scholarly journals When size matters – coordination of growth and cell cycle in bacteria

2019 ◽  
Author(s):  
Joanna Morcinek-Orłowska ◽  
Justyna Galińska ◽  
Monika Katarzyna Glinkowska
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Driving Forces ◽  
Control Strategies ◽  
Bacterial Species ◽  
Control Cell ◽  
Genetic Material ◽  
Alternative View ◽  
Time Interval ◽  
Bacterial Cells

Bacterial cells often inhabit environments where conditions can change rapidly. Therefore, a lot of bacterial species developed control strategies allowing them to grow and divide very fast during feast and slow down both parameters during famine. Under rich nutritional conditions, fast-growing bacteria can divide with time interval equal to half of the period required to synthesize their chromosomes. This is possible due to multifork replication which allows ancestor cells to start copying genetic material for their descendants. This reproduction scheme was most likely selected for, since it enables maximization of growth rate and hence – effective competition for resources, while ensuring that DNA replication will not become limiting for cell division. Even with this complexity of cell cycle, isogenic bacterial cells grown under defined conditions display remarkably narrow distribution of sizes. This may suggest that mechanisms exists to control cell size at division step. Alternative view, with great support in experimental data is that the only step coordinated with cell growth is the initiation of DNA replication. Despite decades of research we are still not sure what the driving forces in bacterial cell cycle are. In this work we review recent advances in understanding coordination of growth with DNA replication coming from single cell studies and systems biology approaches.

scholarly journals Regulation of Cell Division in Bacteria by Monitoring Genome Integrity and DNA Replication Status

2019 ◽  
Vol 202 (2) ◽  
Author(s):  
Peter E. Burby ◽  
Lyle A. Simmons
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Division ◽  
Dna Replication ◽  
Cell Cycle Progression ◽  
Genome Instability ◽  
Sos Response ◽  
Bacterial Cells ◽  
Cycle Progression ◽  
Content Type

ABSTRACT All organisms regulate cell cycle progression by coordinating cell division with DNA replication status. In eukaryotes, DNA damage or problems with replication fork progression induce the DNA damage response (DDR), causing cyclin-dependent kinases to remain active, preventing further cell cycle progression until replication and repair are complete. In bacteria, cell division is coordinated with chromosome segregation, preventing cell division ring formation over the nucleoid in a process termed nucleoid occlusion. In addition to nucleoid occlusion, bacteria induce the SOS response after replication forks encounter DNA damage or impediments that slow or block their progression. During SOS induction, Escherichia coli expresses a cytoplasmic protein, SulA, that inhibits cell division by directly binding FtsZ. After the SOS response is turned off, SulA is degraded by Lon protease, allowing for cell division to resume. Recently, it has become clear that SulA is restricted to bacteria closely related to E. coli and that most bacteria enforce the DNA damage checkpoint by expressing a small integral membrane protein. Resumption of cell division is then mediated by membrane-bound proteases that cleave the cell division inhibitor. Further, many bacterial cells have mechanisms to inhibit cell division that are regulated independently from the canonical LexA-mediated SOS response. In this review, we discuss several pathways used by bacteria to prevent cell division from occurring when genome instability is detected or before the chromosome has been fully replicated and segregated.

scholarly journals Cell Cycle Regulation of DNA Replication Initiator Factor Dbf4p

1999 ◽  
Vol 19 (6) ◽  
pp. 4270-4278 ◽  
Author(s):  
Liang Cheng ◽  
Tim Collyer ◽  
Christopher F. J. Hardy
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Replication ◽  
Genetic Material ◽  
Anaphase Promoting Complex ◽  
Initiator Protein ◽  
Evolutionarily Conserved ◽  
M Phase ◽  
Cycle Regulation ◽  
Replication Initiator

ABSTRACT The precise duplication of eukaryotic genetic material takes place once and only once per cell cycle and is dependent on the completion of the previous mitosis. Two evolutionarily conserved kinases, the cyclin B (Clb)/cyclin-dependent kinase (Cdk/Cdc28p) and Cdc7p along with its interacting factor Dbf4p, are required late in G1 to initiate DNA replication. We have determined that the levels of Dbf4p are cell cycle regulated. Dbf4p levels increase as cells begin S phase and remain high through late mitosis, after which they decline dramatically as cells begin the next cell cycle. We report that Dbf4p levels are sensitive to mutations in key components of the anaphase-promoting complex (APC). In addition, Dbf4p is modified in response to DNA damage, and this modification is dependent upon the DNA damage response pathway. We had previously shown that Dbf4p interacts with the M phase polo-like kinase Cdc5p, a key regulator of the APC late in mitosis. These results further link the actions of the initiator protein, Dbf4p, to the completion of mitosis and suggest possible roles for Dbf4p during progression through mitosis.

