scholarly journals Cell Cycle Characteristics of Crenarchaeota: Unity among Diversity

2008 ◽  
Vol 190 (15) ◽  
pp. 5362-5367 ◽  
Author(s):  
Magnus Lundgren ◽  
Laurence Malandrin ◽  
Stefan Eriksson ◽  
Harald Huber ◽  
Rolf Bernander
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Chromosome Segregation ◽  
Cellular Growth ◽  
Epifluorescence Microscopy ◽  
Hyperthermophilic Archaea ◽  
Time Interval ◽  
Aeropyrum Pernix ◽  
Genome Separation ◽  
Long Time

ABSTRACT The hyperthermophilic archaea Acidianus hospitalis, Aeropyrum pernix, Pyrobaculum aerophilum, Pyrobaculum calidifontis, and Sulfolobus tokodaii representing three different orders in the phylum Crenarchaeota were analyzed by flow cytometry and combined phase-contrast and epifluorescence microscopy. The overall organization of the cell cycle was found to be similar in all species, with a short prereplicative period and a dominant postreplicative period that accounted for 64 to 77% of the generation time. Thus, in all Crenarchaeota analyzed to date, cell division and initiation of chromosome replication occur in close succession, and a long time interval separates termination of replication from cell division. In Pyrobaculum, chromosome segregation overlapped with or closely followed DNA replication, and further genome separation appeared to occur concomitant with cellular growth. Cell division in P. aerophilum took place without visible constriction.

scholarly journals Changes in Cell Size and DNA Content inSulfolobus Cultures during Dilution and Temperature Shift Experiments

1999 ◽  
Vol 181 (18) ◽  
pp. 5669-5675 ◽  
Author(s):  
Karin Hjort ◽  
Rolf Bernander
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Stationary Phase ◽  
Growth Medium ◽  
Temperature Shift ◽  
Chromosome Replication ◽  
Cellular Growth ◽  
Inhibition Of Growth ◽  
Ice Water ◽  
Fresh Growth Medium

ABSTRACT Stationary-phase cultures of different hyperthermophilic species of the archaeal genus Sulfolobus were diluted into fresh growth medium and analyzed by flow cytometry and phase-fluorescence microscopy. After dilution, cellular growth started rapidly but no nucleoid partition, cell division, or chromosome replication took place until the cells had been increasing in size for several hours. Initiation of chromosome replication required that the cells first go through partition and cell division, revealing a strong interdependence between these key cell cycle events. The time points at which nucleoid partition, division, and replication occurred after the dilution were used to estimate the relative lengths of the cell cycle periods. When exponentially growing cultures were diluted into fresh growth medium, there was an unexpected transient inhibition of growth and cell division, showing that the cultures did not maintain balanced growth. Furthermore, when cultures growing at 79°C were shifted to room temperature or to ice-water baths, the cells were found to “freeze” in mid-growth. After a shift back to 79°C, growth, replication, and division rapidly resumed and the mode and kinetics of the resumption differed depending upon the nature and length of the shifts. Dilution of stationary-phase cultures provides a simple protocol for the generation of partially synchronized populations that may be used to study cell cycle-specific events.

scholarly journals Bacterial chromosome segregation.

2005 ◽  
Vol 52 (1) ◽  
pp. 1-34 ◽  
Author(s):  
Aneta A Bartosik ◽  
Grazyna Jagura-Burdzy
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Chromosome Segregation ◽  
Copy Number ◽  
Bacterial Cells ◽  
Replication Machinery ◽  
Rapid Separation ◽  
Dna Segregation ◽  
Low Copy Number ◽  
Bacterial Chromosomes

In most bacteria two vital processes of the cell cycle: DNA replication and chromosome segregation overlap temporally. The action of replication machinery in a fixed location in the cell leads to the duplication of oriC regions, their rapid separation to the opposite halves of the cell and the duplicated chromosomes gradually moving to the same locations prior to cell division. Numerous proteins are implicated in co-replicational DNA segregation and they will be characterized in this review. The proteins SeqA, SMC/MukB, MinCDE, MreB/Mbl, RacA, FtsK/SpoIIIE playing different roles in bacterial cells are also involved in chromosome segregation. The chromosomally encoded ParAB homologs of active partitioning proteins of low-copy number plasmids are also players, not always indispensable, in the segregation of bacterial chromosomes.

scholarly journals Activation of a signaling pathway by the physical translocation of a chromosome

2021 ◽  
Author(s):  
Mathilde Guzzo ◽  
Allen G. Sanderlin ◽  
Lennice K. Castro ◽  
Michael T. Laub
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Dna Replication ◽  
Signaling Pathway ◽  
Chromosome Segregation ◽  
Caulobacter Crescentus ◽  
Replication Initiation ◽  
Dna Replication Initiation ◽  
Cellular Processes ◽  
Initiation Of Dna Replication

