Thematische Bibliographien / Fork restart

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Auswahl der wissenschaftlichen Literatur zum Thema „Fork restart“

Autor: Grafiati

Veröffentlicht am 25. Januar 2025

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Zeitschriftenartikel zum Thema "Fork restart"

Gold, Michaela A., Jenna M. Whalen, Karine Freon, Zixin Hong, Ismail Iraqui, Sarah A. E. Lambert und Catherine H. Freudenreich. „Restarted replication forks are error-prone and cause CAG repeat expansions and contractions“. PLOS Genetics 17, Nr. 10 (21.10.2021): e1009863. http://dx.doi.org/10.1371/journal.pgen.1009863.

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Disease-associated trinucleotide repeats form secondary DNA structures that interfere with replication and repair. Replication has been implicated as a mechanism that can cause repeat expansions and contractions. However, because structure-forming repeats are also replication barriers, it has been unclear whether the instability occurs due to slippage during normal replication progression through the repeat, slippage or misalignment at a replication stall caused by the repeat, or during subsequent replication of the repeat by a restarted fork that has altered properties. In this study, we have specifically addressed the fidelity of a restarted fork as it replicates through a CAG/CTG repeat tract and its effect on repeat instability. To do this, we used a well-characterized site-specific replication fork barrier (RFB) system in fission yeast that creates an inducible and highly efficient stall that is known to restart by recombination-dependent replication (RDR), in combination with long CAG repeat tracts inserted at various distances and orientations with respect to the RFB. We find that replication by the restarted fork exhibits low fidelity through repeat sequences placed 2–7 kb from the RFB, exhibiting elevated levels of Rad52- and Rad8ScRad5/HsHLTF-dependent instability. CAG expansions and contractions are not elevated to the same degree when the tract is just in front or behind the barrier, suggesting that the long-traveling Polδ-Polδ restarted fork, rather than fork reversal or initial D-loop synthesis through the repeat during stalling and restart, is the greatest source of repeat instability. The switch in replication direction that occurs due to replication from a converging fork while the stalled fork is held at the barrier is also a significant contributor to the repeat instability profile. Our results shed light on a long-standing question of how fork stalling and RDR contribute to expansions and contractions of structure-forming trinucleotide repeats, and reveal that tolerance to replication stress by fork restart comes at the cost of increased instability of repetitive sequences.

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Petermann, Eva, und Thomas Helleday. „Pathways of mammalian replication fork restart“. Nature Reviews Molecular Cell Biology 11, Nr. 10 (15.09.2010): 683–87. http://dx.doi.org/10.1038/nrm2974.

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Pepe, Alessandra, und Stephen C. West. „MUS81-EME2 Promotes Replication Fork Restart“. Cell Reports 7, Nr. 4 (Mai 2014): 1048–55. http://dx.doi.org/10.1016/j.celrep.2014.04.007.

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Dyankova-Danovska, Teodora, Sonya Uzunova, Georgi Danovski, Rumen Stamatov, Petar-Bogomil Kanev, Aleksandar Atemin, Aneliya Ivanova, Radoslav Aleksandrov und Stoyno Stoynov. „In and out of Replication Stress: PCNA/RPA1-Based Dynamics of Fork Stalling and Restart in the Same Cell“. International Journal of Molecular Sciences 26, Nr. 2 (14.01.2025): 667. https://doi.org/10.3390/ijms26020667.

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Replication forks encounter various impediments, which induce fork stalling and threaten genome stability, yet the precise dynamics of fork stalling and restart at the single-cell level remain elusive. Herein, we devise a live-cell microscopy-based approach to follow hydroxyurea-induced fork stalling and subsequent restart at 30 s resolution. We measure two distinct processes during fork stalling. One is rapid PCNA removal, which reflects the drop in DNA synthesis. The other is gradual RPA1 accumulation up to 2400 nt of ssDNA per fork despite an active intra-S checkpoint. Restoring the nucleotide pool enables a prompt restart without post-replicative ssDNA and a smooth cell cycle progression. ATR, but not ATM inhibition, accelerates hydroxyurea-induced RPA1 accumulation nine-fold, leading to RPA1 exhaustion within 20 min. Fork restart under ATR inhibition led to the persistence of ~600 nt ssDNA per fork after S-phase, which reached 2500 nt under ATR/ATM co-inhibition, with both scenarios leading to mitotic catastrophe. MRE11 inhibition had no effect on PCNA/RPA1 dynamics regardless of ATR activity. E3 ligase RAD18 was recruited at stalled replication forks in parallel to PCNA removal. Our results shed light on fork dynamics during nucleotide depletion and provide a valuable tool for interrogating the effects of replication stress-inducing anti-cancer agents.

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Longerich, S., und P. Sung. „Clearance of roadblocks in replication fork restart“. Proceedings of the National Academy of Sciences 108, Nr. 34 (08.08.2011): 13881–82. http://dx.doi.org/10.1073/pnas.1110698108.

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Iyer, Divya R., und Alan D. D’Andrea. „Fork restart: unloading FANCD2 to travel ahead“. Molecular Cell 83, Nr. 20 (Oktober 2023): 3590–92. http://dx.doi.org/10.1016/j.molcel.2023.09.027.

