Relevant bibliographies by topics / G1 Phase Cell Cycle Checkpoints

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Academic literature on the topic 'G1 Phase Cell Cycle Checkpoints'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "G1 Phase Cell Cycle Checkpoints"

1

Mantel, Charlie, and Hal E. Broxmeyer. "Embryonic Stem Cells Bypass Numerous Cell Cycle Checkpoints; Not Just G1." Blood 112, no. 11 (November 16, 2008): 1331. http://dx.doi.org/10.1182/blood.v112.11.1331.1331.

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Abstract It was recently demonstrated that human and mouse embryonic stem cells (ESC) have deficiencies in the mitotic spindle assembly checkpoint (SAC) and it’s uncoupling to apoptosis which leads to polyploidy (Mantel et.al. BLOOD10:4518; 2007), a source of genetic instability in ESC in-vitro. The G1 checkpoint is also absent in ESC, a fact already known. It was also shown that p53 phosphorylation is absent in SAC-bypassed murine ESC in contrast to somatic cells with intact checkpoints (Mantel, et.al. CELL CYCLE 7:484; 2008). This lack of p53 phosporylation likely contributes to apoptosis uncoupling and polyploidization in ESC after microtubule/spindle damage and SAC-bypass. Microtubule/spindle damage in somatic cells eventually causes M-phase slippage where cells enter a 4C-G1 state that has 4C DNA content, no cyclin B1, and highly phosphorylated Rb. 4C-G1 status has not been investigated in ESC. We have now begun studies to determine mechanisms of checkpoint-bypass and polyploidization in ESC using intracellular flow cytometric analysis and here we report on the phosphorylation status of Rb in polyploid ESC. Because histone acetylation has been linked to cell cycle checkpoint function and because chromatin structure is more “open” in ESC, we investigated the oscillatory acetylations of the four core nucleosomal histones during checkpoint-bypass in ESC. The effects of DNA strand breaks on cell cycle checkpoints in ESC were also investigated. Results demonstrated that Rb is highly phosphorylated at several sites when ESC are in a cell cycle phase consistent with that seen in somatic cells in 4C-G1 after microtubule damage. It is concluded that ESC polyploidization is accompanied by 4C-G1-exit without apoptosis, which contrasts to 4C-G1-exit in somatic cells that do initiate apoptosis. There were also pronounced differences in acetylation oscillations on histone H4 and histone H2B compared to histone H3 and histone H2A during checkpoint activation and bypass. Total histones increased linearly as DNA content increased, as expected. Bivalent histone acetylation/methylation site, histone H3K9, changed little during checkpoint-bypass. However, DNA strand breakage revealed that S, G2, and the following G1 DNA-damage checkpoints also appeared to be bypassed in ESC. Most unusual is the polyploidization after DNA strand breakage, which may be due to aborted G2/M phases, but not to SAC activation since DNA strand breakage is not known to activate the SAC. DNA damage caused polyploidy without accumulation of cells in 4C-G1, as noted by lack of Rb phosphorylation, lack of p53 phosphorylation (as previously determined), but with an increase in total p53 in all phases of the cell cycle including 8C/polyploid. We conclude that mouse ESC can bypass numerous cell cycle checkpoints and fail to couple them to apoptosis initiation. This could be related to differences in histone acetylation, Rb phosphorylation, and the absence of p53 phosphorylation when compared to results of similar studies of somatic cells. Bypass of numerous checkpoints is a likely source of genetic instability in ESC cultured in-vitro.
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Naiki, Takahiro, Toshiyasu Shimomura, Tae Kondo, Kunihiro Matsumoto, and Katsunori Sugimoto. "Rfc5, in Cooperation with Rad24, Controls DNA Damage Checkpoints throughout the Cell Cycle inSaccharomyces cerevisiae." Molecular and Cellular Biology 20, no. 16 (August 15, 2000): 5888–96. http://dx.doi.org/10.1128/mcb.20.16.5888-5896.2000.

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ABSTRACT RAD24 and RFC5 are required for DNA damage checkpoint control in the budding yeast Saccharomyces cerevisiae. Rad24 is structurally related to replication factor C (RFC) subunits and associates with RFC subunits Rfc2, Rfc3, Rfc4, and Rfc5. rad24Δ mutants are defective in all the G1-, S-, and G2/M-phase DNA damage checkpoints, whereas the rfc5-1 mutant is impaired only in the S-phase DNA damage checkpoint. Both the RFC subunits and Rad24 contain a consensus sequence for nucleoside triphosphate (NTP) binding. To determine whether the NTP-binding motif is important for Rad24 function, we mutated the conserved lysine115 residue in this motif. The rad24-K115E mutation, which changes lysine to glutamate, confers a complete loss-of-function phenotype, while the rad24-K115R mutation, which changes lysine to arginine, shows no apparent phenotype. Although neitherrfc5-1 nor rad24-K115R single mutants are defective in the G1- and G2/M-phase DNA damage checkpoints, rfc5-1 rad24-K115R double mutants become defective in these checkpoints. Coimmunoprecipitation experiments revealed that Rad24K115R fails to interact with the RFC proteins in rfc5-1 mutants. Together, these results indicate that RFC5, like RAD24, functions in all the G1-, S- and G2/M-phase DNA damage checkpoints and suggest that the interaction of Rad24 with the RFC proteins is essential for DNA damage checkpoint control.
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Mantel, Charlie, Stephen E. Braun, Suzanna Reid, Octavian Henegariu, Lisa Liu, Giao Hangoc, and Hal E. Broxmeyer. "p21cip-1/waf-1 Deficiency Causes Deformed Nuclear Architecture, Centriole Overduplication, Polyploidy, and Relaxed Microtubule Damage Checkpoints in Human Hematopoietic Cells." Blood 93, no. 4 (February 15, 1999): 1390–98. http://dx.doi.org/10.1182/blood.v93.4.1390.

