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At least 19 recordsLinked to original sources
PubMed2001

Cell cycle-independent expression of the Arabidopsis cytokinesis-specific syntaxin KNOLLE results in mistargeting to the plasma membrane and is not sufficient for cytokinesis.

The Arabidopsis KNOLLE gene encodes a cytokinesis-specific syntaxin that localises to the plane of division and mediates cell-plate formation. KNOLLE mRNA and protein expression is tightly regulated during the cell cycle. To explore the significance of this regulation, we expressed KNOLLE protein under the control of two constitutive promoters, the flower-specific AP3 and the cauliflower mosaic virus 35S promoter. The transgenic plants developed normally, although KNOLLE mRNA and protein accumulated to high levels in non-proliferating cells and protein was incorporated into membranes. Immunolocalisation studies in transgenic seedling roots revealed mistargeting of KNOLLE protein to the plasma membrane in tip-growing root hairs and in expanding root cells, whereas no mislocalisation was observed in proliferating cells. By comparative in situ hybridisation to embryo sections, the 35S promoter yielded, relative to the endogenous KNOLLE promoter, low levels of KNOLLE mRNA accumulation in proliferating cells that were insufficient to rescue cytokinesis-defective knolle mutant embryos. Our results suggest that in wild type, strong expression of KNOLLE protein during M phase is necessary to ensure efficient vesicle fusion during cytokinesis.

Arabidopsis↗
PubMed2003

The degradation of two mitotic cyclins contributes to the timing of cytokinesis.

BACKGROUND: Cytokinesis occurs just as chromosomes complete segregation and reform nuclei. It has been proposed that cyclin/Cdk kinase inhibits cytokinesis until exit from mitosis; however, the timer of cytokinesis has not been experimentally defined. Whereas expression of a stable version of Drosophila cyclin B blocks cytokinesis along with numerous events of mitotic exit, stable cyclin B3 allows cytokinesis even though it blocks late events of mitotic exit. We examined the interface between mitotic cyclin destruction and the timing of cytokinesis. RESULTS: In embryonic mitosis 14, the cytokinesis furrow appeared 60 s after the metaphase/anaphase transition and closed 90 s later during telophase. In cyclin B or cyclin B3 mutant cells, the cytokinesis furrow appeared at an earlier stage of mitosis. Expression of stable cyclin B3 delayed and prolonged furrow invagination; nonetheless, cytokinesis completed during the extended mitosis. Reduced function of Pebble, a Rho GEF required for cytokinesis, also delayed and slowed furrow invagination, but incomplete furrows were aborted at the time of mitotic exit. In functional and genetic tests, cyclin B and cyclin B3 inhibited Pebble contributions to cytokinesis. CONCLUSIONS: Temporal coordination of mitotic events involves inhibition of cytokinesis by cyclin B and cyclin B3 and punctual relief of the inhibition by destruction of these cyclins. Both cyclins inhibit Pebble-dependent activation of cytokinesis, whereas cyclin B can inhibit cytokinesis by additional modes. Stable cyclin B3 also blocks the later return to interphase that otherwise appears to impose a deadline for the completion of cytokinesis.

Anaphase↗
PubMed2000

Myosin II-independent cytokinesis in Dictyostelium: its mechanism and implications.

Similar to higher animal cells, ameba cells of the cellular slime mold Dictyostelium discoideum form contractile rings containing filaments of myosin II during mitosis, and it is generally believed that contraction of these rings bisects the cells both on substrates and in suspension. In suspension, mutant cells lacking the single myosin II heavy chain gene cannot carry out cytokinesis, become large and multinucleate, and eventually lyze, supporting the idea that myosin II plays critical roles in cytokinesis. These mutant cells are however viable on substrates. Detailed analyses of these mutant cells on substrates revealed that, in addition to "classic" cytokinesis which depends on myosin II ("cytokinesis A"), Dictyostelium has two distinct, novel methods of cytokinesis, 1) attachment-assisted mitotic cleavage employed by myosin II null cells on substrates ("cytokinesis B"), and 2) cytofission, a cell cycle-independent division of adherent cells ("cytokinesis C"). Cytokinesis A, B, and C lose their function and demand fewer protein factors in this order. Cytokinesis B is of particular importance for future studies. Similar to cytokinesis A, cytokinesis B involves formation of a cleavage furrow in the equatorial region, and it may be a primitive but basic mechanism of efficiently bisecting a cell in a cell cycle-coupled manner. Analysis of large, multinucleate myosin II null cells suggested that interactions between astral microtubules and cortices positively induce polar protrusive activities in telophase. A model is proposed to explain how such polar activities drive cytokinesis B, and how cytokinesis B is coordinated with cytokinesis A in wild type cells.