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Thangavel, Saravanabhavan, Matteo Berti, Maryna Levikova, Cosimo Pinto, Shivasankari Gomathinayagam, Marko Vujanovic, Ralph Zellweger et al. „DNA2 drives processing and restart of reversed replication forks in human cells“. Journal of Cell Biology 208, Nr. 5 (02.03.2015): 545–62. http://dx.doi.org/10.1083/jcb.201406100.

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Accurate processing of stalled or damaged DNA replication forks is paramount to genomic integrity and recent work points to replication fork reversal and restart as a central mechanism to ensuring high-fidelity DNA replication. Here, we identify a novel DNA2- and WRN-dependent mechanism of reversed replication fork processing and restart after prolonged genotoxic stress. The human DNA2 nuclease and WRN ATPase activities functionally interact to degrade reversed replication forks with a 5′-to-3′ polarity and promote replication restart, thus preventing aberrant processing of unresolved replication intermediates. Unexpectedly, EXO1, MRE11, and CtIP are not involved in the same mechanism of reversed fork processing, whereas human RECQ1 limits DNA2 activity by preventing extensive nascent strand degradation. RAD51 depletion antagonizes this mechanism, presumably by preventing reversed fork formation. These studies define a new mechanism for maintaining genome integrity tightly controlled by specific nucleolytic activities and central homologous recombination factors.

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Eksi, Sebnem Ece, und Joshua C. Saldivar. „Cohesin Is Out for Stalled Replication Fork Restart“. Developmental Cell 52, Nr. 6 (März 2020): 675–76. http://dx.doi.org/10.1016/j.devcel.2020.03.001.

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Marians, Kenneth J. „PriA-directed replication fork restart in Escherichia coli“. Trends in Biochemical Sciences 25, Nr. 4 (April 2000): 185–89. http://dx.doi.org/10.1016/s0968-0004(00)01565-6.

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Marians, Kenneth J. „Mechanisms of replication fork restart in Escherichia coli“. Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, Nr. 1441 (29.01.2004): 71–77. http://dx.doi.org/10.1098/rstb.2003.1366.

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Replication of the genome is crucial for the accurate transmission of genetic information. It has become clear over the last decade that the orderly progression of replication forks in both prokaryotes and eukaryotes is disrupted with high frequency by encounters with various obstacles either on or in the template strands. Survival of the organism then becomes dependent on both removal of the obstruction and resumption of replication. This latter point is particularly important in bacteria, where the number of replication forks per genome is nominally only two. Replication restart in Escherichia coli is accomplished by the action of the restart primosomal proteins, which use both recombination intermediates and stalled replication forks as substrates for loading new replication forks. These reactions have been reconstituted with purified recombination and replication proteins.

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Dissertationen zum Thema "Fork restart"

Berti, Matteo. „New mechanistic insight into replication fork reversal and restart“. Doctoral thesis, Scuola Normale Superiore, 2013. http://hdl.handle.net/11384/85975.

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An emerging model of how stalled or damaged forks are processed is that replication fork s can reverse to aid repair of the damage. The first evidence that replication forks regress in human cells came from a recent study with topoisomerase I (T op 1) inhibitors, an important class of anticancer drugs currently in clinical use. Their cytotoxicit y, and thus their efficacy, has been generally linked to their ability to cause the accumulation of DNA nicks, which are later converted into double - stranded breaks (DSBs) by the collision of the DNA replication fork with the primary lesion. The discovery that replic ation forks can regress upon Top 1 inhibition provided new insight into the molecular basis of Top 1 cytotoxicity by showing that clinically relevant , nanomolar doses of Top 1 poisons induce replication fork slowing and reversal in a process that c an be uncoupled from DSB formation and requires poly(ADP - ribose) polymerase 1 ( PARP1) activity. However, w hether re versed forks can efficiently restart and wh ich factors are involved in this mechanism was still unknown. In this thesis , u sing a combination of biochemical and cellular approaches, we provided the first evidence that regressed forks can restart in vivo and identified a key role for the human RECQ1 helicase in promoting efficient re plication fork restart after Top 1 inhibition that is not shared by other human RecQ members . Our data also provided the first insight into the molecular role of PARP1 in fork reversal by showing that the poly(ADP - ribosyl)ation activity of PARP inhibits RECQ1 activity on replication forks after Top 1 inhibition. Thus, PARP activity is not required to form, but rather to "accumulate" reversed fork structures by maintaining/protecting them from a counteracting activity (RECQ1), which would otherwise cause an untimely restart of reversed forks, leading to DSB formation. The identification of a specific and controlled biochemical activity that drives the restart of reversed forks strongly supports the physiological relevance of this DNA transaction during replication stress in human cells. Moreover, our studies provide new mec hanistic insights into the roles of RECQ1 and PARP 1 in DNA replication and offer molecular perspectives to potentiate chemo therapeutic regimens based on Top 1 inhibition.

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Schalbetter, Stephanie. „Genome instability induced by structured DNA and replication fork restart“. Thesis, University of Sussex, 2012. http://sro.sussex.ac.uk/id/eprint/38853/.