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Abstract A recent hypothesis suggests that tumor-specific killing by radiation and chemotherapy agents is due to defects or loss of cell cycle checkpoints. An important component of some checkpoints is p53-dependent induction of p21cip-1/waf-1. Both p53 and p21 have been shown to be required for microtubule damage checkpoints in mitosis and in G1 phase of the cell cycle and they thus help to maintain genetic stability. We present here evidence that p21cip-1/waf-1 deficiency relaxes the G1 phase microtubule checkpoint that is activated by microtubule damage induced with nocodazole. Reduced p21cip-1/waf-1expression also results in gross nuclear abnormalities and centriole overduplication. p53 has already been implicated in centrosome regulation. Our findings further suggest that the p53/p21 axis is involved in a checkpoint pathway that links the centriole/centrosome cycle and microtubule organization to the DNA replication cycle and thus helps to maintain genomic integrity. The inability to efficiently upregulate p21cip-1/waf-1 in p21cip-1/waf-1antisense-expressing cells in response to microtubule damage could uncouple the centrosome cycle from the DNA cycle and lead to nuclear abnormalicies and polyploidy. A centrosome duplication checkpoint could be a new target for novel chemotherapy strategies.
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Mantel, Charlie, Stephen E. Braun, Suzanna Reid, Octavian Henegariu, Lisa Liu, Giao Hangoc, and Hal E. Broxmeyer. "p21cip-1/waf-1 Deficiency Causes Deformed Nuclear Architecture, Centriole Overduplication, Polyploidy, and Relaxed Microtubule Damage Checkpoints in Human Hematopoietic Cells." Blood 93, no. 4 (February 15, 1999): 1390–98. http://dx.doi.org/10.1182/blood.v93.4.1390.404k25_1390_1398.

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A recent hypothesis suggests that tumor-specific killing by radiation and chemotherapy agents is due to defects or loss of cell cycle checkpoints. An important component of some checkpoints is p53-dependent induction of p21cip-1/waf-1. Both p53 and p21 have been shown to be required for microtubule damage checkpoints in mitosis and in G1 phase of the cell cycle and they thus help to maintain genetic stability. We present here evidence that p21cip-1/waf-1 deficiency relaxes the G1 phase microtubule checkpoint that is activated by microtubule damage induced with nocodazole. Reduced p21cip-1/waf-1expression also results in gross nuclear abnormalities and centriole overduplication. p53 has already been implicated in centrosome regulation. Our findings further suggest that the p53/p21 axis is involved in a checkpoint pathway that links the centriole/centrosome cycle and microtubule organization to the DNA replication cycle and thus helps to maintain genomic integrity. The inability to efficiently upregulate p21cip-1/waf-1 in p21cip-1/waf-1antisense-expressing cells in response to microtubule damage could uncouple the centrosome cycle from the DNA cycle and lead to nuclear abnormalicies and polyploidy. A centrosome duplication checkpoint could be a new target for novel chemotherapy strategies.
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5

Xu, Bo, Seong-Tae Kim, Dae-Sik Lim, and Michael B. Kastan. "Two Molecularly Distinct G2/M Checkpoints Are Induced by Ionizing Irradiation." Molecular and Cellular Biology 22, no. 4 (February 15, 2002): 1049–59. http://dx.doi.org/10.1128/mcb.22.4.1049-1059.2002.