Animals↗
PubMed2004

Dictyostelium discoideum talin A is crucial for myosin II-independent and adhesion-dependent cytokinesis.

Cytokinesis in myosin II-null (mhcA-) cells of Dictyostelium discoideum requires adhesion to a substratum. Moreover, such myosin II-independent, adhesion-dependent cytokinesis can be divided into two distinct classes: a cell cycle-coupled form (cytokinesis B) and a cell cycle-independent form (cytokinesis C). To better understand the mechanisms underlying cytokinesis B and C, we introduced mutations into mhcA- cells and isolated clones that consistently gave rise to large, multinucleated cells. One such clone was found to have a disrupted talA gene, which codes for one of two Dictyostelium homologues of talin. Time-lapse observation revealed that cytokinesis B is partially impaired in mhcA-/talA- cells and that cytokinesis C is completely blocked. MhcA-/talA- cells took significantly longer to complete cytokinesis B than mhcA- cells on regular polystyrene surfaces, but not on a more adhesive surface. During cytokinesis B in mhcA- cells, GFP-TalA localized in the cortex and in dot-like structures on the ventral surface. Like vertebrate talin, these TalA dots may be involved in substrate adhesion and provide the traction needed to efficiently carry out cytokinesis B. During cytokinesis C in mhcA- cells, GFP-TalA was localized in the cortex of future furrow regions, and was highly enriched in cytoplasmic bridges that formed as the furrowing proceeded. Analysis of furrows in which GFP-TalA concentrations were asymmetric suggested that cortical TalA prevents formation of leading edges in regions where its concentration is high and indirectly promotes formation of leading edges elsewhere, which causes passive furrowing of the TalA-rich regions.

Actins↗
PubMed2006

LET-99, GOA-1/GPA-16, and GPR-1/2 are required for aster-positioned cytokinesis.

At anaphase, the mitotic spindle positions the cytokinesis furrow [1]. Two populations of spindle microtubules are implicated in cytokinesis: radial microtubule arrays called asters and bundled nonkinetochore microtubules called the spindle midzone [2-4]. In C. elegans embryos, these two populations of microtubules provide two consecutive signals that position the cytokinesis furrow: The first signal is positioned midway between the microtubule asters; the second signal is positioned over the spindle midzone [5]. Evidence for two cytokinesis signals came from the identification of molecules that block midzone-positioned cytokinesis [5-7]. However, no molecules that are only required for, and thus define, the molecular pathway of aster-positioned cytokinesis have been identified. With RNAi screening, we identify LET-99 and the heterotrimeric G proteins GOA-1/GPA-16 and their regulator GPR-1/2 [10-12] in aster-positioned cytokinesis. By using mechanical spindle displacement, we show that the anaphase spindle positions cortical LET-99, at the site of the presumptive cytokinesis furrow. LET-99 enrichment at the furrow depends on the G proteins. GPR-1 is locally reduced at the site of cytokinesis-furrow formation by LET-99, which prevents accumulation of GPR-1 at this site. We conclude that LET-99 and the G proteins define a molecular pathway required for aster-positioned cytokinesis.

Anaphase↗
PubMed2004

Cell type-specific regulation of RhoA activity during cytokinesis.

