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 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 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.

Alfalfa Mob1-like proteins are involved in cell proliferation and are localized in the cell division plane during cytokinesis

2006 ◽  
Vol 312 (7) ◽  
pp. 1050-1064 ◽  
Author(s):  
Sandra Citterio ◽  
Simonetta Piatti ◽  
Emidio Albertini ◽  
Roberta Aina ◽  
Serena Varotto ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Division ◽  
Division Plane ◽  
Cell Division Plane

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.

scholarly journals Cell fate clusters in ICM organoids arise from cell fate heredity and division: a modelling approach

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tim Liebisch ◽  
Armin Drusko ◽  
Biena Mathew ◽  
Ernst H. K. Stelzer ◽  
Sabine C. Fischer ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Division ◽  
Cell Fate ◽  
Inner Cell Mass ◽  
Cell Mass ◽  
Cell Lineage ◽  
Cell Fate Decision ◽  
Cell Fate Decisions ◽  
Chemical Signalling ◽  
Fate Decision

AbstractDuring the mammalian preimplantation phase, cells undergo two subsequent cell fate decisions. During the first decision, the trophectoderm and the inner cell mass are formed. Subsequently, the inner cell mass segregates into the epiblast and the primitive endoderm. Inner cell mass organoids represent an experimental model system, mimicking the second cell fate decision. It has been shown that cells of the same fate tend to cluster stronger than expected for random cell fate decisions. Three major processes are hypothesised to contribute to the cell fate arrangements: (1) chemical signalling; (2) cell sorting; and (3) cell proliferation. In order to quantify the influence of cell proliferation on the observed cell lineage type clustering, we developed an agent-based model accounting for mechanical cell–cell interaction, i.e. adhesion and repulsion, cell division, stochastic cell fate decision and cell fate heredity. The model supports the hypothesis that initial cell fate acquisition is a stochastically driven process, taking place in the early development of inner cell mass organoids. Further, we show that the observed neighbourhood structures can emerge solely due to cell fate heredity during cell division.

scholarly journals A possible relation between dietary zinc and cAMP in the regulation of tumour cell proliferation in the rat

1988 ◽  
Vol 59 (3) ◽  
pp. 437-442 ◽  
Author(s):  
Noel S. Skeef ◽  
John R. Duncan
Keyword(s):  
Cell Proliferation ◽  
Cell Division ◽  
Cell Line ◽  
Tumour Cell ◽  
Tumour Growth ◽  
Zn Deficiency ◽  
Regenerating Liver ◽  
Small Reduction ◽  
Dietary Zinc ◽  
Camp Concentration

1. The possibility of an effect of zinc on the rate of tumour cell division, mediated through a regulation of cellular cAMP concentration, was investigated in the present study in rats.2. Dietary Zn deficiency (< 1·5 mg Zn/kg) but not Zn excess (500 mg Zn/kg) resulted in an increased cAMP concentration in transplanted hepatoma cells. Neither treatment had any effect on the cAMP concentration in regenerating liver or normal resting liver. Both the deficient and excess Zn diets resulted in a small reduction in tumour growth (not statistically significant).3. The results seem to indicate that the relation investigated in the present study does not apply in the cell line used.

scholarly journals Role of Cell Division Autoantigen 1 (CDA1) in Cell Proliferation and Fibrosis

Genes ◽  
2010 ◽  
Vol 1 (3) ◽  
pp. 335-348 ◽  
Author(s):  
Ban-Hock Toh ◽  
Yugang Tu ◽  
Zemin Cao ◽  
Mark E. Cooper ◽  
Zhonglin Chai
Keyword(s):  
Cell Proliferation ◽  
Cell Division
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