scholarly journals Instructive simulation of the bacterial cell division cycle

Microbiology ◽  
2011 ◽  
Vol 157 (7) ◽  
pp. 1876-1885 ◽  
Author(s):  
Arieh Zaritsky ◽  
Ping Wang ◽  
Norbert O. E. Vischer
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Dna Replication ◽  
Cell Mass ◽  
Time Lapse ◽  
Replication Initiation ◽  
Bacterial Cells ◽  
Bacterial Cell Division ◽  
Cycle Simulation ◽  
New Ideas

The coupling between chromosome replication and cell division includes temporal and spatial elements. In bacteria, these have globally been resolved during the last 40 years, but their full details and action mechanisms are still under intensive study. The physiology of growth and the cell cycle are reviewed in the light of an established dogma that has formed a framework for development of new ideas, as exemplified here, using the Cell Cycle Simulation (CCSim) program. CCSim, described here in detail for the first time, employs four parameters related to time (replication, division and inter-division) and size (cell mass at replication initiation) that together are sufficient to describe bacterial cells under various conditions and states, which can be manipulated environmentally and genetically. Testing the predictions of CCSim by analysis of time-lapse micrographs of Escherichia coli during designed manipulations of the rate of DNA replication identified aspects of both coupling elements. Enhanced frequencies of cell division were observed following an interval of reduced DNA replication rate, consistent with the prediction of a minimum possible distance between successive replisomes (an eclipse). As a corollary, the notion that cell poles are not always inert was confirmed by observed placement of division planes at perpendicular planes in monstrous and cuboidal cells containing multiple, segregating nucleoids.

scholarly journals Response of single bacterial cells to stress gives rise to complex history dependence at the population level

2016 ◽  
Vol 113 (15) ◽  
pp. 4224-4229 ◽  
Author(s):  
Roland Mathis ◽  
Martin Ackermann
Keyword(s):  
Cell Cycle ◽  
Sodium Chloride ◽  
Caulobacter Crescentus ◽  
Single Cells ◽  
Population Level ◽  
Time Interval ◽  
Bacterial Cells ◽  
History Dependence ◽  
Cell Cycle Synchronization ◽  
Subsequent Exposure

Most bacteria live in ever-changing environments where periods of stress are common. One fundamental question is whether individual bacterial cells have an increased tolerance to stress if they recently have been exposed to lower levels of the same stressor. To address this question, we worked with the bacteriumCaulobacter crescentusand asked whether exposure to a moderate concentration of sodium chloride would affect survival during later exposure to a higher concentration. We found that the effects measured at the population level depended in a surprising and complex way on the time interval between the two exposure events: The effect of the first exposure on survival of the second exposure was positive for some time intervals but negative for others. We hypothesized that the complex pattern of history dependence at the population level was a consequence of the responses of individual cells to sodium chloride that we observed: (i) exposure to moderate concentrations of sodium chloride caused delays in cell division and led to cell-cycle synchronization, and (ii) whether a bacterium would survive subsequent exposure to higher concentrations was dependent on the cell-cycle state. Using computational modeling, we demonstrated that indeed the combination of these two effects could explain the complex patterns of history dependence observed at the population level. Our insight into how the behavior of single cells scales up to processes at the population level provides a perspective on how organisms operate in dynamic environments with fluctuating stress exposure.

scholarly journals Multiplication and division: Archaic modes of DNA replication initiation

2004 ◽  
Vol 26 (3) ◽  
pp. 11-15
Author(s):  
Nicholas P. Robinson ◽  
Stephen D. Bell
Keyword(s):  
Cell Division ◽  
Dna Replication ◽  
Genetic Material ◽  
Replication Initiation ◽  
Eukaryotic Cells ◽  
Bacterial Cells ◽  
Proliferating Cells ◽  
Dna Replication Initiation ◽  
The Third ◽  
Single Origin