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DNA replication is a central mechanism to all forms of life. Errors occurring during DNA replication can result in mutagenesis and genome rearrangements, which can cause various diseases. In this work I have investigated the stability of direct tandem repeats (TRs) in the context of replication and replication-associated repair mechanisms. During DNA replication the replication fork encounters many obstacles, such as DNA-protein barriers, secondary DNA structures and DNA lesions. How and if replication resumes or restarts in these circumstances in order to complete genome replication is not well understood and the ﬁdelity of replication in response to such obstacles remains unclear. I have developed TR assays to assess replication errors in the context of replication fork restart and secondary structures. The results suggest that structured DNA (G4) can cause instability of TRs in the context of normal replication and that restarted replication can be intrinsically error-prone. Surprisingly, the mutagenic effect of G4-DNA on TR stability was not elevated in the context of replication fork restart. Therefore, deletions of TRs containing G4-DNA are not more susceptible to the compromised fidelity of a restarted replication fork. Structures such as stalled replication forks can induce checkpoint responses to maintain genome stability. The stabilisation of replication forks is central in the response to replication stress. These protective mechanisms include the regulation of enzymatic activities. Mus81-Eme1 is a structure-specific endonuclease which is regulated by the DNA replication checkpoint, but has also been shown to be required for replication fork restart in certain circumstances. In collaboration with Professor Neil McDonald I analysed a novel domain identified in Mus81-Eme1. Mutagenesis of key residues deduced from the protein structure and comparison of their genetic analysis to known phenotypes of Mus81-Eme1 suggests distinct requirements for this domain.

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Nguyen, Michael Ong. „Investigating the molecular mechanism of replication restart in fission yeast“. Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:b90fff59-d5b7-43b2-b648-61c0bc977ee9.

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Successful replication of the genome during each cell cycle requires that every replication fork merge with its opposing fork. However, lesions in the template DNA or protein-DNA barriers often impede replication forks and threaten the timely completion of genome duplication. If a fork encounters a replication fork barrier (RFB), it can be subject to a variety of fates. In some cases the replisome is maintained in a manner such that it can resume DNA synthesis when the barrier is removed. Alternatively the stalled fork is simply held in a competent state to merge with the opposing fork when it arrives. However, fork stalling can also precipitate dissociation of the replisome (fork collapse) or even fork breakage. If this happens the recombination machinery can intervene to restore DNA integrity and restart replication, albeit with a risk of causing deleterious genetic change if ectopic homologous sequences are recombined. I have exploited a site-specific RFB in fission yeast termed RTS1 to investigate the consequences of perturbing a single replication fork. RTS1 is a polar RFB (i.e. it blocks fork progression in a unidirectional fashion), enabling replication to be completed by the opposing fork. Despite this, fork blockage at RTS1 triggers a strong recombinational response that is able to restart DNA synthesis, which at least initially is highly error prone. Here, I present my work in establishing a live cell imaging approach to visualizing the recombinational response at the RTS1 RFB, demonstrating that the majority of cells initiate recombination-dependent replication (RDR). RDR begins within a few minutes of fork blockage and is only curtailed by the arrival of the opposing fork. It depends on the Rad52 protein, which remains associated with the restarted fork and whose presence correlates with its infidelity. I also illustrate the significance of various genetic factors, including Rad51, the Rad51 mediators, Fml1 helicase, Rad54 translocase, Pfh1 sweepase, and Cds1 checkpoint kinase, in modulating Rad52 localization and block-induced recombination at the RTS1 RFB.

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Chakraborty, Shrena. „Multifaceted role of SUMOylation in maintaining centromere biology and regulation of replication fork restart in Schizosaccharomyces pombe“. Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL069.