AbstractIn every organism, the cell cycle requires the execution of multiple cellular processes in a strictly defined order. However, the mechanisms used to ensure such order remain poorly understood, particularly in bacteria. Here, we show that the activation of the essential CtrA signaling pathway that triggers cell division in Caulobacter crescentus is intrinsically coupled to the successful initiation of DNA replication via the physical translocation of a newly-replicated chromosome, powered by the ParABS system. We demonstrate that ParA accumulation at the new cell pole during chromosome segregation recruits ChpT, an intermediate component of the CtrA signaling pathway. ChpT is normally restricted from accessing the selective PopZ polar microdomain until the new chromosome and ParA arrive. Consequently, any disruption to DNA replication initiation prevents the recruitment of ChpT and, in turn, cell division. Collectively, our findings reveal how major cell-cycle events are coordinated in Caulobacter and, importantly, how the physical translocation of a chromosome triggers an essential signaling pathway.

Cell growth kinetics, division asymmetry and volume control at division in the marine dinoflagellate Gonyaulax polyedra: a model of circadian clock control of the cell cycle

1989 ◽  
Vol 92 (2) ◽  
pp. 303-318 ◽  
Author(s):  
K. Homma ◽  
J.W. Hastings
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Growth ◽  
Circadian Clock ◽  
Cell Volume ◽  
Conditional Probability ◽  
Growth Patterns ◽  
Time Interval ◽  
Dark Cycle ◽  
Gonyaulax Polyedra

A new method of determining the dependence of cell growth on the initial cell volume in the absence of cell division is presented. The assumptions are that volume in a certain period of time is either increasing or decreasing, but not both, and is independent of the history of cells. Applying this method to Gonyaulax polyedra in a 12h light-12h dark cycle, growth in volume between the 3rd and 12th hours of the light period is found to be more exponential-like than linear. The magnitude of growth in the time period is determined solely by cell volume and environmental conditions, not by cell age. All cells decrease in volume slightly in the dark from the 12th to 23rd hour, and then increase a little from the 23rd to 3rd hour of the following day. Cell division in this species is significantly asymmetric, and the extent of asymmetry is estimated mathematically. Simulations based on the growth patterns and the asymmetric division reveal that cell division must at least partly depend on the volume of cells. The dependence of conditional cell division probability on cell volume is then experimentally determined. The probability is zero up to a certain cell volume, and then it gradually increases to a plateau level, which is less than unity. Neither the strict size control model nor the transition probability model is fully consistent with the observed shape of the conditional probability function. A hybrid model postulating a ‘sloppy’ critical volume with a constant probability of division above that volume adequately accounts for the conditional probability. With the use of the observed volume growth law, cell division dependence on volume, and the extent of asymmetry in cell division, cell volume distributions are successfully simulated for cells growing in a 12h light-12h dark cycle. Another simulation reveals that the true coefficient of variation in generation time is 33%. On the basis of these findings, a model of the cell cycle is presented that incorporates the circadian clock as a cyclic G1 phase. According to this scheme, cells satisfying the minimum cell volume requirement between the 12th and the 18th hour probably exit to the replication/segregation sequence ending in division, and re-enter the cyclic portion after a fixed time interval.

scholarly journals Dynamics of Escherichia coli Chromosome Segregation during Multifork Replication

2007 ◽  
Vol 189 (23) ◽  
pp. 8660-8666 ◽  
Author(s):  
Henrik J. Nielsen ◽  
Brenda Youngren ◽  
Flemming G. Hansen ◽  
Stuart Austin
Keyword(s):  
Escherichia Coli ◽  
Cell Cycle ◽  
Growth Rate ◽  
Cell Division ◽  
Chromosome Segregation ◽  
Replication Forks ◽  
Daughter Cells ◽  
Initiation Of Replication ◽  
Replication Terminus ◽  
Multiple Replication

ABSTRACT Slowly growing Escherichia coli cells have a simple cell cycle, with replication and progressive segregation of the chromosome completed before cell division. In rapidly growing cells, initiation of replication occurs before the previous replication rounds are complete. At cell division, the chromosomes contain multiple replication forks and must be segregated while this complex pattern of replication is still ongoing. Here, we show that replication and segregation continue in step, starting at the origin and progressing to the replication terminus. Thus, early-replicated markers on the multiple-branched chromosomes continue to separate soon after replication to form separate protonucleoids, even though they are not segregated into different daughter cells until later generations. The segregation pattern follows the pattern of chromosome replication and does not follow the cell division cycle. No extensive cohesion of sister DNA regions was seen at any growth rate. We conclude that segregation is driven by the progression of the replication forks.

