scholarly journals MARK2/Par1b kinase present at centrosomes and retraction fibres corrects spindle off-centring induced by actin disassembly

Open Biology ◽  
2019 ◽  
Vol 9 (6) ◽  
pp. 180263 ◽  
Author(s):  
Madeleine Hart ◽  
Ihsan Zulkipli ◽  
Roshan Lal Shrestha ◽  
David Dang ◽  
Duccio Conti ◽  
...  
Keyword(s):  
Cell Division ◽  
Actin Cytoskeleton ◽  
Mitotic Spindle ◽  
Division Plane ◽  
Spatial Regulation ◽  
Molecular Components ◽  
Molecular Framework

Tissue maintenance and development requires a directed plane of cell division. While it is clear that the division plane can be determined by retraction fibres that guide spindle movements, the precise molecular components of retraction fibres that control spindle movements remain unclear. We report MARK2/Par1b kinase as a novel component of actin-rich retraction fibres. A kinase-dead mutant of MARK2 reveals MARK2's ability to monitor subcellular actin status during interphase. During mitosis, MARK2's localization at actin-rich retraction fibres, but not the rest of the cortical membrane or centrosome, is dependent on its activity, highlighting a specialized spatial regulation of MARK2. By subtly perturbing the actin cytoskeleton, we reveal MARK2's role in correcting mitotic spindle off-centring induced by actin disassembly. We propose that MARK2 provides a molecular framework to integrate cortical signals and cytoskeletal changes in mitosis and interphase.

scholarly journals MARK2/Par1b present at retraction fibres corrects spindle off-centering induced by actin disassembly

2018 ◽  
Author(s):  
Madeleine Hart ◽  
Ihsan Zulkipli ◽  
Roshan Lal Shrestha ◽  
David D Dang ◽  
Duccio Conti ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Division ◽  
Actin Cytoskeleton ◽  
Division Plane ◽  
Spatial Regulation ◽  
Molecular Framework

Tissue maintenance requires adequate cell proliferation and a directed plane of cell division. While it is clear that the division-plane can be determined by retraction fibres that direct spindle movements, the components of retraction fibres that direct spindle movements are poorly understood. We report MARK2/Par1b kinase as a novel component of actin-rich retraction fibres, important for directed spindle movements. A kinase-dead mutant of MARK2 reveals the ability of MARK2 to monitor actin status. MARK2 localisation at actin-rich retraction fibres, but not the rest of the cortical membrane or centrosome, is dependent on its activity, highlighting a specialised spatial regulation of MARK2. By subtly perturbing the actin cytoskeleton, we demonstrate MARK2 has a role in correcting spindle off-centering, induced by actin disassembly. In addition to this mitotic role, we show MARK2 has a post-mitotic role in ensuring normal G1-S transition and cell proliferation. We propose that MARK2 provides a molecular framework to integrate cortical signals and cytoskeletal changes in both mitosis and interphase.

scholarly journals Plk1 regulates spindle orientation by phosphorylating NuMA in human cells

2018 ◽  
Vol 1 (6) ◽  
pp. e201800223 ◽  
Author(s):  
Shrividya Sana ◽  
Riya Keshri ◽  
Ashwathi Rajeevan ◽  
Sukriti Kapoor ◽  
Sachin Kotak
Keyword(s):  
Cell Division ◽  
Mitotic Spindle ◽  
Molecular Mechanisms ◽  
Spindle Pole ◽  
Spindle Orientation ◽  
Cell Cortex ◽  
Division Plane ◽  
Evolutionarily Conserved ◽  
Cortical Localization ◽  
Proper Orientation

Proper orientation of the mitotic spindle defines the correct division plane and is essential for accurate cell division and development. In metazoans, an evolutionarily conserved complex comprising of NuMA/LGN/Gαi regulates proper orientation of the mitotic spindle by orchestrating cortical dynein levels during metaphase. However, the molecular mechanisms that modulate the spatiotemporal dynamics of this complex during mitosis remain elusive. Here, we report that acute inactivation of Polo-like kinase 1 (Plk1) during metaphase enriches cortical levels of dynein/NuMA/LGN and thus influences spindle orientation. We establish that this impact of Plk1 on cortical levels of dynein/NuMA/LGN is through NuMA, but not via dynein/LGN. Moreover, we reveal that Plk1 inhibition alters the dynamic behavior of NuMA at the cell cortex. We further show that Plk1 directly interacts and phosphorylates NuMA. Notably, NuMA-phosphorylation by Plk1 impacts its cortical localization, and this is needed for precise spindle orientation during metaphase. Overall, our finding connects spindle-pole pool of Plk1 with cortical NuMA and answers a long-standing puzzle about how spindle-pole Plk1 gradient dictates proper spindle orientation for error-free mitosis.