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Les défauts dans le processus de réplication de l'ADN, connus sous le nom de stress de réplication, sont une source majeure d'instabilité du génome qui favorise le développement du cancer. La résolution du stress de réplication se produit dans un noyau compartimenté qui présente des capacités distinctes de réparation de l'ADN. Les fourches de réplication stressées présentent une mobilité accrue et se déplacent vers la périphérie du noyau pour s'ancrer aux complexes du pore nucléaire, une structure hautement conservée de l'enveloppe nucléaire qui agit comme un site d'amarrage pour permettre à d'autres voies de réparation de l'ADN de se mettre en place. Ces changements dans le positionnement nucléaire sont régulés par le métabolisme des petits modificateurs de type ubiquitine (SUMO), qui jouent un rôle essentiel dans la ségrégation spatiale des activités de la voie de la recombinaison homologue (RH). Nos travaux antérieurs chez la levure de fission ont établi qu'une fourche de réplication bloquée par une protéine liée à l'ADN se relocalise et s'ancre au NPC d'une manière SUMO-dépendante. Les chaînes SUMO déclenchent la relocalisation des fourches arrêtées à la périphérie du noyau pour s'ancrer au NPC. Cet ancrage nécessite les chaînes SUMO et la voie de l'ubiquitine ligase ciblée par les SUMO (STUbL) Slx8. Cependant, les chaînes Cependant, les chaînes SUMO limitent également la voie de redémarrage de la fourche. Ces conjugués SUMO peuvent être éliminés par la protéase SENP Ulp1 et le protéasome, dont les activités sont enrichies à la périphérie nucléaire. Ainsi, une relocalisation vers les NPCs permet un redémarrage de la réplication dépendant de la RH en contrecarrant la toxicité des chaînes SUMO. La formation de chaînes SUMO et la voie Slx8 étant cruciales pour la relocalisation des fourches de réplications bloquées au NPC. Mon projet s'est d'abord attaché à déterminer si Slx8 STUbL pouvait être exploitée en tant que marqueur des chaînes SUMO induites par des dommages à l’ADN. Pour ce faire, j'ai marqué Slx8 avec une étiquette GFP et j’ai suivi le marquage GFP par microscopie à fluorescence. De manière inattendue, je n'ai pas pu détecter de foyers Slx8 spécifiquement induits par le stress de réplication. Cependant, j'ai découvert que Slx8 forme un foyer nucléaire unique, enrichi à la périphérie nucléaire, qui marque à la fois les centromères groupés au niveau du centre organisateur des microtubules et la région silencieuse du mating type. La formation de ce foyer unique de Slx8 nécessite la ligase E3 SUMO Pli1, la poly-SUMOylation et l'histone méthyl transférase Clr4 qui est responsable de la méthylation de l’histone H3K9 qui marque l'hétérochromatine. Enfin, j'ai établi que Slx8 favorise le regroupement des centromères et le silencing des gènes dans les domaines de l'hétérochromatine. Dans l'ensemble, mes données mettent en évidence des relations fonctionnelles et conservées au cours de l'évolution entre STUbL et les domaines de l'hétérochromatine pour promouvoir le silencing des gènes et l'organisation nucléaire. En outre, j'ai mieux caractérisé les voies de redémarrage des fourches bloquées dans l'espace nucléaire. L'équipe a précédemment établi que les fourches arrêtées nécessitent l'activité d'échange de brins de Rad51 pour être acheminées vers le NPC en vue d'un redémarrage. Dans ce contexte, j'ai dévoilé l'existence d'une voie alternative de redémarrage qui implique la mono-SUMOylation, dans le nucléoplasme en absence de relocalisation au NPC. Ici, je révèle le nouveau rôle de Rad52 dans l'orchestration du redémarrage de la fourche dans le nucléoplasme, un rôle qui implique son activité SSA (single strand annealing). Pris ensemble, mes résultats suggèrent deux aspects. Une partie souligne comment la SUMOylation régulée par Slx8 STUbL favorise la maintenance du centromère. L'autre partie élucide le “contrôle SUMO” des voies alternatives de redémarrage de fourches résolues dans l'espace nucléaire
Flaws in the DNA replication process, known as replication stress, is a major source of genome instability that fuels cancer development. Resolution of replication stress occurs within a compartmentalized nucleus that exhibits distinct DNA repair capacities. In different eukaryotic organisms, stressed replication forks (RFs) shift to the nuclear periphery for anchorage to the nuclear pore complexes (NPCs), a highly conserved structure in the nuclear envelope that act as docking sites to allow alternative DNA repair pathways to occur. These changes in nuclear positioning is regulated by the small ubiquitin-like modifier (SUMO) metabolism, which is pivotal to spatially segregate the activities of the homologous recombination (HR) pathway. Our previous work in the fission yeast Schizossacharomyces pombe, has established that a replication fork blocked by a DNA-bound protein relocates and anchors to NPC in a SUMO-dependent manner. SUMO chains trigger the relocation of single arrested forks to the nuclear periphery to anchor to the NPC. This anchorage requires the SUMO chains and the SUMO-targeted ubiquitin ligase (STUbL), Slx8 pathway. However, SUMO chains also limit the Recombination-Dependent Replication (RDR) pathway, necessary to promote fork restart. These SUMO conjugates can be cleared off by the SENP protease Ulp1 and the proteasome, whose activities are enriched at the nuclear periphery. Thus, a routing towards NPCs allows HR-dependent replication restart by counteracting the toxicity of SUMO chains. Since, both SUMO chain formation and the Slx8 STUbL pathway were crucial for NPC routing of arrested replication forks. My thesis project initially focused on unraveling if the Slx8 STUbL can be exploited as a readout of damage-induced SUMO chains. To do so, I tagged Slx8 with a GFP tag and monitored them using the fluorescence microscopy technique. Unexpectedly, I was unable to detect replication stress-induced Slx8 foci. However, I discovered that Slx8 forms a single nuclear focus, enriched at the nuclear periphery, which marks both clustered centromeres at the spindle pole body and the silent mating type region. The formation of this single Slx8 focus requires the E3 SUMO ligase Pli1, poly-SUMOylation and the histone methyl transferase Clr4 that is responsible for the heterochromatin histone mark H3-K9 methylation. Finally, it was established that Slx8 promotes centromere clustering and gene silencing at heterochromatin domains. Altogether, my data highlight evolutionarily conserved and functional relationships between STUbL and heterochromatin domains to promote gene silencing and nuclear organization. Additionally, I have better characterized pathways of fork restart within the nuclear space. The team previously established that arrested RFs require SUMO chains and the strand exchange activity of Rad51 for routing to the NPC for subsequent fork restart. In this context, I unveiled the existence of an alternate fork restart pathway that occurs by mono-SUMOylation, in the nucleoplasm when forks do not shift to the NPC, as SUMO chains are not formed. Here, I revealed that fork restart within the nucleoplasm still depends on the strand exchange activity of Rad51 largely, while the single strand annealing (SSA) activity of Rad52 plays an important role in mediating error-prone fork progression in the absence of SUMO chains. Taken together, my results suggest two different ideas about SUMOylation. One part underscores how Slx8 STUbL-regulated SUMOylation promotes centromere clustering and gene silencing at heterochromatin domains. Whereas, the other section elucidates the “SUMO control” on the spatially segregated, alternative pathways of fork restart within the nuclear space. Therefore highlighting the importance of maintaining SUMO balance for preserving genome integrity