scholarly journals Concurrent processes setE. colicell division

2018 ◽  
Vol 4 (11) ◽  
pp. eaau3324 ◽  
Author(s):  
Gabriele Micali ◽  
Jacopo Grilli ◽  
Matteo Osella ◽  
Marco Cosentino Lagomarsino
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Single Cell ◽  
Chromosome Segregation ◽  
Genetic Material ◽  
Replication Initiation ◽  
Concurrent Processes ◽  
A Cell ◽  
Rate Limiting ◽  
Cell Data

A cell can divide only upon completion of chromosome segregation; otherwise, its daughters would lose genetic material. However, we do not know whether the partitioning of chromosomes is the key event for the decision to divide. We show how key trends in single-cell data reject the classic idea of replication-segregation as the rate-limiting process for cell division. Instead, the data agree with a model where two concurrent processes (setting replication initiation and interdivision time) set cell division on competing time scales. During each cell cycle, division is set by the slowest process (an “AND” gate). The concept of transitions between cell cycle stages as decisional processes integrating multiple inputs instead of cascading from orchestrated steps can affect the way we think of the cell cycle in general.

scholarly journals The structural basis for Ulp2 recruitment to the kinetochore

2021 ◽  
Author(s):  
Yun Quan ◽  
Stephen M. Hinshaw ◽  
Pang-Che Wang ◽  
Stephen C. Harrison ◽  
Huilin Zhou
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Chromosome Segregation ◽  
Structural Basis ◽  
Centromeric Dna ◽  
Step Process ◽  
Sumo Protease ◽  
Daughter Cells ◽  
Sister Chromatids ◽  
Spindle Microtubules

ABSTRACTThe step-by-step process of chromosome segregation defines the stages of the cell division cycle. In eukaryotes, signaling pathways that control these steps converge upon the kinetochore, a multiprotein assembly that connects spindle microtubules to the centromere of each chromosome. Kinetochores control and adapt to major chromosomal transactions, including replication of centromeric DNA, biorientation of sister centromeres on the metaphase spindle, and transit of sister chromatids into daughter cells during anaphase. Although the mechanisms that ensure tight microtubule coupling at anaphase are at least partly understood, kinetochore adaptations that support other cell cycle transitions are not. We report here a mechanism that enables regulated control of kinetochore sumoylation. A conserved surface of the Ctf3/CENP-I kinetochore protein provides a binding site for the SUMO protease, Ulp2. Ctf3 mutations that disable Ulp2 recruitment cause elevated inner kinetochore sumoylation and defective chromosome segregation. The location of the site within the assembled kinetochore suggests coordination between sumoylation and other cell cycle-regulated processes.

scholarly journals The Last Chance Saloon

2021 ◽  
Vol 9 ◽  
Author(s):  
Ye Hong ◽  
Hongtao Zhang ◽  
Anton Gartner
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Chromosome Segregation ◽  
Cell Cycle Progression ◽  
Genome Instability ◽  
Genome Integrity ◽  
Cycle Progression ◽  
Chromosome Fragmentation ◽  
C Elegans ◽  
Chromatin Bridges

Accurate chromosome segregation requires the removal of all chromatin bridges, which link chromosomes before cell division. When chromatin bridges fail to be removed, cell cycle progression may halt, or cytokinesis failure and ensuing polyploidization may occur. Conversely, the inappropriate severing of chromatin bridges leads to chromosome fragmentation, excessive genome instability at breakpoints, micronucleus formation, and chromothripsis. In this mini-review, we first describe the origins of chromatin bridges, the toxic processing of chromatin bridges by mechanical force, and the TREX1 exonuclease. We then focus on the abscission checkpoint (NoCut) which can confer a transient delay in cytokinesis progression to facilitate bridge resolution. Finally, we describe a recently identified mechanism uncovered in C. elegans where the conserved midbody associated endonuclease LEM-3/ANKLE1 is able to resolve chromatin bridges generated by various perturbations of DNA metabolism at the final stage of cell division. We also discuss how LEM-3 dependent chromatin bridge resolution may be coordinated with abscission checkpoint (NoCut) to achieve an error-free cleavage, therefore acting as a “last chance saloon” to facilitate genome integrity and organismal survival.

scholarly journals Cyclin B3 is specifically required for metaphase to anaphase transition in mouse oocyte meiosis I

2018 ◽  
Author(s):  
Yufei Li ◽  
Leyun Wang ◽  
Linlin Zhang ◽  
Zhengquan He ◽  
Guihai Feng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Chromosome Segregation ◽  
Mammalian Species ◽  
Cell Cycle Control ◽  
Special Role ◽  
List Type ◽  
Oocyte Meiosis ◽  
Cyclin B3 ◽  
Meiosis I