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ABSTRACT Cell cycle checkpoints are among the multiple mechanisms that eukaryotic cells possess to maintain genomic integrity and minimize tumorigenesis. Ionizing irradiation (IR) induces measurable arrests in the G1, S, and G2 phases of the mammalian cell cycle, and the ATM (ataxia telangiectasia mutated) protein plays a role in initiating checkpoint pathways in all three of these cell cycle phases. However, cells lacking ATM function exhibit both a defective G2 checkpoint and a prolonged G2 arrest after IR, suggesting the existence of different types of G2 arrest. Two molecularly distinct G2/M checkpoints were identified, and the critical importance of the choice of G2/M checkpoint assay was demonstrated. The first of these G2/M checkpoints occurs early after IR, is very transient, is ATM dependent and dose independent (between 1 and 10 Gy), and represents the failure of cells which had been in G2 at the time of irradiation to progress into mitosis. Cell cycle assays that can distinguish mitotic cells from G2 cells must be used to assess this arrest. In contrast, G2/M accumulation, typically assessed by propidium iodide staining, begins to be measurable only several hours after IR, is ATM independent, is dose dependent, and represents the accumulation of cells that had been in earlier phases of the cell cycle at the time of exposure to radiation. G2/M accumulation after IR is not affected by the early G2/M checkpoint and is enhanced in cells lacking the IR-induced S-phase checkpoint, such as those lacking Nbs1 or Brca1 function, because of a prolonged G2 arrest of cells that had been in S phase at the time of irradiation. Finally, neither the S-phase checkpoint nor the G2 checkpoints appear to affect survival following irradiation. Thus, two different G2 arrest mechanisms are present in mammalian cells, and the type of cell cycle checkpoint assay to be used in experimental investigation must be thoughtfully selected.
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Xu, Bo, Seong-tae Kim, and Michael B. Kastan. "Involvement of Brca1 in S-Phase and G2-Phase Checkpoints after Ionizing Irradiation." Molecular and Cellular Biology 21, no. 10 (May 15, 2001): 3445–50. http://dx.doi.org/10.1128/mcb.21.10.3445-3450.2001.

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ABSTRACT Cell cycle arrests in the G1, S, and G2phases occur in mammalian cells after ionizing irradiation and appear to protect cells from permanent genetic damage and transformation. Though Brca1 clearly participates in cellular responses to ionizing radiation (IR), conflicting conclusions have been drawn about whether Brca1 plays a direct role in cell cycle checkpoints. Normal Nbs1 function is required for the IR-induced S-phase checkpoint, but whether Nbs1 has a definitive role in the G2/M checkpoint has not been established. Here we show that Atm and Brca1 are required for both the S-phase and G2 arrests induced by ionizing irradiation while Nbs1 is required only for the S-phase arrest. We also found that mutation of serine 1423 in Brca1, a target for phosphorylation by Atm, abolished the ability of Brca1 to mediate the G2/M checkpoint but did not affect its S-phase function. These results clarify the checkpoint roles for each of these three gene products, demonstrate that control of cell cycle arrests must now be included among the important functions of Brca1 in cellular responses to DNA damage, and suggest that Atm phosphorylation of Brca1 is required for the G2/M checkpoint.
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Hopkins, Michael, John J. Tyson, and Béla Novák. "Cell-cycle transitions: a common role for stoichiometric inhibitors." Molecular Biology of the Cell 28, no. 23 (November 7, 2017): 3437–46. http://dx.doi.org/10.1091/mbc.e17-06-0349.

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The cell division cycle is the process by which eukaryotic cells replicate their chromosomes and partition them to two daughter cells. To maintain the integrity of the genome, proliferating cells must be able to block progression through the division cycle at key transition points (called “checkpoints”) if there have been problems in the replication of the chromosomes or their biorientation on the mitotic spindle. These checkpoints are governed by protein-interaction networks, composed of phase-specific cell-cycle activators and inhibitors. Examples include Cdk1:Clb5 and its inhibitor Sic1 at the G1/S checkpoint in budding yeast, APC:Cdc20 and its inhibitor MCC at the mitotic checkpoint, and PP2A:B55 and its inhibitor, alpha-endosulfine, at the mitotic-exit checkpoint. Each of these inhibitors is a substrate as well as a stoichiometric inhibitor of the cell-cycle activator. Because the production of each inhibitor is promoted by a regulatory protein that is itself inhibited by the cell-cycle activator, their interaction network presents a regulatory motif characteristic of a “feedback-amplified domineering substrate” (FADS). We describe how the FADS motif responds to signals in the manner of a bistable toggle switch, and then we discuss how this toggle switch accounts for the abrupt and irreversible nature of three specific cell-cycle checkpoints.
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Fulka, Josef, Judy Bradshaw, and Robert Moor. "Meiotic cycle checkpoints in mammalian oocytes." Zygote 2, no. 4 (November 1994): 351–54. http://dx.doi.org/10.1017/s0967199400002197.

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Recent Spectacular achievements have enabled the identification of key molecules responsible for mitotic cell cycle progression through the stages of G1, the gap before DNA replication; S, the phase of DNA synthesis; G2, the gap before chromosome segregation; and M, mitosis itself. The last stage has been most intensively studied, where MPE, maturation promotion factor, has been found responsible for the nuclear events associated with chromosomal segregation and the prodcution of two identical daughter cells (see Murray & Hunt, 1993).
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Morgan, S. E., C. Lovly, T. K. Pandita, Y. Shiloh, and M. B. Kastan. "Fragments of ATM which have dominant-negative or complementing activity." Molecular and Cellular Biology 17, no. 4 (April 1997): 2020–29. http://dx.doi.org/10.1128/mcb.17.4.2020.

