scholarly journals Two distinct pathways responsible for the loading of CENP-A to centromeres in the fission yeast cell cycle

2005 ◽  
Vol 360 (1455) ◽  
pp. 595-607 ◽  
Author(s):  
Kohta Takahashi ◽  
Yuko Takayama ◽  
Fumie Masuda ◽  
Yasuyo Kobayashi ◽  
Shigeaki Saitoh
Keyword(s):  
Cell Cycle ◽  
Fission Yeast ◽  
S Phase ◽  
Histone H4 ◽  
Gata Factor ◽  
Checkpoint Response ◽  
Histone H3 Variant ◽  
Two Factors ◽  
A Cell ◽  
G2 Phase

CENP-A is a centromere-specific histone H3 variant that is- essential for faithful chromosome segregation in all eukaryotes thus far investigated. We genetically identified two factors, Ams2 and Mis6, each of which is required for the correct centromere localization of SpCENP-A (Cnp1), the fission yeast homologue of CENP-A. Ams2 is a cell-cycle-regulated GATA factor that localizes on the nuclear chromatin, including on centromeres, during the S phase. Ams2 may be responsible for the replication-coupled loading of SpCENP-A by facilitating nucleosomal formation during the S phase. Consistently, overproduction of histone H4, but not that of H3, suppressed the defect of SpCENP-A localization in Ams2-deficient cells. We demonstrated the existence of at least two distinct phases for SpCENP-A loading during the cell cycle: the S phase and the late-G2 phase. Ectopically induced SpCENP-A was efficiently loaded onto the centromeres in G2-arrested cells, indicating that SpCENP-A probably undergoes replication-uncoupled loading after the completion of S phase. This G2 loading pathway of SpCENP-A may require Mis6, a constitutive centromere-binding protein that is also implicated in the Mad2-dependent spindle attachment checkpoint response. Here, we discuss the functional relationship between the flexible loading mechanism of CENP-A and the plasticity of centromere chromatin formation in fission yeast.

scholarly journals Biphasic Incorporation of Centromeric Histone CENP-A in Fission Yeast

2008 ◽  
Vol 19 (2) ◽  
pp. 682-690 ◽  
Author(s):  
Yuko Takayama ◽  
Hiroshi Sato ◽  
Shigeaki Saitoh ◽  
Yuki Ogiyama ◽  
Fumie Masuda ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Fission Yeast ◽  
Genome Stability ◽  
Fluorescent Protein ◽  
Gene Activation ◽  
S Phase ◽  
Dependent Manner ◽  
Gata Factor ◽  
Histone H3 Variant ◽  
Green Fluorescent

CENP-A is a centromere-specific histone H3 variant that is essential for kinetochore formation. Here, we report that the fission yeast Schizosaccharomyces pombe has at least two distinct CENP-A deposition phases across the cell cycle: S and G2. The S phase deposition requires Ams2 GATA factor, which promotes histone gene activation. In Δams2, CENP-A fails to retain during S, but it reaccumulates onto centromeres via the G2 deposition pathway, which is down-regulated by Hip1, a homologue of HIRA histone chaperon. Reducing the length of G2 in Δams2 results in failure of CENP-A accumulation, leading to chromosome missegregation. N-terminal green fluorescent protein-tagging reduces the centromeric association of CENP-A, causing cell death in Δams2 but not in wild-type cells, suggesting that the N-terminal tail of CENP-A may play a pivotal role in the formation of centromeric nucleosomes at G2. These observations imply that CENP-A is normally localized to centromeres in S phase in an Ams2-dependent manner and that the G2 pathway may salvage CENP-A assembly to promote genome stability. The flexibility of CENP-A incorporation during the cell cycle may account for the plasticity of kinetochore formation when the authentic centromere is damaged.

Cyclin Dependent Kinases and Regulation of the Fission Yeast Cell Cycle

1999 ◽  
Vol 380 (7-8) ◽  
pp. 729-733 ◽  
Author(s):  
P. Nurse
Keyword(s):  
Cell Cycle ◽  
Yeast Cell ◽  
Fission Yeast ◽  
S Phase ◽  
Yeast Cell Cycle ◽  
Cyclin Dependent Kinases ◽  
Fission Yeast Cell ◽  
Nutritional Deprivation ◽  
Orderly Fashion ◽  
A Cell

AbstractThe cyclin dependent kinases (CDKs), formed by complexes between Cdc2p and the B-cyclins Cig2p and Cdc13p, have a central role in regulating the fission yeast cell cycle and maintaining genomic stability. The CDK Cig2p/Cdc2p controls the onset of S-phase and the CDK Cdc13p/Cdc2p controls the onset of mitosis and ensures that there is only one S-phase in each cell. Cdc13p/Cdc2p can replace Cig2p/Cdc2p for the onset of S-phase, suggesting that the increasing activity of a single CDK during the cell cycle is sufficient to drive a cell in an orderly fashion into S-phase and into mitosis. If S-phase is incomplete, then inhibition of Cdc13p/Cdc2p prevents cells with unreplicated DNA from undergoing a catastrophic entry into mitosis. Control of CDK activity is also important to allow cells to exit the cell cycle and accumulate in G1 in response to nutritional deprivation and the presence of pheromone.