Rho family GTPases play pivotal roles in cytokinesis. By using probes based on the principle of fluorescence resonance energy transfer (FRET), we have shown that in HeLa cells RhoA activity increases with the progression of cytokinesis. Here we show that in Rat1A cells RhoA activity remained suppressed during most of the cytokinesis. Consistent with this observation, the expression of C3 toxin inhibited cytokinesis in HeLa cells but not in Rat1A cells. Furthermore, the expression of a dominant negative mutant of Ect2, a Rho GEF, or Y-27632, an inhibitor of the Rho-dependent kinase ROCK, inhibited cytokinesis in HeLa cells but not in Rat1A cells. In contrast to the activity of RhoA, the activity of Rac1 was suppressed during cytokinesis and started increasing at the plasma membrane of polar sides before the abscission of the daughter cells in both HeLa and Rat1A cells. This type of Rac1 suppression was shown to be essential for cytokinesis because a constitutively active mutant of Rac1 induced a multinucleated phenotype in both HeLa and Rat1A cells. Moreover, the involvement of MgcRacGAP/CYK-4 in this suppression of Rac1 during cytokinesis was shown by the use of a dominant negative mutant. Because ML-7, an inhibitor of myosin light chain kinase, delayed the cytokinesis of Rat1A cells and because Pak, a Rac1 effector, is known to suppress myosin light chain kinase, the suppression of the Rac1-Pak pathway by MgcRacGAP may play a pivotal role in the cytokinesis of Rat1A cells.

ADP Ribose Transferases↗
PubMed2004

Genetic dissection of meiotic cytokinesis in Drosophila males.

We have used Drosophila male meiosis as a model system for genetic dissection of the cytokinesis mechanism. Drosophila mutants defective in meiotic cytokinesis can be easily identified by their multinucleate spermatids. Moreover, the large size of meiotic spindles allows characterization of mutant phenotypes with exquisite cytological resolution. We have screened a collection of 1955 homozygous mutant male sterile lines for those with multinucleate spermatids, and thereby identified mutations in 19 genes required for cytokinesis. These include 16 novel loci and three genes, diaphanous, four wheel drive, and pebble, already known to be involved in Drosophila cytokinesis. To define the primary defects leading to failure of cytokinesis, we analyzed meiotic divisions in male mutants for each of these 19 genes. Examination of preparations stained for tubulin, anillin, KLP3A, and F-actin revealed discrete defects in the components of the cytokinetic apparatus, suggesting that these genes act at four major points in a stepwise pathway for cytokinesis. Our results also indicated that the central spindle and the contractile ring are interdependent structures that interact throughout cytokinesis. Moreover, our genetic and cytological analyses provide further evidence for a cell type-specific control of Drosophila cytokinesis, suggesting that several genes required for meiotic cytokinesis in males are not required for mitotic cytokinesis.

Actomyosin↗
PubMed2006

Cytokinesis in plant and animal cells: endosomes 'shut the door'.

For many years, cytokinesis in eukaryotic cells was considered to be a process that took a variety of forms. This is rather surprising in the face of an apparently conservative mitosis. Animal cytokinesis was described as a process based on an actomyosin-based contractile ring, assembling, and acting at the cell periphery. In contrast, cytokinesis of plant cells was viewed as the centrifugal generation of a new cell wall by fusion of Golgi apparatus-derived vesicles. However, recent advances in animal and plant cell biology have revealed that many features formerly considered as plant-specific are, in fact, valid also for cytokinetic animal cells. For example, vesicular trafficking has turned out to be important not only for plant but also for animal cytokinesis. Moreover, the terminal phase of animal cytokinesis based on midbody microtubule activity resembles plant cytokinesis in that interdigitating microtubules play a decisive role in the recruitment of cytokinetic vesicles and directing them towards the cytokinetic spaces which need to be plugged by fusing endosomes. Presently, we are approaching another turning point which brings cytokinesis in plant and animal cells even closer. As an unexpected twist, new studies reveal that both plant and animal cytokinesis is driven not so much by Golgi-derived vesicles but rather by homotypically and heterotypically fusing endosomes. These are generated from cytokinetic cortical sites defined by preprophase microtubules and contractile actomyosin ring, which induce local endocytosis of both the plasma membrane and cell wall material. Finally, plant and animal cytokinesis meet together at the physical separation of daughter cells despite obvious differences in their preparatory events.

Actomyosin↗
PubMed2006

Dissociation of cytokinesis initiation from mitotic control in a eukaryote.