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The ATM protein has been implicated in pathways controlling cell cycle checkpoints, radiosensitivity, genetic instability, and aging. Expression of ATM fragments containing a leucine zipper motif in a human tumor cell line abrogated the S-phase checkpoint after ionizing irradiation and enhanced radiosensitivity and chromosomal breakage. These fragments did not abrogate irradiation-induced G1 or G2 checkpoints, suggesting that cell cycle checkpoint defects alone cannot account for chromosomal instability in ataxia telangiectasia (AT) cells. Expression of the carboxy-terminal portion of ATM, which contains the PI-3 kinase domain, complemented radiosensitivity and the S-phase checkpoint and reduced chromosomal breakage after irradiation in AT cells. These observations suggest that ATM function is dependent on interactions with itself or other proteins through the leucine zipper region and that the PI-3 kinase domain contains much of the significant activity of ATM.
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Koledova, Zuzana, Leona Kafkova, Sonja Hennemann, Alwin Kraemer, and Vladimir Divoky. "Cdk2 Kinase Activity Is Not Abrogated after DNA Damage in Mouse Embryonic Stem Cells." Blood 110, no. 11 (November 16, 2007): 3371. http://dx.doi.org/10.1182/blood.v110.11.3371.3371.

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Abstract Stem cells have gained special attention for their implication in medicine where stem-cell based therapies promise powerful approach to treat different disorders, and, on the other hand, cancer stem cells have been suggested as important novel targets for the treatment of cancer. To successfully develop new therapies, a deeper understanding of the biology of stem cells is necessary. Embryonic stem (ES) cells are naturally immortalized pluripotent cells derived from early mammalian embryos. ES cells are characterized by unique self-renewal and differentiation abilities, as well as by special features of cell cycle regulation and DNA damage response. In general, when DNA damage occurs, checkpoint pathways are activated, preventing replication of damaged DNA and/or division of cells with damaged DNA. Somatic cells employ checkpoints throughout the whole cell cycle; in ES cells functional checkpoints have been described in S and G2 phases only. In somatic cells the G1/S transition is governed by Cdk2-cyclin E complex. G1-checkpoint mechanisms lead to inhibition of Cdk2 activity via two parallel pathways: Chk1/Chk2-Cdc25A and p53-p21. It has been suggested proteins of these pathways are not functional in ES cells. We aimed to unravel the causes of G1 checkpoint non-functionality in mouse ES (mES) cells. To analyze the events after DNA damage in G1 phase, we synchronized mES cells (lines HM-1 and V6.5) in M phase by nocodazole treatment. After release from nocodazole arrest the cells were gamma-irradiated (γ) in early and late G1 phase. We observed activation of both Chk2-Cdc25A and p53-p21 pathways in mES cells after DNA damage by γ-irradiation. However, FACS cell cycle analysis revealed that after γ-induced DNA damage mES cells did not arrest in G1; instead, cell cycle arrest occurred only at the G2/M boundary. Measurements of Cdk2 kinase activity in γ-irradiated and mock-treated mES cells revealed that although Cdk2-activating phosphatase Cdc25A is degraded after γ-irradiation, Cdk2 activity is not diminished. Since it has been reported earlier that in mES cells Chk2 is mislocalized to centrosomes, we speculated that full function of other cell cycle regulatory proteins might be hampered by aberrant localization as well. Our immunolocalization studies showed that both Cdk2 and its phosphorylated, inactive form (P-Thr14/Tyr15-Cdk2) localize to centrosomes in mES cells. This could, at least partially, influence its accessibility by interacting factors such as Cdc25A and explain the lack of Cdk2 activity downregulation after DNA damage despite activated checkpoint pathways. In conclusion, DNA damage in mES cells (lines HM-1 and V6.5) elicits fast activation of both Chk2-Cdc25A and p53-p21 G1 checkpoint pathways. However, since Cdk2 activity is not reduced after DNA damage, mES cells do not arrest in G1 phase. Other factors than those identified in somatic cells, including aberrant localization of cell cycle regulatory proteins, could play important roles in the regulation of cell cycle progression in mES cells. These factors lead to sustained Cdk2 kinase activity even in the presence of DNA damage.
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Dissertations / Theses on the topic "G1 Phase Cell Cycle Checkpoints"

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Martinsson, Hanna-Stina. "Single cell analysis of checkpoints in G₁ /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-455-4/.

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Pope, Patricia A. "Investigation of Multiple Concerted Mechanisms Underlying Stimulus-induced G1 Arrest in Yeast: A Dissertation." eScholarship@UMMS, 2006. http://escholarship.umassmed.edu/gsbs_diss/680.