scholarly journals Subunit interactions and arrangements in the fission yeast Mis16–Mis18–Mis19 complex

2019 ◽  
Vol 2 (4) ◽  
pp. e201900408 ◽  
Author(s):  
Melanie Korntner-Vetter ◽  
Stéphane Lefèvre ◽  
Xiao-Wen Hu ◽  
Roger George ◽  
Martin R Singleton
Keyword(s):  
Cell Cycle ◽  
Binding Site ◽  
Fission Yeast ◽  
Histone H3 ◽  
Histone H4 ◽  
Subunit Interactions ◽  
Centromeric Chromatin ◽  
Partner Protein ◽  
Histone H3 Variant

Centromeric chromatin in fission yeast is distinguished by the presence of nucleosomes containing the histone H3 variant Cnp1CENP-A. Cell cycle–specific deposition of Cnp1 requires the Mis16–Mis18–Mis19 complex, which is thought to direct recruitment of Scm3-chaperoned Cnp1/histone H4 dimers to DNA. Here, we present the structure of the essential Mis18 partner protein Mis19 and describe its interaction with Mis16, revealing a bipartite-binding site. We provide data on the stoichiometry and overall architecture of the complex and provide detailed insights into the Mis18–Mis19 interface.

The Effect of Cell Mass on the Cell Cycle Timing and Duration of S-Phase in Fission Yeast

1979 ◽  
Vol 39 (1) ◽  
pp. 215-233
Author(s):  
KIM NASMYTH ◽  
PAUL NURSE ◽  
R. S. S. FRASER
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Fission Yeast ◽  
Critical Level ◽  
Single Cells ◽  
Cell Mass ◽  
S Phase ◽  
Pulse Labelling ◽  
Random Transition ◽  
A Cell

Request for reprints to Paul Nurse. Two isotopic methods for measuring DNA replication in the fission yeast Schizosaccharomyces pombe are described. The first is a method for measuring the total quantity of [3H]uracil incorporated into DNA after pulse labelling. The second is a means of detecting DNA replication in single cells by autoradiography. Both of these techniques have been used to investigate the timing and duration of S-phase in a series of mutant strains whose cell mass at division varies over a 3-fold range. The results support the hypothesis that in S. pombe there are 2 different controls over the timing of S-phase: an attainment of a critical cell mass and a dependency upon the completion of the previous mitosis coupled with a short minimum time in G1. Strains whose cell mass at birth is above this critical level initiate DNA replication almost immediately after septation, that is, very soon after the previous mitosis. Strains whose cell mass at birth is below the critical level do not initiate replication until the critical cell mass is attained. The duration of S-phase has been estimated from the proportion of cells whose nuclei are labelled after a pulse of given duration. S-phase is short in S. pombe, lasting only about 0.1 of a cell cycle in wild type. Cell mass at S-phase does not have any consistent effect on this length. We have also investigated the degree of synchrony of S-phase initiation in daughter cells, and have found that, in a cell cycle 240 min long, their S-phases are initiated within 1–2 min of each other. This result indicates that between sisters variability in the duration of the G1 phase is small compared with variability in the total cell cycle time, and argues against the hypothesis that the rate of cell cycle traverse is determined by a random transition in G1.

The Wellcome Lecture, 1992. Cell cycle control

1993 ◽  
Vol 341 (1298) ◽  
pp. 449-454 ◽  
Keyword(s):  
Cell Cycle ◽  
Fission Yeast ◽  
Gene Network ◽  
Cell Cycle Control ◽  
Regulatory Gene ◽  
Eukaryotic Cell ◽  
S Phase ◽  
M Phase ◽  
A Cell ◽  
Future Work

Genetic analysis using the fission yeast has provided a powerful methodology to investigate the eukaryotic cell cycle and its control. The onset of M -phase in fission yeast is controlled by a regulatory gene network which activates the p34 cdc2 protein kinase encoded by the cdc 2 + gene. The coupling of M -phase to the completion of S-phase also works through p34 cdc2 . A similar network is operative in vertebrate cells. Future work will focus on the controls regulating onset of S-phase and on the mechanisms by which a cell duplicates itself in space during division.

scholarly journals Transcription of alpha-tubulin and histone H4 genes begins at the same point in the Physarum cell cycle.