Cytokinesis is initiated only after mitotic exit in eukaryotes. However, in the insect (procyclic) form of an ancient protist, Trypanosoma brucei, a blockade at the G2/M checkpoint results in an enrichment of anucleate cells (zoids), suggesting separated regulations between mitosis and cytokinesis (X. Tu and C. C. Wang, J. Biol. Chem. 279:20519-20528, 2004). Polo-like kinases (Plks) are known to play critical roles in controlling both mitosis and cytokinesis. A single Plk homologue in T. brucei, TbPLK, was found to be capable of complementing the Plk (Cdc5) functions in Saccharomyces cerevisiae, thus raising the question of how it may function in the trypanosome with cytokinesis dissociated from mitosis. Depletion of TbPLK in the procyclic form of T. brucei by RNA interference resulted in growth arrest with accumulation of multiple nuclei, kinetoplasts, basal bodies, and flagella in approximately equal numbers among individual cells. There were, however, few zoids detectable, indicating inhibited cytokinesis with unblocked mitosis and kinetoplast segregation. TbPLK is thus apparently involved only in initiating cytokinesis in T. brucei. Overexpression of TbPLK in the trypanosome did not affect cell growth, but 13% of the resulting population was in the zoid form, suggesting runaway cytokinesis. An immunofluorescence assay indicated that TbPLK was localized in a chain of likely flagellum attachment zones in the cytoskeleton. In a dividing cell, a new line of such zones appeared closely paralleling the existing one, which could constitute the cleavage furrow. An exposed region of TbPLK at the anterior tip of the cell may provide the trigger of cytokinesis. Taken together, our results revealed a novel mechanism of cytokinesis initiation in the trypanosome that may serve as a useful model for further in-depth investigations.

Animals↗
PubMed2002

Nir2, a human homolog of Drosophila melanogaster retinal degeneration B protein, is essential for cytokinesis.

Cytokinesis, the final stage of eukaryotic cell division, ensures the production of two daughter cells. It requires fine coordination between the plasma membrane and cytoskeletal networks, and it is known to be regulated by several intracellular proteins, including the small GTPase Rho and its effectors. In this study we provide evidence that the protein Nir2 is essential for cytokinesis. Microinjection of anti-Nir2 antibodies into interphase cells blocks cytokinesis, as it results in the production of multinucleate cells. Immunolocalization studies revealed that Nir2 is mainly localized in the Golgi apparatus in interphase cells, but it is recruited to the cleavage furrow and the midbody during cytokinesis. Nir2 colocalizes with the small GTPase RhoA in the cleavage furrow and the midbody, and it associates with RhoA in mitotic cells. Its N-terminal region, which contains a phosphatidylinositol transfer domain and a novel Rho-inhibitory domain (Rid), is required for normal cytokinesis, as overexpression of an N-terminal-truncated mutant blocks cytokinesis completion. Time-lapse videomicroscopy revealed that this mutant normally initiates cytokinesis but fails to complete it, due to cleavage furrow regression, while Rid markedly affects cytokinesis due to abnormal contractility. Rid-expressing cells exhibit aberrant ingression and ectopic cleavage sites; the cells fail to segregate into daughter cells and they form a long unseparated bridge-like cytoplasmic structure. These results provide new insight into the cellular functions of Nir2 and introduce it as a novel regulator of cytokinesis.

Animals↗
PubMed2002

Genetic and morphological evidence for two parallel pathways of cell-cycle-coupled cytokinesis in Dictyostelium.

Myosin-II-null cells of Dictyostelium discoideum cannot divide in suspension, consistent with the dogma that myosin II drives constriction of the cleavage furrow and, consequently, cytokinesis (cytokinesis A). Nonetheless, when grown on substrates, these cells exhibit efficient, cell-cycle-coupled division, suggesting that they possess a novel, myosin-II-independent, adhesion-dependent method of cytokinesis (cytokinesis B). Here we show that double mutants lacking myosin II and either AmiA or coronin, both of which are implicated in cytokinesis B, are incapable of cell-cycle-coupled cytokinesis. These double mutants multiplied mainly by cytokinesis C, a third, inefficient, method of cell division, which requires substrate adhesion and is independent of cell cycle progression. In contrast, double mutants lacking AmiA and coronin were no sicker than each of the single mutants, indicating that the severe defects of myosin II(-)/AmiA(-) or myosin II(-)/coronin(-) mutants are not simple additive effects of two mutations. We take this as genetic evidence for two parallel pathways both of which lead to cell-cycle-coupled cytokinesis. This conclusion is supported by differences in morphological changes during cytokinesis in the mutant cell lines.