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Progression through the cell cycle is tightly controlled, and the decision whether or not to enter a new cell cycle can be influenced by both internal and external cues. For budding yeast one such external cue is pheromone treatment, which can induce G1 arrest. Two distinct mechanisms are known to be involved in this arrest, one dependent on the arrest protein Far1 and one independent of Far1, but the exact mechanisms have remained enigmatic. The studies presented here further elucidate both of these mechanisms. We looked at two distinct aspects of the Far1-independent arrest mechanism. First, we studied the role of the G1/S regulatory system in G1 arrest. We found that deletion of the G1/S transcriptional repressors Whi5 and Stb1 compromises Far1-independent arrest, but only partially, and that this partial arrest failure correlates to partial de-repression of G1/S transcripts. Deletion of the CKI Sic1, however, is more strongly required for arrest in the absence of Far1, though not when Far1 is present. Together, this demonstrates that functionally overlapping regulatory circuits controlling the G1/S transition collectively provide robustness to the G1 arrest response. We also sought to reexamine the phenomenon of pheromone-induced loss of G1/S cyclin proteins, which we suspected could be another Far1-independent arrest mechanism. We confirmed that pheromone treatment has an effect on G1 cyclin protein levels independent of transcriptional control. Our findings suggest that this phenomenon is dependent on SCFGrr1but is at least partly independent of Cdc28 activity, the CDK phosphorylation sites in Cln2, and Far1. We were not, however, able to obtain evidence that pheromone increases the degradation rate of Cln1/2, which raises the possibility that pheromone reduces their synthesis rate instead. Finally, we also studied the function of Far1 during pheromone-induced G1 arrest. Although it has been assumed that Far1 acts as a G1/S cyclin specific CDK inhibitor, there has been no conclusive evidence that this is the case. Our data, however, suggests that at least part of Far1’s function may actually be to interfere with Cln-CDK/substrate interactions since we saw a significant decrease of co-pulldown of Cln2 and substrates after treatment with pheromone. All together, the results presented here demonstrate that there are numerous independent mechanisms in place to help robustly arrest cells in G1.
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Pope, Patricia A. "Investigation of Multiple Concerted Mechanisms Underlying Stimulus-induced G1 Arrest in Yeast: A Dissertation." eScholarship@UMMS, 2013. https://escholarship.umassmed.edu/gsbs_diss/680.

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Progression through the cell cycle is tightly controlled, and the decision whether or not to enter a new cell cycle can be influenced by both internal and external cues. For budding yeast one such external cue is pheromone treatment, which can induce G1 arrest. Two distinct mechanisms are known to be involved in this arrest, one dependent on the arrest protein Far1 and one independent of Far1, but the exact mechanisms have remained enigmatic. The studies presented here further elucidate both of these mechanisms. We looked at two distinct aspects of the Far1-independent arrest mechanism. First, we studied the role of the G1/S regulatory system in G1 arrest. We found that deletion of the G1/S transcriptional repressors Whi5 and Stb1 compromises Far1-independent arrest, but only partially, and that this partial arrest failure correlates to partial de-repression of G1/S transcripts. Deletion of the CKI Sic1, however, is more strongly required for arrest in the absence of Far1, though not when Far1 is present. Together, this demonstrates that functionally overlapping regulatory circuits controlling the G1/S transition collectively provide robustness to the G1 arrest response. We also sought to reexamine the phenomenon of pheromone-induced loss of G1/S cyclin proteins, which we suspected could be another Far1-independent arrest mechanism. We confirmed that pheromone treatment has an effect on G1 cyclin protein levels independent of transcriptional control. Our findings suggest that this phenomenon is dependent on SCFGrr1but is at least partly independent of Cdc28 activity, the CDK phosphorylation sites in Cln2, and Far1. We were not, however, able to obtain evidence that pheromone increases the degradation rate of Cln1/2, which raises the possibility that pheromone reduces their synthesis rate instead. Finally, we also studied the function of Far1 during pheromone-induced G1 arrest. Although it has been assumed that Far1 acts as a G1/S cyclin specific CDK inhibitor, there has been no conclusive evidence that this is the case. Our data, however, suggests that at least part of Far1’s function may actually be to interfere with Cln-CDK/substrate interactions since we saw a significant decrease of co-pulldown of Cln2 and substrates after treatment with pheromone. All together, the results presented here demonstrate that there are numerous independent mechanisms in place to help robustly arrest cells in G1.
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Campbell, Callum James. "Time to quit? : non-genetic heterogeneity in cell fate propensity after DNA damage." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/275600.

