scholarly journals Requirement for ESP1 in the nuclear division of Saccharomyces cerevisiae.

1992 ◽  
Vol 3 (12) ◽  
pp. 1443-1454 ◽  
Author(s):  
J T McGrew ◽  
L Goetsch ◽  
B Byers ◽  
P Baum
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Normal Cell ◽  
Cell Cycle Progression ◽  
Nuclear Division ◽  
Flow Cytometric Analysis ◽  
Spindle Pole ◽  
Spindle Pole Bodies ◽  
Mutant Cells ◽  
Normal Cell Cycle

Mutations in the ESP1 gene of Saccharomyces cerevisiae disrupt normal cell-cycle control and cause many cells in a mutant population to accumulate extra spindle pole bodies. To determine the stage at which the esp1 gene product becomes essential for normal cell-cycle progression, synchronous cultures of ESP1 mutant cells were exposed to the nonpermissive temperature for various periods of time. The mutant cells retained viability until the onset of mitosis, when their viability dropped markedly. Examination of these cells by fluorescence and electron microscopy showed the first detectable defect to be a structural failure in the spindle. Additionally, flow cytometric analysis of DNA content demonstrated that massive chromosome missegregation accompanied this failure of spindle function. Cytokinesis occurred despite the aberrant nuclear division, which often resulted in segregation of both spindle poles to the same cell. At later times, the missegregated spindle pole bodies entered a new cycle of duplication, thereby leading to the accumulation of extra spindle pole bodies within a single nucleus. The DNA sequence predicts a protein product similar to those of two other genes that are also required for nuclear division: the cut1 gene of Schizosaccharomyces pombe and the bimB gene of Aspergillus nidulans.

scholarly journals Disturbance of normal cell cycle progression enhances the establishment of transcriptional silencing in Saccharomyces cerevisiae.

1995 ◽  
Vol 15 (7) ◽  
pp. 3608-3617 ◽  
Author(s):  
H Laman ◽  
D Balderes ◽  
D Shore
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Normal Cell ◽  
Cell Cycle Progression ◽  
Position Effect ◽  
General Effect ◽  
Cell Cycle Regulators ◽  
Cycle Progression ◽  
Cyclin Genes ◽  
Normal Cell Cycle

Previous studies have indicated that mutation of RAP1 (rap1s) or of the HMR-E silencer ARS consensus element leads to metastable repression of HMR. A number of extragenic suppressor mutations (sds, suppressors of defective silencing) that increase the fraction of repressed cells in rap1s hmr delta A strains have been identified. Here we report the cloning of three SDS genes. SDS11 is identical to SWI6, a transcriptional regulator of genes required for DNA replication and of cyclin genes. SDS12 is identical to RNR1, which encodes a subunit of ribonucleotide reductase. SDS15 is identical to CIN8, whose product is required for spindle formation. We propose that mutations in these genes improve the establishment of silencing by interfering with normal cell cycle progression. In support of this idea, we show that exposure to hydroxyurea, which increases the length of S phase, also restores silencing in rap1s hmr delta A strains. Mutations in different cyclin genes (CLN3, CLB5, and CLB2) and two cell cycle transcriptional regulators (SWI4 and MBP1) also suppress the silencing defect at HMR. The effect of these cell cycle regulators is not specific to the rap1s or hmr delta A mutation, since swi6, swi4, and clb5 mutations also suppress mutations in SIR1, another gene implicated in the establishment of silencing. Several mutations also improve the efficiency of telomeric silencing in wild-type strains, further demonstrating that disturbance of the cell cycle has a general effect on position effect repression in Saccharomyces cerevisiae. We suggest several possible models to explain this phenomenon.

scholarly journals Chk1-mediated Cdc25A degradation as a critical mechanism for normal cell cycle progression

2019 ◽  
Vol 132 (2) ◽  
pp. jcs223123 ◽  
Author(s):  
Hidemasa Goto ◽  
Toyoaki Natsume ◽  
Masato T. Kanemaki ◽  
Aika Kaito ◽  
Shujie Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Normal Cell ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Normal Cell Cycle

scholarly journals The decision to enter mitosis: feedback and redundancy in the mitotic entry network