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Jalan, Manisha. „Investigating the recombinational response to replication fork barriers in fission yeast“. Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:aed1673a-f967-41a5-9643-2e432052e174.

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Timely completion of DNA replication in each cell cycle is crucial for maintaining genomic integrity. This is often challenged by the presence of various replication fork barriers (RFBs). On collision with a RFB, the fate of the replication fork remains uncertain. In some cases, the integrity of the fork is maintained until the barrier is removed or the fork is rescued by merging with the incoming fork. However, fork stalling can cause dissociation of all of the associated replication proteins (fork collapse). If this occurs, the cell's recombination machinery can intervene to help restart replication in a process called recombination-dependent replication (RDR). Programmed protein-DNA barriers like the Replication Terminator Sequence-1 (RTS1) have been used to demonstrate that replication fork blockage can induce recombination. However, it remains unclear how efficiently this recombination gives rise to replication restart and whether the restarted replication fork exhibits the same fidelity as an origin-derived fork. It is also unknown whether accidental replication barriers induce recombination in the same manner as programmed barriers. In this study, I introduce recombination reporters at various sites downstream of RTS1 to obtain information on both the fidelity and efficiency of replication restart. I find that unlike break induced replication (BIR), the restarted fork gives rise to hyper-recombination at least 75 kb downstream of the barrier. Surprisingly, fork convergence, rather than inducing recombination, acts to prevent or curtail genetic instability associated with RDR. I also investigate a number of genetic factors that have a role in either preventing or promoting genome instability associated with the progression of the restarted fork. To compare RTS1 with an accidental protein-DNA barrier, a novel site-specific barrier system (called MarBl) was established based on the human mariner transposase, Hsmar1, binding to its transposon end. Replication fork blockage at MarBl strongly induces recombination, more so than at RTS1. This appears to be a general feature of accidental barriers as introduction of the E. coli TusB-TerB site-specific barrier in S. pombe gives rise to a similar effect. Here, I compare and contrast accidental barriers with programmed barriers. I observe that there is very little replication restart, if any, at MarBl measured by direct repeat recombination downstream. This points to the fact that accidental barriers do not trigger fork collapse in the same way as programmed RFBs and that the increased recombination that they cause may be a consequence of the inability of replication forks to terminate correctly, owing to the bi-directional nature of the barrier. Several genetic factors are assessed for their impact on MarBl-induced recombination, which further highlights both similarities and differences with RTS1-induced recombination.

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Richards, Jodi D. „Helicases and DNA dependent ATPases of Sulfolobus solfataricus“. Thesis, University of St Andrews, 2008. http://hdl.handle.net/10023/474.

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DNA is susceptible to various types of damage as a result of normal cellular metabolism or from environmental sources. In order to maintain genome stability a number of different, partially overlapping DNA repair pathways have evolved to tackle specific lesions or distortions in the DNA. Nucleotide excision repair (NER) is highly conserved throughout eukarya, bacteria and archaea and predominantly targets lesions that result from exposure to UV light, for example cyclobutane pyrimidine dimers and 6-4 photoproducts. The majority of archaea possess homologous of the eukaryotic repair genes and this thesis describes the isolation and the characterization of two XPB homologues identified in the crenarchaeon Sulfolobus solfataricus, SsoXPB1 and SsoXPB2. Human XPB is one of 10 proteins that make up the TFIIH transcription complex. The activity of XPB is tightly controlled by protein interactions, in particular with p52, which stimulates the ATPase activity of XPB. Rather than a conventional helicase, human XPB is thought to act as an ATP dependent conformational switch. Consistent with human XPB, however, the S. solfataricus proteins were unable to catalyse strand separation and the identification of an archaeal protein partner, Bax1, for SsoXPB2 was one of the focuses of this project. In order to maintain genome stability, the DNA must be replicated accurately with each cell cycle. When the advancing replication fork stalls at a lesion or a DNA break, it is crucial that the fork is reset and that replication continues to completion. The helicase Hel308 is thought to clear the lagging strand template of a stalled replication fork in order for replication restart to proceed via homologous recombination (HR). Although the specific function of Hel308 is not well understood, the possibilities are described in this thesis. Strand exchange proceeds to form a D-loop, followed by branch migration to increase regions of heterology during the synapsis stage of HR. No motors for branch migration have previously been recognised in archaea, although the identification of a possible candidate was investigated during this project.

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Tolleson, Terry. „Restart an alternative for reclaiming churches /“. Theological Research Exchange Network (TREN) Access this title online, 1999. http://www.tren.com/search.cfm?p068-0167.

