scholarly journals The function of the prereplicative complex and SCF complex components during Drosophila wing development

2017 ◽  
Author(s):  
Hidetsugu Kohzaki
Keyword(s):  
Dna Replication ◽  
Protein Degradation ◽  
Cell Cycle Progression ◽  
Control Cell ◽  
Wing Development ◽  
Replication Machinery ◽  
Chromosomal Dna ◽  
Scf Complex ◽  
Prereplicative Complex ◽  
Complex Components

AbstractChromosomal DNA replication machinery functions in the growing cells and organs in multicellular organisms. We previously demonstrated that its knockdown in several tissues of Drosophila led to a rough eye phenotype, the loss of bristles in the eye and female sterile. In this paper, we investigated in detail the wing phenotype using RNAi flies, and observed that the knockdown not only of Mcm10 but also of some other prereplicative complex components demonstrated wing phenotypes, using Gal4-driver flies. Surprisingly, some SCF complex components, which control cell cycle progression via protein degradation, also showed the wing phenotype. These results showed that the DNA replication machinery contributes to wing development independent of growth, probably through defects in DNA replication and protein degradation at specific places and times.Summary statementWe recently outlined the prereplicative complex components, including Mcm10 and SCF complex functions, during Drosophila wing development. In this paper, we detail these findings.

scholarly journals Asymmetric division yields progeny cells with distinct modes of regulating cell cycle-dependent chromosome methylation

2019 ◽  
Vol 116 (31) ◽  
pp. 15661-15670 ◽  
Author(s):  
Xiaofeng Zhou ◽  
Jiarui Wang ◽  
Jonathan Herrmann ◽  
W. E. Moerner ◽  
Lucy Shapiro
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Single Molecule ◽  
Transcriptional Activation ◽  
Dna Methyltransferase ◽  
Cell Cycle Progression ◽  
Asymmetric Cell Division ◽  
Chromosomal Dna ◽  
C Terminus ◽  
Cycle Dependent

The cell cycle-regulated methylation state of Caulobacter DNA mediates the temporal control of transcriptional activation of several key regulatory proteins. Temporally controlled synthesis of the CcrM DNA methyltransferase and Lon-mediated proteolysis restrict CcrM to a specific time in the cell cycle, thereby allowing the maintenance of the hemimethylated state of the chromosome during the progression of DNA replication. We determined that a chromosomal DNA-based platform stimulates CcrM degradation by Lon and that the CcrM C terminus both binds to its DNA substrate and is recognized by the Lon protease. Upon asymmetric cell division, swarmer and stalked progeny cells employ distinct mechanisms to control active CcrM. In progeny swarmer cells, CcrM is completely degraded by Lon before its differentiation into a replication-competent stalked cell later in the cell cycle. In progeny stalked cells, however, accumulated CcrM that has not been degraded before the immediate initiation of DNA replication is sequestered to the cell pole. Single-molecule imaging demonstrated physical anticorrelation between sequestered CcrM and chromosomal DNA, thus preventing DNA remethylation. The distinct control of available CcrM in progeny swarmer and stalked cells serves to protect the hemimethylated state of DNA during chromosome replication, enabling robustness of cell cycle progression.

scholarly journals The dynamics of replication licensing in live Caenorhabditis elegans embryos

2012 ◽  
Vol 196 (2) ◽  
pp. 233-246 ◽  
Author(s):  
Remi Sonneville ◽  
Matthieu Querenet ◽  
Ashley Craig ◽  
Anton Gartner ◽  
J. Julian Blow
Keyword(s):  
Caenorhabditis Elegans ◽  
Dna Replication ◽  
Dna Binding ◽  
Feedback Loop ◽  
Origin Recognition Complex ◽  
S Phase ◽  
Chromosomal Dna ◽  
M Phase ◽  
Prereplicative Complex

Accurate DNA replication requires proper regulation of replication licensing, which entails loading MCM-2–7 onto replication origins. In this paper, we provide the first comprehensive view of replication licensing in vivo, using video microscopy of Caenorhabditis elegans embryos. As expected, MCM-2–7 loading in late M phase depended on the prereplicative complex (pre-RC) proteins: origin recognition complex (ORC), CDC-6, and CDT-1. However, many features we observed have not been described before: GFP–ORC-1 bound chromatin independently of ORC-2–5, and CDC-6 bound chromatin independently of ORC, whereas CDT-1 and MCM-2–7 DNA binding was interdependent. MCM-3 chromatin loading was irreversible, but CDC-6 and ORC turned over rapidly, consistent with ORC/CDC-6 loading multiple MCM-2–7 complexes. MCM-2–7 chromatin loading further reduced ORC and CDC-6 DNA binding. This dynamic behavior creates a feedback loop allowing ORC/CDC-6 to repeatedly load MCM-2–7 and distribute licensed origins along chromosomal DNA. During S phase, ORC and CDC-6 were excluded from nuclei, and DNA was overreplicated in export-defective cells. Thus, nucleocytoplasmic compartmentalization of licensing factors ensures that DNA replication occurs only once.

The haloarchaeal chromosome replication machinery

2009 ◽  
Vol 37 (1) ◽  
pp. 108-113 ◽  
Author(s):  
Stuart A. MacNeill
Keyword(s):  
Dna Replication ◽  
Replication Fork ◽  
Biochemical Analysis ◽  
Structure And Function ◽  
Haloferax Volcanii ◽  
Eukaryotic Cells ◽  
Replication Machinery ◽  
Chromosomal Dna ◽  
Biochemical Studies ◽  
And Function

The powerful combination of genetic and biochemical analysis has provided many key insights into the structure and function of the chromosomal DNA replication machineries of bacterial and eukaryotic cells. In contrast, in the archaea, biochemical studies have dominated, mainly due to the absence of efficient genetic systems for these organisms. This situation is changing, however, and, in this regard, the genetically tractable haloarchaea Haloferax volcanii and Halobacterium sp. NRC-1 are emerging as key models. In the present review, I give an overview of the components of the replication machinery in the haloarchaea, with particular emphasis on the protein factors presumed to travel with the replication fork.

scholarly journals Regulated Proteolysis in Bacteria

2018 ◽  
Vol 87 (1) ◽  
pp. 677-696 ◽  
Author(s):  
Samar A. Mahmoud ◽  
Peter Chien
Keyword(s):  
Protein Degradation ◽  
Cell Cycle Progression ◽  
Control Cell ◽  
Regulatory Proteins ◽  
Cycle Progression ◽  
Balanced Growth ◽  
Living Things ◽  
Energy Dependent ◽  
Shed Light ◽  
Control Cell Cycle Progression

Regulated proteolysis is a vital process that affects all living things. Bacteria use energy-dependent AAA+ proteases to power degradation of misfolded and native regulatory proteins. Given that proteolysis is an irreversible event, specificity and selectivity in degrading substrates are key. Specificity is often augmented through the use of adaptors that modify the inherent specificity of the proteolytic machinery. Regulated protein degradation is intricately linked to quality control, cell-cycle progression, and physiological transitions. In this review, we highlight recent work that has shed light on our understanding of regulated proteolysis in bacteria. We discuss the role AAA+ proteases play during balanced growth as well as how these proteases are deployed during changes in growth. We present examples of how protease selectivity can be controlled in increasingly complex ways. Finally, we describe how coupling a core recognition determinant to one or more modifying agents is a general theme for regulated protein degradation.

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 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.

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