Animals↗
PubMed2001

Genetic approaches to dissect the mechanisms of two distinct pathways of cell cycle-coupled cytokinesis in Dictyostelium.

Dictyostelium discoideum is a unique experimental organism which allows genetic analysis of the mechanism of cytokinesis of the animal type, and a number of mutations which affect cytokinesis in one way or other have been identified. Myosin II filaments accumulate in the equatorial region, and myosin II-null cells cannot divide in suspension, indicating that active, myosin II-dependent constriction of the cleavage furrow contributes to bisection of the cell. We refer to this method of cytokinesis as cytokinesis A. On substrates, however, myosin II-null cells divide efficiently in a cell cycle-coupled manner. This adhesion-dependent but myosin II-independent division method, which we termed cytokinesis B, is carried out by a pathway that is genetically distinct from that of cytokinesis A. Morphological analyses suggested that cytokinesis B is driven by radial traction forces generated along polar peripheries, which indirectly cause furrow ingression. Identification of two redundant pathways have allowed us to search genes involved in either pathway by mutagenizing cells which are already defective in one of the pathways. This approach enabled us to identify a number of novel cytokinesis-related genes, as well as to reclassify known genes as cytokinesis-related.

Animals↗
PubMed2004

Comparative analysis of cytokinesis in budding yeast, fission yeast and animal cells.

Cytokinesis is a temporally and spatially regulated process through which the cellular constituents of the mother cell are partitioned into two daughter cells, permitting an increase in cell number. When cytokinesis occurs in a polarized cell it can create daughters with distinct fates. In eukaryotes, cytokinesis is carried out by the coordinated action of a cortical actomyosin contractile ring and targeted membrane deposition. Recent use of model organisms with facile genetics and improved light-microscopy methods has led to the identification and functional characterization of many proteins involved in cytokinesis. To date, this analysis indicates that some of the basic components involved in cytokinesis are conserved from yeast to humans, although their organization into functional machinery that drives cytokinesis and the associated regulatory mechanisms bear species-specific features. Here, we briefly review the current status of knowledge of cytokinesis in the budding yeast Saccharomyces cerevisiae, the fission yeast Schizosaccharomyces pombe and animal cells, in an attempt to highlight both the common and the unique features. Although these organisms diverged from a common ancestor about a billion years ago, there are eukaryotes that are far more divergent. To evaluate the overall evolutionary conservation of cytokinesis, it will be necessary to include representatives of these divergent branches. Nevertheless, the three species discussed here provide substantial mechanistic diversity.

Animals↗
PubMed2005

A cytokinesis furrow is positioned by two consecutive signals.

The position of the cytokinesis furrow in a cell determines the relative sizes of its two daughter cells as well as the distribution of their contents. In animal cells, the position of the cytokinesis furrow is specified by the position of the mitotic spindle. The cytokinesis furrow bisects the spindle midway between the microtubule asters, at the site of the microtubule-based midzone, producing two daughter cells. Experiments in some cell types have suggested that the midzone positions the furrow, but experiments in other cells have suggested that the asters position the furrow. One possibility is that different organisms and cell types use different mechanisms to position the cytokinesis furrow. An alternative possibility is that both asters and the midzone contribute to furrow positioning. Recent work in C. elegans has suggested that centrosome separation and the midzone are implicated in cytokinesis. Here we examine the relative contributions of different parts of the mitotic spindle to positioning of the cytokinesis furrow in the C. elegans zygote. By spatially separating the spindle midzone from one of the asters using an ultraviolet laser, we show that the cytokinesis furrow is first positioned by a signal determined by microtubule asters, and then by a second signal that is derived from the spindle midzone. Thus, the position of the cytokinesis furrow is specified by two consecutive furrowing activities.

Actomyosin↗
PubMed2005

Endocytosis resumes during late mitosis and is required for cytokinesis.