Proliferating cells must produce a complete and accurate copy of their genetic material by DNA replication prior to cell division, and in all organisms this duplication begins at discrete sites known as replication origins. In eukaryotic cells, DNA synthesis is initiated from a large number of these regions, whereas bacterial cells replicate less complex genomes from a single origin. It is only in recent years that the process of replication initiation has become elucidated in the third domain of life, the Archaea.

scholarly journals Multi-generational Analysis and Manipulation of Chromosomes in a Polyploid Cyanobacterium

2019 ◽  
Author(s):  
Kristin A. Moore ◽  
Jian Wei Tay ◽  
Jeffrey C. Cameron
Keyword(s):  
Dna Replication ◽  
Cell Growth ◽  
Photosynthetic Bacteria ◽  
Bacterial Species ◽  
Genetic Material ◽  
Time Lapse ◽  
Time Lapse Microscopy ◽  
Life On Earth ◽  
Microbial Dna

ABSTRACTFaithful inheritance of genetic material from one generation to the next is an essential process for all life on earth. Much of what is known about microbial DNA replication and inheritance has been learned from a small number of bacterial species that share many common traits. Whether these pathways are conserved across the great diversity of the microbiome remains unclear. To address this question, we studied chromosome dynamics in a polyploid photosynthetic bacteria using single cell, time-lapse microscopy over multi-generation lineages in conjunction with inducible CRISPR-interference and fluorescent chromosome labeling. With this method we demonstrated the long-term consequences of manipulating parameters such as cell growth, cell division, and DNA replication and segregation on chromosome regulation in a polyploid bacterial species. We find that these bacteria are surprisingly resilient to chromosome disruption resulting in continued cell growth when DNA replication is inhibited and even in the complete absence of chromosomes.

scholarly journals PAR-4/LKB1 regulates DNA replication during asynchronous division of the early C. elegans embryo

2014 ◽  
Vol 205 (4) ◽  
pp. 447-455 ◽  
Author(s):  
Laura Benkemoun ◽  
Catherine Descoteaux ◽  
Nicolas T. Chartier ◽  
Lionel Pintard ◽  
Jean-Claude Labbé
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Control Cell ◽  
Cycle Duration ◽  
Cell Stage ◽  
C Elegans ◽  
Stage Embryo ◽  
Regulation Of Cell Cycle

Regulation of cell cycle duration is critical during development, yet the underlying molecular mechanisms are still poorly understood. The two-cell stage Caenorhabditis elegans embryo divides asynchronously and thus provides a powerful context in which to study regulation of cell cycle timing during development. Using genetic analysis and high-resolution imaging, we found that deoxyribonucleic acid (DNA) replication is asymmetrically regulated in the two-cell stage embryo and that the PAR-4 and PAR-1 polarity proteins dampen DNA replication dynamics specifically in the posterior blastomere, independently of regulators previously implicated in the control of cell cycle timing. Our results demonstrate that accurate control of DNA replication is crucial during C. elegans early embryonic development and further provide a novel mechanism by which PAR proteins control cell cycle progression during asynchronous cell division.

scholarly journals Effects of oriC relocation on control of replication initiation in Bacillus subtilis

Microbiology ◽  
2009 ◽  
Vol 155 (9) ◽  
pp. 3070-3082 ◽  
Author(s):  
Shigeki Moriya ◽  
Yoshikazu Kawai ◽  
Sakiko Kaji ◽  
Adrian Smith ◽  
Elizabeth J. Harry ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bacillus Subtilis ◽  
Dna Replication ◽  
Negative Control ◽  
Replication Initiation ◽  
Control Mechanisms ◽  
Bacterial Cells ◽  
Wild Type ◽  
Dna Replication Initiation ◽  
In The Wild

In bacteria, DNA replication initiation is tightly regulated in order to coordinate chromosome replication with cell growth. In Escherichia coli, positive factors and negative regulatory mechanisms playing important roles in the strict control of DNA replication initiation have been reported. However, it remains unclear how bacterial cells recognize the right time for replication initiation during the cell cycle. In the Gram-positive bacterium Bacillus subtilis, much less is known about the regulation of replication initiation, specifically, regarding negative control mechanisms which ensure replication initiation only once per cell cycle. Here we report that replication initiation was greatly enhanced in strains that had the origin of replication (oriC) relocated to various loci on the chromosome. When oriC was relocated to new loci further than 250 kb counterclockwise from the native locus, replication initiation became asynchronous and earlier than in the wild-type cells. In two oriC-relocated strains (oriC at argG or pnbA, 25 ° or 30 ° on the 36 ° chromosome map, respectively), DnaA levels were higher than in the wild-type but not enough to cause earlier initiation of replication. Our results suggest that the initiation capacity of replication is accumulated well before the actual time of initiation, and its release may be suppressed by a unique DNA structure formed near the native oriC locus.