scholarly journals A molecular framework for control of oriented cell division in the Arabidopsis embryo

2021 ◽  
Author(s):  
Prasad Vaddepalli ◽  
Thijs de Zeeuw ◽  
Sören Strauss ◽  
Katharina Bürstenbinder ◽  
Che-Yang Liao ◽  
...  
Keyword(s):  
Cell Division ◽  
Actin Cytoskeleton ◽  
Plant Development ◽  
Transcriptome Profiling ◽  
Cell Geometry ◽  
Auxin Response ◽  
Division Plane ◽  
Asymmetric Divisions ◽  
Extensive Cell ◽  
Minimal Surface Area

SummaryPremitotic control of cell division orientation is critical for plant development, as cell walls prevent extensive cell remodelling or migration. Whilst many divisions are proliferative and add cells to existing tissues, some divisions are formative, and generate new tissue layers or growth axes. Such formative divisions are often asymmetric in nature, producing daughters with different fates. We have previously shown that in the Arabidopsis thaliana embryo, developmental asymmetry is correlated with geometric asymmetry, creating daughter cells of unequal volume. Such divisions are generated by division planes that deviate from a default “minimal surface area” rule. Inhibition of auxin response leads to reversal to this default, yet the mechanisms underlying division plane choice in the embryo have been unclear. Here we show that auxin-dependent division plane control involves alterations in cell geometry, but not in cell polarity or nuclear position. Through transcriptome profiling, we find that auxin regulates genes controlling cell wall and cytoskeleton properties. We confirm the involvement of microtubule (MT)-binding proteins in embryo division control. Topology of both MT and Actin cytoskeleton depend on auxin response, and genetically controlled MT or Actin depolymerization in embryos leads to disruption of asymmetric divisions, including reversion to the default. Our work shows how auxin-dependent control of MT- and Actin cytoskeleton properties interacts with cell geometry to generate asymmetric divisions during the earliest steps in plant development.

scholarly journals IFT88 controls NuMA enrichment at k-fibers minus-ends to facilitate their reincorporation into mitotic spindles

2019 ◽  
Author(s):  
Nicolas Taulet ◽  
Audrey Douanier ◽  
Benjamin Vitre ◽  
Christelle Anguille ◽  
Justine Maurin ◽  
...  
Keyword(s):  
Cell Division ◽  
Laser Ablation ◽  
Molecular Motors ◽  
Mitotic Spindle ◽  
Intraflagellar Transport ◽  
Mitotic Spindles ◽  
Spatial Regulation ◽  
Main Spindle

ABSTRACTTo build and maintain mitotic spindle architecture, molecular motors exert spatially regulated forces on microtubules (MT) minus-ends. This spatial regulation is required to allow proper chromosomes alignment through the organization of kinetochore fibers (k-fibers). NuMA was recently shown to target dynactin to MT minus-ends and thus to spatially regulate dynein activity. However, given that k-fibers are embedded in the spindle, our understanding of the machinery involved in the targeting of proteins to their minus-ends remains limited. Intraflagellar transport (IFT) proteins were primarily studied for their ciliary roles but they also emerged as key regulators of cell division. Taking advantage of MT laser ablation, we show here that IFT88 concentrates at k-fibers minus-ends and is required for their re-anchoring into spindles by controlling NuMA accumulation. Indeed, IFT88 interacts with NuMA and is required for its enrichment at newly generated k-fibers minus-ends. Combining nocodazole washout experiments and IFT88 depletion, we further show that IFT88 is required for the reorganization of k-fibers into spindles and thus for efficient chromosomes alignment in mitosis. Overall, we propose that IFT88 could serve as a mitotic MT minus-end adaptor to concentrate NuMA at minus-ends thus facilitating k-fibers incorporation into the main spindle.

scholarly journals SepF is the FtsZ anchor in archaea, with features of an ancestral cell division system