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Wong, Hing Choi. „Schedulability analysis for the abort-and-restart model“. Thesis, University of York, 2014. http://etheses.whiterose.ac.uk/8574/.

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In real-time systems, a schedulable task-set guarantees that all tasks complete before their deadlines. In functional programming, atomic execution provides the correctness of the program. Priority-based functional reactive programming (P-FRP) allows the usage of functional programming in the real-time system environment. The abort-and-restart (AR) is a scheme to implement P-FRP but an appropriate scheduling approach does not exist at the moment. Hence, efficient analysis is needed for the AR model. In this thesis, the schedulability analysis for the AR model is introduced and it shows that finding the critical instant for the AR model with periodic and sporadic tasks is intractable, and a new formulation is derived. Afterwards, a new priority assignment scheme is developed that has the performance close to the exhaustive search method, which is intractable for large systems. The technique of deferred preemption is employed and a new model, deferred abort (DA), provides better schedulability and dominates the non-preemptive model. Lastly, a tighter analysis is introduced and the technique of the multi-set approach from the analysis of cache related preemption delay is employed to introduce a new approach, multi-bag. The multi-bag approach can apply to both the AR model and the DA model. In the experiments, the schedulability of the AR model is improved at each stage of the research in this thesis.

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Ahmed, Nisar. „Implicit restart schemes for Krylov subspace model reduction methods“. Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340535.

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Papakos, Vasilios. „Restarted Lanczos algorithms for model reduction“. Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404818.

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Bücher zum Thema "Fork restart"

Marcaccini, Pierluigi. Villa delle Panche: Il restauro. Firenze: Centro Di, 1993.

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Grisotti, Marcello. Barletta, il castello: La storia, il restauro. Bari: M. Adda, 1995.

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Torsello, Alberto. Venezia, Cinema Teatro Italia: Restauro e riuso. Venezia: Marsilio, 2017.

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Aldo, Pinto, Valerio Adriana 1952- und Fondazione Pasquale Valerio per la storia delle donne., Hrsg. Sant'Antoniello a Port'Alba: Storia, arte, restauro. Napoli: Fridericiana editrice universitaria, 2009.

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1944-, Amendolagine Francesco, Hrsg. Molino Stucky: Ricerche storiche e ipotesi di restauro. Venezia: Il cardo, 1995.

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Zanirato, Claudio. La Badia del Lavino: Studi e restauri. Bologna: Libreria Piani, 2011.

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Massimiliano, Ghilardi, und Baiani Serena, Hrsg. Crypta Balbi, Fori imperiali: Archeologia urbana a Roma e interventi di restauro nell'anno del grande giubileo. Roma: Kappa, 2000.

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Serena, Baiani, und Ghilardi Massimiliano, Hrsg. Crypta Balbi - Fori imperiali: Archeologia urbana a Roma e interventi di restauro nell'anno del Grande Giubileo. Roma: Kappa, 2000.

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Bottini, Massimo. Il Sant'Agostino: Storia e restauro di un convento cesenate. Cesena [Italy]: Il ponte vecchio, 1998.

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Stocco, Bruno. La fornace Morandi: Processo di restauro e metodologia di recupero. Bologna: Compositori, 2010.

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Mehr Quellen

Buchteile zum Thema "Fork restart"

Wolter, Katinka. „Applicability Analysis of Restart“. In Stochastic Models for Fault Tolerance, 35–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11257-7_3.

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Wolter, Katinka. „Meeting Deadlines Through Restart“. In Stochastic Models for Fault Tolerance, 95–115. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11257-7_5.

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Jørgensen, Sveinung, und Lars Jacob Tynes Pedersen. „Avenues for Future Research“. In RESTART Sustainable Business Model Innovation, 193–208. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91971-3_15.

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van Eenennaam, Fred, und Hagar Michel. „Fraud Governance Case“. In Management for Professionals, 91–93. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-48606-8_18.

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AbstractThe Imtech case is about a Dutch listed company that tried a restart and failed at that restart.A couple of spinning questions are in the case among which.• Why did the supervisory board and the management board dynamics prevent from taking appropriate actions?• Why did the decentral local entrepreneurial model fail and to what extend were missing Corp governance systems to blame?• What should the supervisory board have done to mitigate their company and personal risks?

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Jørgensen, Sveinung, und Lars Jacob Tynes Pedersen. „Case Study: A RESTART for Scanship“. In RESTART Sustainable Business Model Innovation, 209–19. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91971-3_16.

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Jørgensen, Sveinung, und Lars Jacob Tynes Pedersen. „A Process Model for Sustainable Business Model Innovation“. In RESTART Sustainable Business Model Innovation, 183–92. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91971-3_14.

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Jørgensen, Sveinung, und Lars Jacob Tynes Pedersen. „Case Study: A Circular Business Model for Orkla and BIR?“ In RESTART Sustainable Business Model Innovation, 221–29. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91971-3_17.

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Fukunaga, Alex S. „Restart scheduling for genetic algorithms“. In Lecture Notes in Computer Science, 357–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0056878.

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Wolter, Katinka. „Moments of Completion Time Under Restart“. In Stochastic Models for Fault Tolerance, 51–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11257-7_4.

