

confidence: 87%

Section: Soce Inactivates During Mitosismentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Regulation of store-operated Ca2+ entry during the cell cycle

Arredouani

Sun

et al. 2010

Journal of Cell Science

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“…Similar indings were reported in COS-7 cells, where the treatment with nocodazole triggered the retraction of tubulin ilaments from cell periphery leading to the progressive loss of SOCE, similarly to what is found in mitosis. On the contrary, placlitaxel, which stabilizes microtubules, enhanced SOCE [36], supporting for a role of microtubules in the normal function of SOCE.…”

Section: Cytoskeletal Components Involved In the Control Of Socementioning

confidence: 74%

The Interplay between Cytoskeleton and Calcium Dynamics

Martı́n-Romero¹,

López-Guerrero²,

CarlosPascual-Caro³

et al. 2017

Cytoskeleton - Structure, Dynamics, Function and Disease

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Cell motility is a complex cellular event that involves reorganization of cytoskeleton. This reorganization encompasses the transient polarization of the cell to facilitate the plasma membrane ruling, a rearrangement of cortical actin cytoskeleton required for the development of cellular protrusions. It is known that extracellular Ca 2+ inlux is essential for cell migration and for the positive-feedback cycle that maintains leading-edge structures and ruling activity. The aim of this review is to summarize our knowledge regarding the Ca 2+ -dependent signaling pathways, Ca 2+ transporters and sensors involved in cell migration. Also, we show here reported evidences that support for a crosstalk between Ca 2+ transport and the reorganization of the cytoskeleton required for cell migration. In this regard, we will analyze the role of store-operated Ca 2+ entry (SOCE) as a modulator of cytoskeleton and cell migration, but also the modulation of this Ca 2+ entry pathway by microtubules and the actin cytoskeleton. As a main conclusion, this review will show that data reported in the last years support a role for SOCE in shaping cytoskeleton, but at the same time, SOCE is strongly dependent on cytoskeletal proteins, in an interesting interplay between cytoskeleton and Ca 2+ dynamics.

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Extracellular Calcium Has Multiple Targets to Control Cell Proliferation

Capiod

2016

Advances in Experimental Medicine and Biology

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Calcium channels and the two G-protein coupled receptors sensing extracellular calcium, calcium-sensing receptor (CaSR) and GPRC6a, are the two main means by which extracellular calcium can signal to cells and regulate many cellular processes including cell proliferation, migration and invasion of tumoral cells. Many intracellular signaling pathways are sensitive to cytosolic calcium rises and conversely intracellular signaling pathways can modulate calcium channel expression and activity. Calcium channels are undoubtedly involved in the former while the CaSR and GPRC6a are most likely to interfere with the latter. As for neurotransmitters, calcium ions use plasma membrane channels and GPCR to trigger cytosolic free calcium concentration rises and intracellular signaling and regulatory pathways activation. Calcium sensing GPCR, CaSR and GPRC6a, allow a supplemental degree of control and as for metabotropic receptors, they not only modulate calcium channel expression but they may also control calcium-dependent K+ channels. The multiplicity of intracellular signaling pathways involved, their sensitivity to local and global intracellular calcium increase and to CaSR and GPRC6a stimulation, the presence of membrane signalplex, all this confers the cells the plasticity they need to convert the effects of extracellular calcium into complex physiological responses and therefore determine their fate.

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Microtubule remodeling mediates the inhibition of store-operated calcium entry (SOCE) during mitosis in COS-7 cells

Cited by 18 publications

References 51 publications

Regulation of store-operated Ca2+ entry during the cell cycle

Regulation of store-operated Ca2+ entry during the cell cycle

The Interplay between Cytoskeleton and Calcium Dynamics

Extracellular Calcium Has Multiple Targets to Control Cell Proliferation

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