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Cellular checkpoints are typically considered to both facilitate the ordered execution of the cell cycle and to act as a barrier to oncogene driven cell cycles and the transmission of unresolved genetic lesions from one phase to the next. Furthermore, these mechanisms are also believed to underpin the responses of cells, both in normal and cancerous tissues, to those therapies that either directly or indirectly generate DNA damage. In recent studies however, it has become clear these checkpoints permit the passage of significant genomic aberrations into subsequent cell cycle phases and even descendant cells, and that heterogeneous responses are apparent amongst genetically identical cells. The consequences of this checkpoint ‘negligence’ remain relatively uncharacterised despite the importance of checkpoints in current models for how genomic instability is avoided in the face of ubiquitous DNA damage. Unresolved DNA damage is presumably inherited by subsequent cell cycle phases and descendant cells yet characterisation of the consequences of this has been relatively limited to date. I therefore utilised microscopy-based lineage tracing of cells expressing genetically encoded fluorescent sensors, particularly the Fluorescent Ubiquitination-based Cell Cycle Indicator (FUCCI) probes (Sakaue-Sawano et al., 2008), with semi-automated image analysis to characterise the response of single cells and their descendants to DNA lesions across multiple cell cycle generations. This approach, complemented by generational tracing by flow cytometry, permitted me to characterise the timing of cell fate determination in treated and descendant cells, the non-genetic heterogeneity in checkpoint responses and overall lineage behaviour, correlations between cells (similarly to Sandler et al., 2015) and cell cycle timing dependencies in the response to DNA damaging agents. With these single cell analytical approaches I show that the consequences of DNA damage on descendant cell fate is dramatic, suggesting checkpoint mechanisms may have consequences and even cooperate across phases and generations. U2OS cell lineages traced for three generations following the induction of DNA damage in the form of strand breaks showed greatly induced cell death in the daughters and granddaughters of DNA damaged cells, termed delayed death. Furthermore, lineage behaviour was characterised as highly heterogeneous in when and whether cell death occurred. Complementary flow cytometric approaches validated the findings in U2OS cells and suggested HeLa cells may show similar behaviour. These findings indicate that checkpoint models need to incorporate multigenerational behaviour in order to better describe the response of cells to DNA damage. Understanding the processes governing cell fate determination in descendant cells will impact upon our understanding of the development of genomic instability during carcinogenesis and how DNA-damaging chemotherapeutics drive cells to ‘quit’ the cell cycle.
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Edgerton, Heather Dawn. "Functions of Gamma-tubulin in the Spindle Assembly Checkpoint and APC/C Regulation in Aspergillus nidulans." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1374159200.

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Pilaz, Louis-Jan. "Role of G1 phase regulators during corticogenesis." Thesis, Lyon 1, 2009. http://www.theses.fr/2009LYO10277.

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Les mécanismes développementaux qui spécifient le nombre et le phénotype laminaire des neurones du cortex cérébral jouent un rôle essentiel dans l’établissement de la cytoarchitecture corticale. Le nombre de neurones dans chaque couche d'une aire donnée est déterminé par le taux de production neuronale, qui dépend étroitement de l'équilibre entre les divisions prolifératives et différenciatives. Des observations clés suggèrent que la durée de la phase G1 (TG1) ferait partie intégrante d'un mécanisme cellulaire régulant le mode de division des précurseurs du cortex. Nous avons testé cette hypothèse par l'accélération expérimentale de la progression dans la phase G1 de précurseurs corticaux de souris in vivo, via la surexpression des cyclines E1 et D1. A E15, la réduction de TG1 promeut la rentrée dans le cycle cellulaire aux dépens de la différenciation neuronale, résultant en une modification de la cytoarchitecture du cortex adulte. Des données de modélisation confirment que les effets induits par la réduction de TG1 sont médiés par des changements du mode de division. Les effets de la surexpression des cyclines E1 et D2 à E13 sont plus modérés qu'à E15, indiquant des différences intrinsèques entre les précurseurs corticaux précoces et tardifs. La mesure des phases du cycle cellulaire des populations de précurseurs corticaux à l’aide de différentes techniques révèle un niveau important d’hétérogénéité et souligne la nécessité de prendre en compte la diversité des précurseurs co‐existant dans les zones germinales du télencéphale
In the cerebral cortex, area‐specific differences in neuron number and phenotype are distinguishing features both within and across species. The developmental mechanisms that specify the number of neurons and their laminar fate are instrumental in specifying cortical cytoarchitecture. Neuron number in layers and areas correlate with changes in the rate of neuron production, largely determined by the balance between proliferative and differentiative divisions in cortical precursors. Key observations suggest a concerted regulation between the duration of the G1 phase (TG1) and mode of division and have led to the hypothesis that TG1 could be an integral part of a cellular mechanism regulating the mode of division of cortical precursors. To test this hypothesis we experimentally accelerated TG1 in mouse cortical precursors in vivo, via the forced expression of cyclinE1 and cyclinD1. At E15, TG1 reduction promoted cell‐cycle re‐entry at the expense of differentiation and led to cytoarchitectural modifications. Modeling confirms that the TG1‐induced changes in neuron production and laminar fate are mediated via the changes in the mode of division. Forced expression of G1 cyclins was also applied to early cortical precursors. The effects of cyclinD1 and cyclinE1 up‐regulation at E13 were milder than those observed at E15, pointing to intrinsic differences between early and late cortical precursors. The used of various techniques to measure cell‐cycle kinetics in distinct precursor populations underlined the necessity of taking the full diversity of neural precursors co‐existing in the GZ of the telencephalon into account when performing cellcycle kinetics analysis
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Scuderi, Richard. "G1-phase cyclin expression in neoplastic B cells /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-292-2/.