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Loshchilov, Ilya, Marc Schoenauer und Michèle Sebag. „Alternative Restart Strategies for CMA-ES“. In Lecture Notes in Computer Science, 296–305. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-32937-1_30.

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Konferenzberichte zum Thema "Fork restart"

Davy, Leo, Nelly Pustelnik und Patrice Abry. „Restart Strategies Enabling Automatic Differentiation for Hyperparameter Tuning in Inverse Problems“. In 2024 32nd European Signal Processing Conference (EUSIPCO), 1811–15. IEEE, 2024. http://dx.doi.org/10.23919/eusipco63174.2024.10715077.

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Ai, Zekai, Xiaoming Shi, Heming Jia, Jie Yang, Bowen Xue und Yilong Du. „Beta Random Restart Strategy-Based Remora Optimization Algorithm for Global Optimization“. In 2024 14th International Conference on Information Science and Technology (ICIST), 724–29. IEEE, 2024. https://doi.org/10.1109/icist63249.2024.10805347.

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Weekes, Daniel, Elodie Noel, Callum Walker, Nick Balan, Vandna Shah, Bhavna Sidhu, Anna Pardix et al. „Abstract 3363:PUM3is a triple-negative breast cancer dependency gene that functions in replication fork restart and repair“. In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3363.

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Ferrand, Antoine, Marc Bellenoue, Yves Bertin und Patrick Marconi. „Improvement of Turboshaft Restart Time Through an Experimental and Numerical Investigation“. In ASME Turbo Expo 2020: Turbomachinery Technical Conference and Exposition. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/gt2020-14143.

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Abstract Inflight shutdown of one engine for twin-engine helicopters have proven beneficial for fuel consumption. A new flight mode is then considered, in which one engine is put into sleep mode (the gas generator is kept at a stabilized, sub-idle speed by means of an electric motor, with no combustion), while the second engine runs almost at nominal load. The ability to restart the engine in sleep mode is then critical for safety reasons. Indeed, the certification of this flight mode involves ensuring a close-to-zero failure rate for in-flight restarts as well as a fast restart capability of the shutdown engine. In this paper, the focus is made on improving the restart time of the shutdown turboshaft engine. Fast restart capability is necessary for flight management reasons. Indeed, in case of a failure of the engine operating close to nominal load while the other one is in sleep mode, there is no more power available and the helicopter can lose up to 15–20 meters per second during autorotation. The restart time becomes a critical parameter to limit the loss of altitude. In the configuration studied, the fast restart is achieved thanks to the electric motor designed to deliver a high torque to the gas generator shaft. This electric motor is powered by an additional battery, more powerful than the conventional one dedicated for standard restarts. The aim of the paper is to assess the potential restart time saving using an approach combining test rig data analysis and numerical results generated by a thermodynamic model able to simulate at very low rotational speed. A gas turbine engine starting process is composed of two main phases: the light-up phase and the acceleration phase. It is important to understand the detailed phenomenology of these two phases as well as the various sub-systems involved, first to highlight the influencing parameters of both phases and then to establish an exhaustive listing of the possible time optimizations. From the test rig campaign, conducted at Safran Helicopter Engines on a high power free turbine turboshaft engine, we are able to accurately break down the phases of the start-up sequence, which helps us to identify what steps of the sequence worth shortening. With the engine performance thermodynamic model, we can then use the information gathered from the test rig analysis to further predict how to save time and to give guidelines for developing new control strategies. The results of this study show that a fast restart going from sleep mode to max power speed can be up to 60% faster than a conventional restart going from sleep mode to idle speed. This is significantly faster, especially if one takes into account the higher final speed targeted by the fast restart.

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Gankevich, I., I. Petriakov, A. Gavrikov, D. Tereshchenko und G. Mozhaiskii. „VERIFIABLE APPLICATION-LEVEL CHECKPOINT AND RESTART FRAMEWORK FOR PARALLEL COMPUTING“. In 9th International Conference "Distributed Computing and Grid Technologies in Science and Education". Crossref, 2021. http://dx.doi.org/10.54546/mlit.2021.45.84.001.

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Fault tolerance of parallel and distributed applications is one of the concerns that becomes topical for large computer clusters and large distributed systems. For a long time the common solution to this problem was checkpoint and restart mechanisms implemented on operating system level, however, they are inefficient for large systems and now application-level checkpoint and restart is considered as a more efficient alternative. In this paper we implement application-level checkpoint and restart manually for the well-known parallel computing benchmarks to evaluate this alternative approach. We measure the overheads introduced by creating and restarting from a checkpoint, and the amount of effort that is needed to implement and verify the correctness of the resulting programme. Based on the results we propose generic framework for application-level checkpointing that simplifies the process and allows to verify that the application gives correct output when restarted from any checkpoint.

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Balaji, Budharaju, N. Om Prakash Raj, Mahesh P. Padwale und G. P. Ravishankar. „Modelling, Analysis and Flight Testing of a Military Turbofan Engine Under Windmilling Conditions“. In ASME 2019 Gas Turbine India Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/gtindia2019-2353.