2009 ◽  
Vol 185 (2) ◽  
pp. 193-202 ◽  
Author(s):  
Arne Lindqvist ◽  
Verónica Rodríguez-Bravo ◽  
René H. Medema
Keyword(s):  
Cell Cycle ◽  
Normal Cell ◽  
Cell Cycle Progression ◽  
Feedback Loops ◽  
Cyclin B ◽  
Cycle Progression ◽  
Mitotic Entry ◽  
Different Levels ◽  
Normal Cell Cycle

The decision to enter mitosis is mediated by a network of proteins that regulate activation of the cyclin B–Cdk1 complex. Within this network, several positive feedback loops can amplify cyclin B–Cdk1 activation to ensure complete commitment to a mitotic state once the decision to enter mitosis has been made. However, evidence is accumulating that several components of the feedback loops are redundant for cyclin B–Cdk1 activation during normal cell division. Nonetheless, defined feedback loops become essential to promote mitotic entry when normal cell cycle progression is perturbed. Recent data has demonstrated that at least three Plk1-dependent feedback loops exist that enhance cyclin B–Cdk1 activation at different levels. In this review, we discuss the role of various feedback loops that regulate cyclin B–Cdk1 activation under different conditions, the timing of their activation, and the possible identity of the elusive trigger that controls mitotic entry in human cells.

scholarly journals A novel form of Deleted in breast cancer 1 (DBC1) lacking the N-terminal domain does not bind SIRT1 and is dynamically regulated in vivo

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Leonardo Santos ◽  
Laura Colman ◽  
Paola Contreras ◽  
Claudia C. Chini ◽  
Adriana Carlomagno ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Liver Regeneration ◽  
Partial Hepatectomy ◽  
Normal Cell ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Quiescent Cells ◽  
Normal Cell Cycle

Abstract The protein Deleted in Breast Cancer-1 is a regulator of several transcription factors and epigenetic regulators, including HDAC3, Rev-erb-alpha, PARP1 and SIRT1. It is well known that DBC1 regulates its targets, including SIRT1, by protein-protein interaction. However, little is known about how DBC1 biological activity is regulated. In this work, we show that in quiescent cells DBC1 is proteolytically cleaved, producing a protein (DN-DBC1) that misses the S1-like domain and no longer binds to SIRT1. DN-DBC1 is also found in vivo in mouse and human tissues. Interestingly, DN-DBC1 is cleared once quiescent cells re-enter to the cell cycle. Using a model of liver regeneration after partial hepatectomy, we found that DN-DBC1 is down-regulated in vivo during regeneration. In fact, WT mice show a decrease in SIRT1 activity during liver regeneration, coincidentally with DN-DBC1 downregulation and the appearance of full length DBC1. This effect on SIRT1 activity was not observed in DBC1 KO mice. Finally, we found that DBC1 KO mice have altered cell cycle progression and liver regeneration after partial hepatectomy, suggesting that DBC1/DN-DBC1 transitions play a role in normal cell cycle progression in vivo after cells leave quiescence. We propose that quiescent cells express DN-DBC1, which either replaces or coexist with the full-length protein, and that restoring of DBC1 is required for normal cell cycle progression in vitro and in vivo. Our results describe for the first time in vivo a naturally occurring form of DBC1, which does not bind SIRT1 and is dynamically regulated, thus contributing to redefine the knowledge about its function.

scholarly journals Dynamic regulation of the PR-Set7 histone methyltransferase is required for normal cell cycle progression

2010 ◽  
Vol 24 (22) ◽  
pp. 2531-2542 ◽  
Author(s):  
S. Wu ◽  
W. Wang ◽  
X. Kong ◽  
L. M. Congdon ◽  
K. Yokomori ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Normal Cell ◽  
Cell Cycle Progression ◽  
Histone Methyltransferase ◽  
Cycle Progression ◽  
Dynamic Regulation ◽  
Normal Cell Cycle

scholarly journals Involvement of DNA-dependent Protein Kinase in Normal Cell Cycle Progression through Mitosis

2011 ◽  
Vol 286 (14) ◽  
pp. 12796-12802 ◽  
Author(s):  
Kyung-Jong Lee ◽  
Yu-Fen Lin ◽  
Han-Yi Chou ◽  
Hirohiko Yajima ◽  
Kazi R. Fattah ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Protein Kinase ◽  
Normal Cell ◽  
Cell Cycle Progression ◽  
Dependent Protein Kinase ◽  
Cycle Progression ◽  
Dependent Protein ◽  
Normal Cell Cycle

scholarly journals Budding Yeast Bub2 Is Localized at Spindle Pole Bodies and Activates the Mitotic Checkpoint via a Different Pathway from Mad2