Recent work has underscored the importance of membrane trafficking events during cytokinesis. For example, targeted membrane secretion occurs at the cleavage furrow in animal cells, and proteins that regulate endocytosis also influence the process of cytokinesis. Nonetheless, the prevailing dogma is that endosomal membrane trafficking ceases during mitosis and resumes after cell division is complete. In this study, we have characterized endocytic membrane trafficking events that occur during mammalian cell cytokinesis. We have found that, although endocytosis ceases during the early stages of mitosis, it resumes during late mitosis in a temporally and spatially regulated pattern as cells progress from anaphase to cytokinesis. Using fixed and live cell imaging, we have found that, during cleavage furrow ingression, vesicles are internalized from the polar region and subsequently trafficked to the midbody area during later stages of cytokinesis. In addition, we have demonstrated that cytokinesis is inhibited when clathrin-mediated endocytosis is blocked using a series of dominant negative mutants. In contrast to previous thought, we conclude that endocytosis resumes during the later stages of mitosis, before cytokinesis is completed. Furthermore, based on our findings, we propose that the proper regulation of endosomal membrane traffic is necessary for the successful completion of cytokinesis.

ADP-Ribosylation Factor 6↗
PubMed2005

Inhibition of cyclin-dependent kinase 1 induces cytokinesis without chromosome segregation in an ECT2 and MgcRacGAP-dependent manner.

Cleavage furrow formation marks the onset of cell division during early anaphase. The small GTPase RhoA and its regulators ECT2 and MgcRacGAP have been implicated in furrow ingression in mammalian cells, but the signaling upstream of these molecules remains unclear. We now show that the inhibition of cyclin-dependent kinase (Cdk)1 is sufficient to initiate cytokinesis. When mitotically synchronized cells were treated with the Cdk-specific inhibitor BMI-1026, the initiation of cytokinesis was induced precociously before chromosomal separation. Cytokinesis was also induced by the Cdk1-specific inhibitor purvalanol A but not by Cdk2/Cdk5- or Cdk4-specific inhibitors. Consistent with initiation of precocious cytokinesis by Cdk1 inhibition, introduction of anti-Cdk1 monoclonal antibody resulted in cells with aberrant nuclei. Depolymerization of mitotic spindles by nocodazole inhibited BMI-1026-induced precocious cytokinesis. However, in the presence of a low concentration of nocodazole, BMI-1026 induced excessive membrane blebbing, which appeared to be caused by formation of ectopic cleavage furrows. Depletion of ECT2 or MgcRacGAP by RNA interference abolished both of the phenotypes (precocious furrowing after nocodazole release and excessive blebbing in the presence of nocodazole). RNA interference of RhoA or expression of dominant-negative RhoA efficiently reduced both phenotypes. RhoA was localized at the cleavage furrow or at the necks of blebs. We propose that Cdk1 inactivation is sufficient to activate a signaling pathway leading to cytokinesis, which emanates from mitotic spindles and is regulated by ECT2, MgcRacGAP, and RhoA. Chemical induction of cytokinesis will be a valuable tool to study the initiation mechanism of cytokinesis.

Anaphase↗
PubMed2000

The role of pre- and post-anaphase microtubules in the cytokinesis phase of the cell cycle.

The cytokinesis phase, or C phase, of the cell cycle results in the separation of one cell into two daughter cells after the completion of mitosis. Although it is known that microtubules are required for proper positioning of the cytokinetic furrow [1] [2], the role of pre-anaphase microtubules in cytokinesis has not been clearly defined for three key reasons. First, inducing microtubule depolymerization or stabilization before the onset of anaphase blocks entry into anaphase and cytokinesis via the spindle checkpoint [3]. Second, microtubule organization changes rapidly at anaphase onset as the mitotic kinase, Cdc2-cyclin B, is inactivated [4]. Third, the time between the onset of anaphase and the initiation of cytokinesis is very short, making it difficult to unambiguously alter microtubule polymer levels before cytokinesis, but after inactivation of the spindle checkpoint. Here, we have taken advantage of the discovery that microinjection of antibodies to the spindle checkpoint protein Mad2 (mitotic arrest deficient) in prometaphase abrogates the spindle checkpoint, producing premature chromosome separation, segregation, and normal cytokinesis [5] [6]. To test the role of pre-anaphase microtubules in cytokinesis, microtubules were disassembled in prophase and prometaphase cells, the cells were then injected with anti-Mad2 antibodies and recorded through C phase. The results show that exit from mitosis in the absence of microtubules triggered a 50 minute period of cortical contractility that was independent of microtubules. Furthermore, upon microtubule reassembly during this contractile C-phase period, approximately 30% of the cells underwent chromosome poleward movement, formed a midzone microtubule complex, and completed cytokinesis.

Anaphase↗