Spatio-temporally separated cortical flows and spindle geometry establish physical asymmetry in fly neural stem cells

Roubinet, Chantal; Tsankova, Anna; Pham, Tri; Monnard, Arnaud; Caussinus, Emmanuel; Affolter, Markus; Cabernard, Clemens

doi:10.1038/s41467-017-01391-w

Cited by 60 publications

(101 citation statements)

References 66 publications

(89 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since the wide field data were not sufficiently reliable to extract Myosin intensity, we imaged third instar neuroblasts expressing Sqh::GFP with spinning disc microscopy and correlated the resulting intensity and curvature profiles with AFM stiffness data by calculating the relative change between Myosin and curvature, and Myosin and stiffness. As reported previously (Roubinet et al, 2017), apical Myosin intensity started to decrease at anaphase onset, albeit stiffness increased again apically. In the mid and sub-basal region, both Myosin intensity and stiffness increased.…”

Section: Neuroblast Stiffness Is a Combination Of Actomyosin Contractsupporting

confidence: 87%

“…The most noticeable curvature changes became apparent in the furrow region from 120s after anaphase onset onwards ( Figure 1E,F,G). The resulting deviation coefficients revealed that Myosin intensity and curvature strongly correlate on the early (-120 -30s) apical neuroblast cortex and later in the cleavage furrow region (120s -240s); the shift in Myosin intensity from the apical cell cortex towards the furrow region -previously described as a cortical flow (Roubinet et al, 2017) was accompanied with a shift in curvature changes. Until 120s after anaphase onset, stiffness correlated best with Myosin intensity in the cleavage furrow region.…”

Section: Neuroblast Stiffness Is a Combination Of Actomyosin Contractmentioning

confidence: 88%

“…On the basal neuroblast cortex, spindle-dependent cues induce an apically directed cortical Myosin flow to flow to the cleavage furrow. The correct timing of these Myosin flowsregulated by polarity and spindle cues -is instrumental in establishing biased Myosin localization and sibling cell size asymmetry in fly neuroblasts (Roth et al, 2015;Roubinet et al, 2017;Tsankova et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Spatiotemporally controlled Myosin relocalization and internal pressure cause biased cortical extension to generate sibling cell size asymmetry

Pham

Monnard

Helenius

et al. 2018

Preprint

Self Cite

View full text Add to dashboard Cite

Metazoan cells can generate unequal sized sibling cells during cell division. This form of asymmetric cell division depends on spindle geometry andMyosin distribution but the underlying mechanics are unclear. Here, we use atomic force microscopy and live cell imaging to elucidate the biophysical forces involved in the establishment of physical asymmetry in Drosophila neural stem cells. We show that the force driving initial apical membrane expansion is provided by hydrostatic pressure, peaking shortly after anaphase onset, and enabled by a relieve of actomyosin contractile tension on the apical cell cortex. The subsequent increase in contractile forces at the cleavage furrow, combined with the relocalization of basally located Myosin results in basal membrane extension and sustained apical expansion. We propose that spatiotemporally controlled actomyosin contractile tension and hydrostatic pressure enables stereotypic biased membrane expansion to generate sibling cell size asymmetry.

show abstract

Section: Neuroblast Stiffness Is a Combination Of Actomyosin Contractsupporting

confidence: 87%

Section: Neuroblast Stiffness Is a Combination Of Actomyosin Contractmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Spatiotemporally controlled Myosin relocalization and internal pressure cause biased cortical extension to generate sibling cell size asymmetry

Pham

Monnard

Helenius

et al. 2018

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

“…The promotion of spindle asymmetry in 1:0 cells would in this case represent an excessive reaction of such a feedback system. Alternatively, in naturally asymmetric spindles (Delaunay et al, 2014;Greenan et al, 2010;Ren and Weisblat, 2006;Roubinet et al, 2017), HURP asymmetry could reinforce the spindle asymmetry by freezing the dynamics of the shorter k-fibers, and thus promote asymmetric cell divisions. This potential function of HURP was not only visible in 1:0 cells, but also in 0:0 cells ( Fig.…”