1999 ◽  
Vol 145 (5) ◽  
pp. 979-991 ◽  
Author(s):  
Roberta Fraschini ◽  
Elisa Formenti ◽  
Giovanna Lucchini ◽  
Simonetta Piatti
Keyword(s):  
Cell Cycle ◽  
Mitotic Spindle ◽  
Cell Cycle Progression ◽  
Budding Yeast ◽  
Spindle Pole Body ◽  
Mitotic Checkpoint ◽  
Spindle Pole ◽  
Cycle Progression ◽  
Spindle Pole Bodies

The mitotic checkpoint blocks cell cycle progression before anaphase in case of mistakes in the alignment of chromosomes on the mitotic spindle. In budding yeast, the Mad1, 2, 3, and Bub1, 2, 3 proteins mediate this arrest. Vertebrate homologues of Mad1, 2, 3, and Bub1, 3 bind to unattached kinetochores and prevent progression through mitosis by inhibiting Cdc20/APC-mediated proteolysis of anaphase inhibitors, like Pds1 and B-type cyclins. We investigated the role of Bub2 in budding yeast mitotic checkpoint. The following observations indicate that Bub2 and Mad1, 2 probably activate the checkpoint via different pathways: (a) unlike the other Mad and Bub proteins, Bub2 localizes at the spindle pole body (SPB) throughout the cell cycle; (b) the effect of concomitant lack of Mad1 or Mad2 and Bub2 is additive, since nocodazole-treated mad1 bub2 and mad2 bub2 double mutants rereplicate DNA more rapidly and efficiently than either single mutant; (c) cell cycle progression of bub2 cells in the presence of nocodazole requires the Cdc26 APC subunit, which, conversely, is not required for mad2 cells in the same conditions. Altogether, our data suggest that activation of the mitotic checkpoint blocks progression through mitosis by independent and partially redundant mechanisms.

scholarly journals Multiple SWI6-dependent cis-acting elements control SWI4 transcription through the cell cycle.

1993 ◽  
Vol 13 (6) ◽  
pp. 3792-3801 ◽  
Author(s):  
R Foster ◽  
G E Mikesell ◽  
L Breeden
Keyword(s):  
Cell Cycle ◽  
Normal Cell ◽  
Cell Cycle Regulation ◽  
Cell Cycle Progression ◽  
Cis Acting ◽  
Upstream Activating Sequence ◽  
A Cell ◽  
Cis And Trans ◽  
Cycle Regulation ◽  
Normal Cell Cycle

The Saccharomyces cerevisiae SWI4 gene encodes an essential transcription factor which controls gene expression at the G1/S transition of the cell cycle. SWI4 transcription itself is cell cycle regulated, and this periodicity is crucial for the normal cell cycle regulation of HO and at least two of the G1 cyclins. Since the regulation of SWI4 is required for normal cell cycle progression, we have characterized cis- and trans-acting regulators of SWI4 transcription. Deletion analysis of the SWI4 promoter has defined a 140-bp region which is absolutely required for transcription and can function as a cell cycle-regulated upstream activating sequence (UAS). The SWI4 UAS contains three potential MluI cell cycle boxes (MCBs), which are known cell cycle-regulated promoter elements. Deletion of all three MCBs in the SWI4 UAS decreases the level of SWI4 mRNA 10-fold in asynchronous cultures but does not abolish periodicity. These data suggest that MCBs are involved in SWI4 UAS activity, but at least one other periodically regulated element must be present. Since SWI6 is known to bind to MCBs and regulate their activity, the role of SWI6 in SWI4 expression was analyzed. Although the MCBs cannot account for the full cell cycle regulation of SWI4, mutations in SWI6 eliminate the normal periodicity of SWI4 transcription. This suggests that the novel cell cycle-regulated element within the SWI4 promoter is also SWI6 dependent. The constitutive transcription of SWI4 in SWI6 mutant cells occurs at an intermediate level, which indicates that SWI6 is required for the full activation and repression of SWI4 transcription through the cell cycle. It also suggests that there is another pathway which can activate SWI4 transcription in the absence of SWI6. The second activator may also target MCB elements, since SWI4 transcription drops dramatically when they are deleted.

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