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nika Pende ◽  
Adrià Sogues ◽  
Daniela Megrian ◽  
Anna Sartori-Rupp ◽  
Patrick England ◽  
...  
Keyword(s):  
Cell Division ◽  
Common Ancestor ◽  
Phylogenetic Analyses ◽  
Super Resolution ◽  
Binding Mode ◽  
Last Universal Common Ancestor ◽  
Division Plane ◽  
Multiple Factors ◽  
Universal Common Ancestor ◽  
Super Resolution Microscopy

AbstractMost archaea divide by binary fission using an FtsZ-based system similar to that of bacteria, but they lack many of the divisome components described in model bacterial organisms. Notably, among the multiple factors that tether FtsZ to the membrane during bacterial cell constriction, archaea only possess SepF-like homologs. Here, we combine structural, cellular, and evolutionary analyses to demonstrate that SepF is the FtsZ anchor in the human-associated archaeon Methanobrevibacter smithii. 3D super-resolution microscopy and quantitative analysis of immunolabeled cells show that SepF transiently co-localizes with FtsZ at the septum and possibly primes the future division plane. M. smithii SepF binds to membranes and to FtsZ, inducing filament bundling. High-resolution crystal structures of archaeal SepF alone and in complex with the FtsZ C-terminal domain (FtsZCTD) reveal that SepF forms a dimer with a homodimerization interface driving a binding mode that is different from that previously reported in bacteria. Phylogenetic analyses of SepF and FtsZ from bacteria and archaea indicate that the two proteins may date back to the Last Universal Common Ancestor (LUCA), and we speculate that the archaeal mode of SepF/FtsZ interaction might reflect an ancestral feature. Our results provide insights into the mechanisms of archaeal cell division and pave the way for a better understanding of the processes underlying the divide between the two prokaryotic domains.

Asymmetric cell division in fucoid algae: a role for cortical adhesions in alignment of the mitotic apparatus

2001 ◽  
Vol 114 (23) ◽  
pp. 4319-4328
Author(s):  
Sherryl R. Bisgrove ◽  
Darryl L. Kropf
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
Cell Cortex ◽  
Mitotic Apparatus ◽  
Pharmacological Agents ◽  
Division Plane ◽  
Adhesion Sites ◽  
Spindle Poles ◽  
Pelvetia Compressa ◽  
Two Phases

The first cell division in zygotes of the fucoid brown alga Pelvetia compressa is asymmetric and we are interested in the mechanism controlling the alignment of this division. Since the division plane bisects the mitotic apparatus, we investigated the timing and mechanism of spindle alignments. Centrosomes, which give rise to spindle poles, aligned with the growth axis in two phases – a premetaphase rotation of the nucleus and centrosomes followed by a postmetaphase alignment that coincided with the separation of the mitotic spindle poles during anaphase and telophase. The roles of the cytoskeleton and cell cortex in the two phases of alignment were analyzed by treatment with pharmacological agents. Treatments that disrupted cytoskeleton or perturbed cortical adhesions inhibited pre-metaphase alignment and we propose that this rotational alignment is effected by microtubules anchored at cortical adhesion sites. Postmetaphase alignment was not affected by any of the treatments tested, and may be dependent on asymmetric cell morphology.

glsA, a Volvox gene required for asymmetric division and germ cell specification, encodes a chaperone-like protein

Development ◽  
1999 ◽  
Vol 126 (4) ◽  
pp. 649-658 ◽  
Author(s):  
S.M. Miller ◽  
D.L. Kirk
Keyword(s):  
Mitotic Spindle ◽  
Site Directed Mutagenesis ◽  
Cell Specification ◽  
Division Plane ◽  
Binding Domains ◽  
Acid Protein ◽  
Germ Cell Specification ◽  
Asymmetric Divisions ◽  
Dividing Cells ◽  
Amino Acid Protein

The gls genes of Volvox are required for the asymmetric divisions that set apart cells of the germ and somatic lineages during embryogenesis. Here we used transposon tagging to clone glsA, and then showed that it is expressed maximally in asymmetrically dividing embryos, and that it encodes a 748-amino acid protein with two potential protein-binding domains. Site-directed mutagenesis of one of these, the J domain (by which Hsp40-class chaperones bind to and activate specific Hsp70 partners) abolishes the capacity of glsA to rescue mutants. Based on this and other considerations, including the fact that the GlsA protein is associated with the mitotic spindle, we discuss how it might function, in conjunction with an Hsp70-type partner, to shift the division plane in asymmetrically dividing cells.

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