The Role of Mitotic Cell-Substrate Adhesion Re-modeling in Animal Cell Division

Dix, Christina L.; Matthews, Helen K.; Uroz, Marina; McLaren, Susannah B. P.; Wolf, Lucie; Heatley, Nicholas; Win, Zaw; Almada, Pedro; Henriques, Ricardo; Boutros, Michael; Trepat, Xavier; Baum, Buzz

doi:10.1016/j.devcel.2018.03.009

Cited by 111 publications

(146 citation statements)

References 71 publications

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“…While almost all proliferating animal cells undergo a degree of mitotic rounding, different cell types exhibit striking differences in the extent to which they round 1,12 . In this context, we previously noted that cancer cell lines tend to round up more than many non-transformed cells 2 . There are two likely explanations for this.…”

Section: Introductionmentioning

confidence: 97%

Oncogenic signaling alters cell shape and mechanics to facilitate cell division under confinement

Matthews

Ganguli

Plak

et al. 2019

Preprint

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When cells enter mitosis, they become spherical and mechanically stiffen. We used MCF10A cell lines as a model system in which to investigate the effect of induced oncogene expression on mitotic entry. We find that activation of oncogenic Ras V12 , for as little as five hours, changes the way cells divide. Ras V12 -dependent activation of the MEK-ERK signalling cascade alters acto-myosin contractility to enhance mitotic rounding. Ras V12 also affects cell mechanics, so that Ras V12 expressing cells are softer in interphase but stiffen more upon entry into mitosis. As a consequence, Ras V12 expression augments the ability of cells to round up and divide faithfully when confined underneath a stiff hydrogel. Conversely, inhibition of the Ras-ERK pathway reduces mitotic rounding under confinement, resulting in chromosome segregation defects. These data suggest a novel mechanism by which oncogenic Ras-ERK signalling can aid division in stiff environments like those found in tumours.

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Section: Introductionmentioning

confidence: 97%

Oncogenic signaling alters cell shape and mechanics to facilitate cell division under confinement

Matthews

Ganguli

Plak

et al. 2019

Preprint

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“…This likely frees up a pool of actin monomers (Kaur et al, 2014), which is then used to assemble a thin (Clark et al, 2013), mechanically rigid (Fischer-Friedrich et al, 2015), cortical actomyosin network that drives mitotic rounding (Reinsch & Karsenti, 1994;Ragkousi & Gibson, 2014;Sorce et al, 2015). While the mechanisms underlying this mitotic switch in actin organisation are not well understood, the process likely involves the following: (i) the loss of interphase focal adhesions (Dix et al, 2018;Lock et al, 2018), (ii) the loss of Arp2/3-dependent lamellipodia (Ibarra et al, 2005;Bovellan et al, 2014;Rosa et al, 2015) and (iii) the activation of formins downstream of Ect2/Pbl and the GTPase Rho (Maddox & Burridge, 2003;Matthews et al, 2012;Rosa et al, 2015;Chugh et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

“…This leads to the de-phosphorylation of ERM proteins, which crosslink actin to the plasma membrane (Rodrigues et al, 2015), to the loss of anillin (Kiyomitsu & Cheeseman, 2013) and to activation of SCAR/WAVE and the Arp2/3 complex at opposing cell poles (Zhang & Robinson, 2005;King et al, 2010;Nezis et al, 2010;Bastos et al, 2012;Luo et al, 2014). In some instances, the process of polar relaxation and cell re-spreading is sufficient to drive division in cells that lack an actomyosin ring (Neujahr et al, 1997;Dix et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Local actin nucleation tunes centrosomal microtubule nucleation during passage through mitosis

et al. 2019

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Cells going through mitosis undergo precisely timed changes in cell shape and organisation, which serve to ensure the fair partitioning of cellular components into the two daughter cells. These structural changes are driven by changes in actin filament and microtubule dynamics and organisation. While most evidence suggests that the two cytoskeletal systems are remodelled in parallel during mitosis, recent work in interphase cells has implicated the centrosome in both microtubule and actin nucleation, suggesting the potential for regulatory crosstalk between the two systems. Here, by using both in vitro and in vivo assays to study centrosomal actin nucleation as cells pass through mitosis, we show that mitotic exit is accompanied by a burst in cytoplasmic actin filament formation that depends on WASH and the Arp2/3 complex. This leads to the accumulation of actin around centrosomes as cells enter anaphase and to a corresponding reduction in the density of centrosomal microtubules. Taken together, these data suggest that the mitotic regulation of centrosomal WASH and the Arp2/3 complex controls local actin nucleation, which may function to tune the levels of centrosomal microtubules during passage through mitosis.

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“…In ~70% of the cps1-191 spheroplasts (37 out of 53 spheroplasts) that underwent cytofission, the rings contracted till mid-phase of division and disassembled before division into two entities. We Previous studies suggested under certain circumstances, some eukaryotic cells are able to divide without an actomyosin ring (Flor-Parra et al, 2014;Proctor et al, 2012;Dix et al, 2018;Choudhary et al, 2013). To see if the cytofission was driven by contraction of the actomyosin ring, we first perturbed the functions of rings using Latrunculin-A (Lat-A) to inhibit actin polymerization (Fujiwara et al, 2018;Morton et al, 2000).…”

Section: Resultsmentioning

confidence: 98%

Inhibition of cell membrane ingression at the division site by cell wall in fission yeast

Chew

Lim

Osaki³

et al. 2020

Preprint

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Eukaryotic cells assemble an actomyosin ring during cytokinesis to function as a force-generating machine to drive membrane invagination, and to counteract the intracellular pressure and the cell surface tension. It is unclear whether additional factors such as the extracellular matrix (cell wall in yeasts and fungi) affect the actomyosin ring contraction. While studying the fission yeast β-glucan synthase mutant cps1-191, which is defective in division septum synthesis and actomyosin ring contraction, we found that significantly weakening of the extracellular glycan matrix caused the spheroplasts to divide at the non-permissive condition. This division was dependent on a functional actomyosin ring and vesicular trafficking, but independent of normal septum synthesis. cps1-191 cells with weakened extracellular glycan matrix divide non-medially with a much slower ring contraction rate compared to wild type cells under similar conditions, which we term as cytofission.Interestingly, the high turgor pressure appears to play minimal roles in inhibiting ring contraction in cps1-191 mutants as decreasing the turgor pressure alone does not enable cytofission. We propose that during cytokinesis, the extracellular glycan matrix restricts actomyosin ring contraction and membrane ingression, and remodeling of the extracellular components through division septum synthesis relieves the inhibition and facilitates actomyosin ring contraction.

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The Role of Mitotic Cell-Substrate Adhesion Re-modeling in Animal Cell Division

Cited by 111 publications

References 71 publications

Oncogenic signaling alters cell shape and mechanics to facilitate cell division under confinement

Oncogenic signaling alters cell shape and mechanics to facilitate cell division under confinement

Local actin nucleation tunes centrosomal microtubule nucleation during passage through mitosis

Inhibition of cell membrane ingression at the division site by cell wall in fission yeast

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