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Abstract Flight testing of a military low bypass turbofan engine involves multitudes of tests to ensure the Engine - Aircraft compatibility across the flight envelope. One of the safety critical tests is to conduct In-Flight restart of the engine. Detailed planning and careful execution is mandated for a single engine aircraft. Accurate modelling of sub-idle performance characteristics of the engine during windmilling conditions enables better prediction of engine behavior during in-Flight shutdown and restart. Typically, Engine manufacturer provides a Performance Cycle Deck (PCD) to predict and assess the performance of the engine across the flight envelope for all throttle positions. However, the PCD does not include sub-idle behavior. The present work focusses on developing a torque based engine behavior model which enables prediction of time dependent fan and compressor characteristics during sub-idle operations. The proposed model is divided into two parts. The first part deals with deceleration characteristics during engine shut-off and spool down, and the second part deals with the acceleration characteristics during spooling up and engine restart. In-flight spool-down (a quick relight without windmilling) restart data obtained through flight tests was used to validate the present model. The model is intended to be used for future flight tests which include windmill restarts under various operating conditions. The model is expected to accurately predict the correlation between aircraft speed and engine windmilling rotor speeds for arriving at a windmill restart envelope for the aircraft.

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van Moorsel, A. P. A., und K. Wolter. „Analysis and algorithms for restart“. In First International Conference on the Quantitative Evaluation of Systems, 2004. QEST 2004. Proceedings. IEEE, 2004. http://dx.doi.org/10.1109/qest.2004.1348034.

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Eiling, Niklas, Stefan Lankes und Antonello Monti. „Checkpoint/Restart for CUDA Kernels“. In SC-W 2023: Workshops of The International Conference on High Performance Computing, Network, Storage, and Analysis. New York, NY, USA: ACM, 2023. http://dx.doi.org/10.1145/3624062.3624254.

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Pardee, Otway O. „Checkpoint---Restart for APL applications“. In the international conference. New York, New York, USA: ACM Press, 1986. http://dx.doi.org/10.1145/22415.22040.

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Freeman, John, Kevin Ramsden und Paul Kovacs. „Dresden Units 2 and 3 Isolation Condenser Waterhammer Prevention During Restart Operations“. In 16th International Conference on Nuclear Engineering. ASMEDC, 2008. http://dx.doi.org/10.1115/icone16-48808.

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The Dresden Units 2 and 3 have a history of hydraulic transients occurring in the Isolation Condenser System piping. One of the most significant transients occurred following a spurious trip and isolation of the Isolation Condenser when operators restarted the system. Piping support damage occurred on supports in the condensate return line. A detailed RELAP5 M3 analysis of the Isolation Condenser and reactor system was performed to study the thermal hydraulic behavior of the system through system initiation and subsequently to system isolation and restart. Several post isolation restart times were analyzed to provide guidance for operating procedure changes. Isolation valve operation sequence was also considered. Piping segment force time histories in the condensate return line were generated to evaluate the pipe loadings. The loads computed compared favorably with the historical damage observed and demonstrated that allowing sufficient time for post isolation void transients to complete will allow system restart with minimal loading on the system.

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Berichte der Organisationen zum Thema "Fork restart"

Sangli, S., E. Chen, R. Fernando, J. Scudder und Y. Rekhter. Graceful Restart Mechanism for BGP. RFC Editor, Januar 2007. http://dx.doi.org/10.17487/rfc4724.

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Shand, M., und L. Ginsberg. Restart Signaling for IS-IS. RFC Editor, Oktober 2008. http://dx.doi.org/10.17487/rfc5306.

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Duell, Jason, Paul H. Hargrove und Eric S. Roman. Requirements for Linux Checkpoint/Restart. Office of Scientific and Technical Information (OSTI), Februar 2002. http://dx.doi.org/10.2172/793773.

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Ginsberg, L., und P. Wells. Restart Signaling for IS-IS. RFC Editor, Februar 2020. http://dx.doi.org/10.17487/rfc8706.

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Crocker, D., N. Freed und A. Cargille. SMTP Service Extension for Checkpoint/Restart. RFC Editor, September 1995. http://dx.doi.org/10.17487/rfc1845.

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Uttaro, J., E. Chen, B. Decraene und J. Scudder. Long-Lived Graceful Restart for BGP. RFC Editor, November 2023. http://dx.doi.org/10.17487/rfc9494.

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Leelanivas, M., Y. Rekhter und R. Aggarwal. Graceful Restart Mechanism for Label Distribution Protocol. RFC Editor, Februar 2003. http://dx.doi.org/10.17487/rfc3478.

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Rekhter, Y., und R. Aggarwal. Graceful Restart Mechanism for BGP with MPLS. RFC Editor, Januar 2007. http://dx.doi.org/10.17487/rfc4781.

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Patel, K., R. Fernando, J. Scudder und J. Haas. Notification Message Support for BGP Graceful Restart. RFC Editor, März 2019. http://dx.doi.org/10.17487/rfc8538.

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Riesen, Rolf E., Patrick G. Bridges, Jon R. Stearley, James H. ,. III Laros, Ron A. Oldfield, Dorian Arnold, Kevin Thomas Tauke Pedretti, Kurt Brian Ferreira und Ronald Brian Brightwell. Keeping checkpoint/restart viable for exascale systems. Office of Scientific and Technical Information (OSTI), September 2011. http://dx.doi.org/10.2172/1029780.

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