Section: Discussionmentioning

confidence: 99%

Centrosomes control kinetochore-fiber plus-end dynamics via HURP to ensure symmetric divisions

Dudka

Liaudet

Vassal

et al. 2019

Preprint

View full text Add to dashboard Cite

During mitosis centrosomes can affect the length of kinetochore-fibers (k-fibers) and the stability of kinetochore-microtubule attachments, implying that they regulate k-fiber dynamics. The exact cellular and molecular mechanisms by which centrosomes regulate kfibers remain, however, unknown. Here, we created human non-cancerous cells with only one centrosome to investigate these mechanisms. Such cells formed highly asymmetric bipolar spindles that resulted in asymmetric cell divisions. K-fibers in acentrosomal spindles were shorter, more stable, had a reduced poleward microtubule flux at minus-ends, and more frequent pausing events at their plus-ends. This indicates that centrosomes regulate k-fiber dynamics both locally at minus-ends and far away at plus-ends. At the molecular level we find that the microtubule-stabilizing protein HURP is enriched on the k-fiber plus-ends in the acentrosomal spindles of cells with only one centrosome. HURP depletion rebalance k-fiber stability and dynamics in such cells, and improved spindle and cell division symmetry. Our data further indicate that HURP accumulates on k-fibers inversely proportionally to halfspindle length. We propose that centrosomes regulate k-fiber plus-ends indirectly via lengthdependent accumulation of HURP. Thus by ensuring equal k-fiber length, centrosomes promote HURP symmetry, reinforcing the symmetry of the mitotic spindle and of cell division.

show abstract

“…Rotational flow emerges after formation of cell-cell contacts, where contact-dependent asymmetries determine cortical flow dynamics, which in turn determine spindle orientation through coupling to microtubule dynamics (Sugioka and Bowerman, 2018). These roles of cortical flow in patterning are orthologous in higher organisms, where they have been shown to drive decision making processes in development (Woolner and Papalopulu, 2012;Maitre et al, 2016;Roubinet et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Planar cell polarity in the C. elegans embryo emerges by differential retention of aPARs at cell-cell contacts

Dutta

Odedra

Pohl

2019

Preprint

View full text Add to dashboard Cite

Formation of the anteroposterior and dorsoventral body axis in the Caenorhabditis elegans embryo depends on cortical actomyosin flows and advection of polarity determinants. The role of this patterning mechanism in tissue polarization immediately after formation of cell-cell contacts is not fully understood.Here, we demonstrate that planar cell polarity (PCP) is established in the C. elegans embryo at the time of left-right (l/r) symmetry breaking. At this stage, centripetal cortical flows asymmetrically and differentially advect anterior polarity determinants (aPARs) PAR-3, PAR-6 and PKC-3 from cell-cell contacts to the medial cortex, which results in their unmixing from apical myosin. Advection generally requires GSK-3 and CDC-42, while advection of PAR-6 specifically depends on the RhoGAP PAC-1. Concurrent asymmetric retention of PAR-3, E-cadherin/HMR-1, PAC-1 and opposing retention of the antagonistic Wnt pathway components APC/APR-1 and Frizzled/MOM-5 at apical cell-cell contacts leads to planar asymmetries. The most obvious mark of PCP, asymmetric retention of PAR-3 at posterior cell-cell contacts on the left side of the embryo, is required for proper cytokinetic cell intercalation. Hence, our data uncover how PCP can be established through Wnt signaling as well as dissociation and planar asymmetric retention of aPARs mediated by distinct Rho GTPases and their regulators.

show abstract

Spatio-temporally separated cortical flows and spindle geometry establish physical asymmetry in fly neural stem cells

Cited by 60 publications

References 66 publications

Spatiotemporally controlled Myosin relocalization and internal pressure cause biased cortical extension to generate sibling cell size asymmetry

Spatiotemporally controlled Myosin relocalization and internal pressure cause biased cortical extension to generate sibling cell size asymmetry

Centrosomes control kinetochore-fiber plus-end dynamics via HURP to ensure symmetric divisions

Planar cell polarity in the C. elegans embryo emerges by differential retention of aPARs at cell-cell contacts

Contact Info

Product

Resources

About