AbstractMeiosis, a cell division to generate gametes for sexual reproduction in eukaryotes, executes a single round of DNA replication and two successive rounds of chromosome segregation [1]. The extraordinary reliability of the meiotic cycle requires the activities of cyclin-dependent kinases (Cdks) associated with specific cyclins [2-4]. Cyclins are the regulatory subunits of protein kinases, which are the main regulators of maturation promoting factor or mitosis promoting factor (MPF) [5, 6] and anaphase-promoting complex/cyclosome (APC/C) [7, 8] in eukaryotic cell division. But how cyclins collaborate to control meiosis is still largely unknown. Cyclin B3 (Ccnb3) shares homology with A- and B-type cyclins [9], and is conserved during higher eukaryote evolution [10-17]. Previous studies have shown that Ccnb3-deleted females are sterile with oocytes unable to complete meiosis I in Drosophila [18], implying that Ccnb3 may have a special role in meiosis. To clarify the function of Ccnb3 in meiosis in mammalian species, we generated Ccnb3 mutant mice by CRISPR/Cas9, and found that Ccnb3 mutation caused female infertility with the failure of metaphase-anaphase transition in meiosis I. Ccnb3 was necessary for APC/C activation to initiate anaphase I, but not required for oocytes maturation, meiosis II progression, or early embryonic development. Our study reveals the differential cell cycle regulation between meiosis I and meiosis II, as well as meiosis between males and females, which shed light on the cell cycle control of meiosis.HighlightsIdentification of a female meiosis-specific cyclin in mouseCyclin B3 is required for metaphase-anaphase transition in oocyte meiosis ICyclin B3 is not essential for oocyte maturation and sister chromosome segregationCyclin B3 is necessary for APC/C activation and MPF kinase activity through Cdk1

FANCA Controls Mitotic Phosphosignaling Networks To Ensure Genome Stability During Cell Division

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 801-801
Author(s):  
Rikki Enzor ◽  
Zahi Abdul Sater ◽  
Donna Cerabona ◽  
Zejin Sun ◽  
Su-jung Park ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Chromosome Segregation ◽  
Fanconi Anemia ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Signaling Network ◽  
Mitotic Apparatus ◽  
Risk Of Cancer

Abstract Fanconi anemia (FA) is a heterogenous genome instability syndrome with a high risk of cancer. The FA proteins are essential for interphase DNA damage repair. However, it is incompletely understood why FA-deficient cells also develop gross aneuploidy and multinucleation, which are symptoms of error-prone chromosome segregation. Emerging evidence indicates that the FA signaling network functions as a guardian of the genome throughout the cell cycle, including chromosome segregation during mitosis. However, the mechanistic aspects of the critical role of the FA signaling in mitosis remain poorly understood. We have recently shown that the FA signaling network localizes to the mitotic apparatus to control the spindle assembly checkpoint and centrosome maintenance (J Clin Invest 2013, in press). The spindle assembly checkpoint (SAC) is a complex tumor suppressor signaling network that prevents premature separation of sister chromatids by delaying the metaphase-to-anaphase transition until all the kinetochores are properly attached to the mitotic spindle. Since weakened SAC promotes stochastic chromosome segregation, mutagenesis and cancer, these findings shed new light on the role of FA signaling in maintenance of genomic stability. We found the subcellular localization of FA proteins to the mitotic apparatus is spatiotemporally regulated as cells divide. Our new data revealed the pathways connecting the FANCA protein with canonical mitotic phosphosignaling networks. We have employed unbiased kinome-wide phospho-mass spectrometry to compare the landscape of abnormalities of mitotic signaling pathways in primary FANCA-/- patient cells and gene-corrected isogenic cells. These experiments led us to identify and quantify a wide range of phosphorylation abnormalities of multiple FANCA-dependent centrosome-, kinetochore- and chromosome-associated regulators of mitosis. Our data illuminated the role for FA signaling in three critical stages of cell division: (1) the spindle assembly checkpoint, (2) anaphase and (3) cytokinesis. Thus, we employed live phase-contrast imaging of primary FANCA-/- patient cells in comparison to gene-corrected cells to separately quantify aberrations in (1) chromosome congression and metaphase-anaphase transition (SAC malfunction), (2) execution of anaphase and (3) completion of cytokinesis. Our findings further our understanding of human cell cycle control and provide new insights into the origins of genomic instability in Fanconi anemia by establishing mechanistic connection between the FANCA protein and key mitotic signaling networks. The identification of cell division pathways regulated by FANCA has implications for future targeted drug development in Fanconi anemia and FA-deficient malignancies in the general population. Disclosures: No relevant conflicts of interest to declare.

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