1986 ◽  
Vol 102 (5) ◽  
pp. 1666-1670 ◽  
Author(s):  
J J Carrino ◽  
T G Laffler
Keyword(s):  
Cell Cycle ◽  
Gene Transcription ◽  
Blot Hybridization ◽  
S Phase ◽  
Histone Gene ◽  
Histone H4 ◽  
Alpha Tubulin ◽  
Periodic Cell ◽  
G2 Phase ◽  
Histone Gene Transcription

In naturally synchronous plasmodia of Physarum polycephalum, both tubulin and histone gene transcription define periodic cell cycle-regulated events. Using a slot-blot hybridization assay and Northern blot analysis, we have demonstrated that a major peak of accumulation of both alpha-tubulin and histone H4 transcripts occurs in late G2 phase. Nuclear transcription assays indicate that both genes are transcriptionally activated at the same point in the cell cycle: mid G2 phase. While the rate of tubulin gene transcription drops sharply at the M/S-phase boundary, the rate of histone gene transcription remains high through most of S phase. We conclude that the cell cycle regulation of tubulin expression occurs primarily at the level of transcription, while histone regulation involves both transcriptional and posttranscriptional controls. It is possible that the periodic expression of both histone and tubulin genes is triggered by a common cell cycle regulatory mechanism.

scholarly journals A Cell Cycle-Regulated GATA Factor Promotes Centromeric Localization of CENP-A in Fission Yeast

2003 ◽  
Vol 11 (1) ◽  
pp. 175-187 ◽  
Author(s):  
Ee Sin Chen ◽  
Shigeaki Saitoh ◽  
Mitsuhiro Yanagida ◽  
Kohta Takahashi
Keyword(s):  
Cell Cycle ◽  
Fission Yeast ◽  
Gata Factor ◽  
A Cell

scholarly journals JunB Breakdown in Mid-/Late G2 Is Required for Down-Regulation of Cyclin A2 Levels and Proper Mitosis

2008 ◽  
Vol 28 (12) ◽  
pp. 4173-4187 ◽  
Author(s):  
Rosa Farràs ◽  
Véronique Baldin ◽  
Sandra Gallach ◽  
Claire Acquaviva ◽  
Guillaume Bossis ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Genetic Instability ◽  
S Phase ◽  
Subsequent Reduction ◽  
Suppressor Activity ◽  
Cell Synchronization ◽  
Tumor Suppressor Activity ◽  
A Cell ◽  
Cyclin A2

ABSTRACT JunB, a member of the AP-1 family of dimeric transcription factors, is best known as a cell proliferation inhibitor, a senescence inducer, and a tumor suppressor, although it also has been attributed a cell division-promoting activity. Its effects on the cell cycle have been studied mostly in G1 and S phases, whereas its role in G2 and M phases still is elusive. Using cell synchronization experiments, we show that JunB levels, which are high in S phase, drop during mid- to late G2 phase due to accelerated phosphorylation-dependent degradation by the proteasome. The forced expression of an ectopic JunB protein in late G2 phase indicates that JunB decay is necessary for the subsequent reduction of cyclin A2 levels in prometaphase, the latter event being essential for proper mitosis. Consistently, abnormal JunB expression in late G2 phase entails a variety of mitotic defects. As these aberrations may cause genetic instability, our findings contrast with the acknowledged tumor suppressor activity of JunB and reveal a mechanism by which the deregulation of JunB might contribute to tumorigenesis.

Excision and replication of extrachromosomal DNA of pea (Pisum sativum)

1983 ◽  
Vol 3 (2) ◽  
pp. 172-181
Author(s):  
J Van't Hof ◽  
C A Bjerknes ◽  
N C Delihas
Keyword(s):  
Cell Cycle ◽  
Pisum Sativum ◽  
S Phase ◽  
Velocity Sedimentation ◽  
Extrachromosomal Dna ◽  
Chromosomal Dna ◽  
Root Tips ◽  
Dividing Cells ◽  
G2 Phase ◽  
Pea Roots

Experiments with cultured pea roots were conducted to determine (i) whether extrachromosomal DNA was produced by cells in the late S phase or in the G2 phase of the cell cycle, (ii) whether the maturation of nascent DNA replicated by these cells achieved chromosomal size, (iii) when extrachromosomal DNA was removed from the chromosomal duplex, and (iv) the replication of nascent chains by the extrachromosomal DNA after its release from the chromosomal duplex. Autoradiography and cytophotometry of cells of carbohydrate-starved root tips revealed that extrachromosomal DNA was produced by a small fraction of cells accumulated in the late S phase after they had replicated about 80% of their DNA. Velocity sedimentation of nascent chromosomal DNA in alkaline sucrose gradients indicated that the DNA of cells in the late S phase failed to achieve chromosomal size. After reaching sizes of 70 X 10(6) to 140 X 10(6) daltons, some of the nascent chromosomal molecules were broken, presumably releasing extrachromosomal DNA several hours later. Sedimentation of selectively extracted extrachromosomal DNA either from dividing cells or from those in the late S phase showed that it replicated two nascent chains, one of 3 X 10(6) daltons and another of 7 X 10(6) daltons. Larger molecules of extrachromosomal DNA were detectable after cells were labeled for 24 h. These two observations were compatible with the idea that the extrachromosomal DNA was first replicated as an integral part of the chromosomal duplex, was cut from the duplex, and then, once free of the chromosome, replicated two smaller chains of 3 X 10(6) and 7 X 10(6) daltons.

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