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Gad, Annica. "Cell cycle control by components of cell anchorage /." Stockholm : Division of Pathology, Karolinska institutet, 2005. http://diss.kib.ki.se/2005/91-7140-359-0/.

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Ekholm-Reed, Susanna. "The role of cyclin E in cell cycle regulation and genomic instability /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-894-7/.

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Fong, Wai Gin. "The candidate tumour suppressor, XIAP associated factor 1 (XAF1), directly inhibits XIAP activity and induces G1 phase cell cycle arrest." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/28983.

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X&barbelow;IAP a&barbelow;ssociated f&barbelow;actor 1&barbelow; (XAF1) was initially isolated as novel 34 kDa protein which bound XIAP in a two-hybrid screening. The XAF1A protein consists of 301 a.a. and contains seven potential zinc finger domains. Two alternatively splice variants of XAF1 were later isolated. One isoform (XAF1B) was formed by the removal of a 57 bp exon, which leads to an in-frame deletion of the third zinc finger and the creation of a shorter 32.5 kDa protein. The other splice variant (XAF1C) contains a 154 bp exon insertion, which truncates the sixth and seventh zinc fingers to produce an 18.7 kDa protein. XAF1A and XAF1B, but not XAF1C, bound XIAP in in vitro pull down assays. Northern blot analysis showed at least four distinct sizes of xaf1 mRNA ranging between 3.9 and 7.0 kb, which may indicate other XAF1 isoforms yet to be discovered. Though the possible role of these zinc fingers on the XAF1/XIAP interaction has yet to be determined, recent experiments indicate that XAF1A can block the ability of XIAP to inhibit caspase-3 in vitro. Furthermore, overexpression of XAF1A in HEL299 cells triggered a G1 cell cycle arrest. This G1 arrest coincides with an increase in p21, but not p53. The ability of XAF1 to block XIAP function and induce cell cycle arrest suggests a role for XAF1 in the control of both apoptosis and cell growth. The coding regions of XAF1A, B and C are encoded on a total of 9 exons within a span of 20 kb. The single copy xaf1 gene has been mapped, using FISH analysis, distal to the TP53 gene on 17p13.2. Southern blot analysis of YACS within this region further localizes the xaf1 gene on YAC 746 C 10, which contains the markers D17S1831, D17S796, and D17S1881. These markers are located approximately 3 cM telomeric to the TP53 gene. Since the xaf1 gene is located in a region commonly deleted in numerous types of cancers, this may suggest a tumour suppressor role for XAF1 in cancer. To test this theory, a 60 cell line panel from the NCl was analyzed for xaf1 RNA expression by Taqman and heterozygosity status of markers proximal to xaf1. Taqman analysis indicated that the majority of cell lines expressed little or no xaf1 RNA while xiap levels were relatively high. A PCR study of markers near xaf1 showed significant loss of heterozygosity (LOH) in this region. The loss of xaf1 expression and significant LOH near the xaf1 gene indicate that the down-regulation of XAF1 may be important in the development of the transformed phenotype.
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Books on the topic "G1 Phase Cell Cycle Checkpoints"

1

Boonstra, Johannes. G1 phase progression. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2003.

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G1 phase progression. Georgetown, TX: Landes Bioscience/Eurekah.com ; Kluwer Academic/Plenum, 2004.

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Johannes, Boonstra, ed. G1 phase progression. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2003.

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Boonstra, Johannes. Regulation of G1 Phase Progression. Springer, 2003.

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Book chapters on the topic "G1 Phase Cell Cycle Checkpoints"

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DeRan, Michael, Mary Pulvino, and Jiyong Zhao. "Assessing G1-to-S-Phase Progression After Genotoxic Stress." In Cell Cycle Checkpoints, 221–30. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-273-1_16.

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Willis, Nicholas, and Nicholas Rhind. "Studying S-Phase DNA Damage Checkpoints Using the Fission Yeast Schizosaccharomyces pombe." In Cell Cycle Checkpoints, 13–21. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-273-1_2.

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Davidson, Jean M., and Robert J. Duronio. "Using Drosophila S2 Cells to Measure S phase-Coupled Protein Destruction via Flow Cytometry." In Cell Cycle Checkpoints, 205–19. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-273-1_15.

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Rampino, Nicholas J., and Vilhelm A. Bohr. "Preferential Repair of Cisplatin Adducts in the Human DHFR Gene During G1 Phase Assayed with T4 DNA Polymerase." In The Cell Cycle, 167–71. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_19.

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Welsh, Catherine F. "Regulation of G1 to S Phase Transition by Adhesion and Growth Factor Signaling." In Steroid Hormones and Cell Cycle Regulation, 19–32. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0965-3_2.