Mechanisms of Antibiotic Resistance

2019 ◽  
Author(s):  
Ruaridh Buchanan ◽  
David Wareham
Keyword(s):  
Antibiotic Resistance ◽  
Dna Replication ◽  
Selection Pressure ◽  
Bacterial Species ◽  
Resistance Mechanisms ◽  
Drug Resistant ◽  
Bacterial Cells ◽  
Gram Negative ◽  
The Times ◽  
Gram Negative Organisms

Although antibiotic resistance has come to the fore in the media and clinical practice relatively recently, it is by no means a new issue; Alexander Fleming discussed the risks of penicillin resistance more than sixty years ago, but even he was behind the times. Bacteria have been competing with each other for millions of years, producing compounds which kill or inhibit other species—it is not surprising that bacteria have evolved defence mechanisms. Current major concerns are the rise of pan-drug resistant gram-negative organisms and the spread of multi-drug resistant TB. Bacterial cells turn over rapidly—this rate of reproduction leads to many errors in DNA replication. Many of these mutations are deleterious to the organism, but others confer new properties, such as changing the structure of an enzyme. The application of selection pressure in the form of antimicrobial therapy leads to the survival of mutants that have randomly acquired resistance mechanisms. There are two useful ways to categorize resistance mechanisms: by how bacterial cells acquire them and by the physical mechanism of action. The types of acquisition have important infection control ramifications. Resistance can be subdivided into three separate categories: ● Intrinsic resistance— mechanisms hard coded into all members of a bacterial species at the chromosomal level. If an organism’s antibiogram suggests susceptibility to an agent to which it should be intrinsically resistant, further work should be done to check that the identification is correct. Examples include gram-negative bacteria being resistant to glycopeptides due to the outer cell membrane, anaerobes being resistant to aminoglycosides due to lack of an uptake mechanism, and amoxicillin resistance in Klebsiella due to beta-lactamase production. ● Mutational resistance—resistance that arises randomly due to DNA replication errors in conjunction with selection pressure applied by antimicrobial agents. This is the basis of the majority of the mechanisms detailed in this chapter. ● Transferrable resistance— mutational resistance that is passed horizontally from the bacterium in which it arose to another cell, possibly of a different species entirely. This happens through either transposons (DNA that incorporates into the bacterial chromosome) or plasmids (rings of DNA that replicate independent of the main chromosome).

scholarly journals The Effect of Dia2 Protein Deficiency on the Cell Cycle, Cell Size, and Recruitment of Ctf4 Protein in Saccharomyces cerevisiae

Molecules ◽  
2021 ◽  
Vol 27 (1) ◽  
pp. 97
Author(s):  
Aneliya Ivanova ◽  
Aleksandar Atemin ◽  
Sonya Uzunova ◽  
Georgi Danovski ◽  
Radoslav Aleksandrov ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Replication ◽  
Cell Size ◽  
Ubiquitin Ligase ◽  
Driving Forces ◽  
S Phase ◽  
Cycle Duration ◽  
Cell Cycles ◽  
Cell Cycle Duration

Cells have evolved elaborate mechanisms to regulate DNA replication machinery and cell cycles in response to DNA damage and replication stress in order to prevent genomic instability and cancer. The E3 ubiquitin ligase SCFDia2 in S. cerevisiae is involved in the DNA replication and DNA damage stress response, but its effect on cell growth is still unclear. Here, we demonstrate that the absence of Dia2 prolongs the cell cycle by extending both S- and G2/M-phases while, at the same time, activating the S-phase checkpoint. In these conditions, Ctf4—an essential DNA replication protein and substrate of Dia2—prolongs its binding to the chromatin during the extended S- and G2/M-phases. Notably, the prolonged cell cycle when Dia2 is absent is accompanied by a marked increase in cell size. We found that while both DNA replication inhibition and an absence of Dia2 exerts effects on cell cycle duration and cell size, Dia2 deficiency leads to a much more profound increase in cell size and a substantially lesser effect on cell cycle duration compared to DNA replication inhibition. Our results suggest that the increased cell size in dia2∆ involves a complex mechanism in which the prolonged cell cycle is one of the driving forces.

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