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Wiederrecht, Gregory J., Candace J. Sabers, Gregory J. Brunn, Mary M. Martin, Francis J. Dumont, and Robert T. Abraham. "Mechanism of action of rapamycin: New insights into the regulation of G1-phase progression in eukaryotic cells." In Progress in Cell Cycle Research, 53–71. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1809-9_5.

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Mirisola, M. G., G. Seidita, C. Kavounis, and O. Fasano. "Phosphorylation of an Overexpressed Yeast Ras2 Protein During the G1 Phase of the Cell Cycle." In Topics in Molecular Organization and Engineering, 353–61. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0822-5_32.

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Yoshiba, Sayaka, Daisuke Ito, Tatsuhito Nagumo, Tatsuo Shirota, Masashi Hatori, and Satoru Shintani. "Hypoxia Induces Resistance to 5-Fluorouracil in Oral Cancer Cells Via G1 Phase Cell Cycle Arrest." In New Trends in the Molecular and Biological Basis for Clinical Oncology, 184–90. Tokyo: Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-88663-1_19.

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Ravitz, Michael J., and Charles E. Wenner. "Cyclin-Dependent Kinase Regulation during G1 Phase and Cell Cycle Regulation by TGF-ß." In Advances in Cancer Research, 165–207. Elsevier, 1997. http://dx.doi.org/10.1016/s0065-230x(08)60099-8.

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Fasullo, Michael. "Checkpoint Control of DNA Repair in Yeast." In Saccharomyces. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96966.

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Budding yeast has been a model organism for understanding how DNA damage is repaired and how cells minimize genetic instability caused by arresting or delaying the cell cycle at well-defined checkpoints. However, many DNA damage insults are tolerated by mechanisms that can both be error-prone and error-free. The mechanisms that tolerate DNA damage and promote cell division are less well-understood. This review summarizes current information known about the checkpoint response to agents that elicit both the G2/M checkpoint and the intra-S phase checkpoint and how cells adapt to unrepaired DNA damage. Tolerance to particular bulky DNA adducts and radiomimetic agents are discussed, as well as possible mechanisms that may control phosphatases that deactivate phosphorylated proteins.
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Conference papers on the topic "G1 Phase Cell Cycle Checkpoints"

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Patel, Deven, and David Foster. "Abstract 2716: Lipid mediated “nutrients sensing” checkpoint in G1 phase of the cell cycle." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2716.

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Schmidt, Keon R., Yingjia Ni, and Siyuan Zhang. "Abstract LB-321: Cytoplasmic DEDD promotes G1- to S-phase cell cycle transition." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-321.

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ko, Hyeonseok, Young-Joo Kim, Jin-Soo Park, Evangeline C. Amor, Jong Wha Lee, and Hyun Ok Yang. "Abstract 780: Dimethyl cardamonin induces G1-phase cell cycle arrest, apoptosis, and autophagy in HCT116 cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-780.

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Gulappa, Thippeswamy, Rama S. Reddy, Suman Suman, and Chendil Damodaran. "Abstract 559: The molecular kinetics of p21 and Cdk4 dictates irreversible G0/G1 phase cell cycle arrest in CRPC cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-559.

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Gao, Jingchun. "Abstract 905: Mirk/Dyrk1B mediates cell survival and G0/G1 phase of cell cycle via interacting with MAPK/ERK pathway in human cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-905.

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Kabolizadeh, Peyman, Ralph Kipping, Vijay Menon, John Ryan, Erica Peterson, Lawrence Povirk, and Nicholas Farrell. "Abstract 2494: A non-covalent binding platinum drug, TriplatinNC, induces a G1 phase cell cycle arrest and p53-independent mechanisms of apoptosis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2494.

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Sin, Eun Ah, Eun J. Sohn, Ji Hoon Jung, Duckgue Lee, Bonglee Kim, Duck-Beom Jung, Ji-Hyun Kim, Hyo-Jeong Lee, and Sung Hoon Kim. "Abstract 1740: SATB2 localizes to mitotic microtubules and centrosome of cell cycles and regulates G1 phase cell cycle via proteosomal-dependent CDK2 in SKOV-3 ovarian cancer cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1740.

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Babcook, Melissa A., R. Michael Sramkoski, Hisashi Fujioka, Firouz Daneshgari, Alexandru Almasan, Sanjeev Shukla, and Sanjay Gupta. "Abstract 16: Combination simvastatin and metformin induces G1-phase cell cycle arrest and Ripk1- and Ripk3-dependent necroptosis in C4-2B osseous metastatic castration-resistant prostate cancer cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-16.

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Hafeez, Bilal B., Nancy E. Dreckschmidt, Laurie A. Colson, and Ajit K. Verma. "Abstract 3800: Dietary agent α-Mangostin inhibits growth of pancreatic cancer BxPC3 and PANC1 cells and arrests the cell cycle in G0/G1 phase: Involvement of Ras, Hedgehog, NF-kB, and STAT3 signaling networks." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3800.

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