Publications of Steve Haase :chronological combined listing:
%% Papers Published
@article{fds141048,
Author = {SB Haase and DJ Lew},
Title = {Microtubule organization: cell shape is destiny.},
Journal = {Current biology : CB, England},
Volume = {17},
Number = {7},
Pages = {R249-51},
Year = {2007},
Month = {April},
Keywords = {Animals • Cell Shape* • Microtubules •
Mitotic Spindle Apparatus • Plants •
Schizosaccharomyces • cytology • metabolism •
metabolism*},
Abstract = {A simple self-assembly pathway generates cytoplasmic
microtubule bundles that can locate the cell center and
guide spindle assembly in fission yeast. The cylindrical
cell shape automatically corrects spindle orientation
errors, rendering a checkpoint unnecessary.},
Key = {fds141048}
}
@article{fds141047,
Author = {DA Orlando and CY Lin and A Bernard and ES Iversen and AJ Hartemink and SB
Haase},
Title = {A probabilistic model for cell cycle distributions in
synchrony experiments.},
Journal = {Cell cycle (Georgetown, Tex.), United States},
Volume = {6},
Number = {4},
Pages = {478-88},
Year = {2007},
Month = {February},
Keywords = {Cell Division • Flow Cytometry • Models,
Biological* • Models, Statistical • Saccharomyces
cerevisiae • Schizosaccharomyces • Time Factors
• cytology • cytology* • growth & development
• metabolism • physiology*},
Abstract = {Synchronized populations of cells are often used to study
dynamic processes during the cell division cycle. However,
the analysis of time series measurements made on
synchronized populations is confounded by the fact that
populations lose synchrony over time. Time series
measurements are thus averages over a population
distribution that is broadening over time. Moreover, direct
comparison of measurements taken from multiple synchrony
experiments is difficult, as the kinetics of progression
during the time series are rarely comparable. Here, we
present a flexible mathematical model that describes the
dynamics of population distributions resulting from
synchrony loss over time. The model was developed using S.
cerevisiae, but we show that it can be easily adapted to
predict distributions in other organisms. We demonstrate
that the model reliably fits data collected from populations
synchronized by multiple techniques, and can accurately
predict cell cycle distributions as measured by other
experimental assays. To indicate its broad applicability, we
show that the model can be used to compare global periodic
transcription data sets from different organisms: S.
cerevisiae and S. pombe.},
Key = {fds141047}
}
@article{fds52648,
Author = {LP Jackson and SI Reed and SB Haase},
Title = {Distinct mechanisms control the stability of the related
S-phase cyclins Clb5 and Clb6.},
Journal = {Molecular and cellular biology, United States},
Volume = {26},
Number = {6},
Pages = {2456-66},
Year = {2006},
Month = {March},
ISSN = {0270-7306},
Keywords = {Amino Acid Motifs • Amino Acid Sequence • Base
Sequence • CDC28 Protein Kinase, S cerevisiae •
Cell Cycle Proteins • Cyclin B • Cyclin-Dependent
Kinases • F-Box Proteins • Gene Expression
Regulation, Fungal • Molecular Sequence Data •
Mutation • Peptide Fragments • Phosphorylation
• Promoter Regions (Genetics) • S Phase •
Saccharomyces cerevisiae Proteins • Ubiquitin •
Ubiquitin-Protein Ligase Complexes • Ubiquitin-Protein
Ligases • genetics • metabolism • metabolism*
• physiology*},
Abstract = {The yeast S-phase cyclins Clb5 and Clb6 are closely related
proteins that are synthesized late in G1. Although often
grouped together with respect to function, Clb5 and Clb6
exhibit differences in their ability to promote S-phase
progression. DNA replication is significantly slowed in
clb5Delta mutants but not in clb6Delta mutants. We have
examined the basis for the differential functions of Clb5
and Clb6 and determined that unlike Clb5, which is stable
until mitosis, Clb6 is degraded rapidly at the G1/S border.
N-terminal deletions of CLB6 were hyperstabilized,
suggesting that the sequences responsible for directing the
destruction of Clb6 reside in the N terminus. Clb6 lacks the
destruction box motif responsible for the anaphase promoting
complex-mediated destruction of Clb5 but contains putative
Cdc4 degron motifs in the N terminus. Clb6 was
hyperstabilized in cdc34-3 and cdc4-3 mutants at restrictive
temperatures and when S/T-P phosphorylation sites in the N
terminus were mutated to nonphosphorylatable residues.
Efficient degradation of Clb6 requires the activities of
both Cdc28 and Pho85. Finally, hyperstabilized Clb6
expressed from the CLB6 promoter rescued the slow S-phase
defect exhibited by clb5Delta cells. Taken together, these
findings suggest that the SCF(Cdc4) ubiquitin ligase complex
regulates Clb6 turnover and that the functional differences
exhibited by Clb5 and Clb6 arise from the distinct
mechanisms controlling their stability.},
Key = {fds52648}
}
@article{fds17346,
Author = {S. Haase},
Title = {Cell Cycle Analysis of Budding Yeast Using SYTOX
Green},
Pages = {7.23.1-7.23.5},
Booktitle = {Curr. Prot. Cytom.},
Publisher = {John Wiley and Sons, Inc.},
Editor = {J. Paul Robinson},
Year = {2003},
Month = {Fall},
Key = {fds17346}
}
@article{fds17352,
Author = {S.B. Haase and S.I. Reed},
Title = {Improved flow cytometric analysis of the budding yeast cell
cycle},
Journal = {Cell Cycle},
Volume = {1},
Number = {2},
Pages = {132-136},
Year = {2002},
Abstract = {The budding yeast, Saccharomyces cerevisiae has been a
remarkably useful model system for the study of eukaryotic
cell cycle regulation. Flow cytometric analysis of DNA
content in budding yeast has become a standard tool for the
analysis of cell cycle progression. However, popular
protocols utilizing the DNA binding dye, propidium iodide,
suffer from a number of drawbacks that confound accurate
analysis by flow cytometry. Here we show the utility of the
DNA binding dye, SYTOX Green, in the cell cycle analysis of
yeast. Samples analyzed using SYTOX Green exhibited better
coefficients of variation, improved linearity between DNA
content and fluorescence, and decreased peak drift
associated with changes in dye concentration, growth
conditions or cell size.},
Key = {fds17352}
}
@article{fds141051,
Author = {SB Haase and DJ Clarke},
Title = {A festival of cell-cycle controls.},
Journal = {Trends in cell biology, England},
Volume = {11},
Number = {11},
Pages = {445-6},
Year = {2001},
Month = {November},
Keywords = {Animals • Cell Cycle • Cell Cycle Proteins •
Chromatin • DNA Replication • Genes, cdc •
Humans • Kinetochores • Mitosis • chemistry
• metabolism • metabolism* • physiology
• physiology*},
Abstract = {The second biennial Salk Cell Cycle meeting convened on 22
June 2001 in San Diego, California. Organized by Tony Hunter
and Susan Forsburg of the Salk Institute, the five-day
conference was highlighted by enlightening science and
plenty of San Diego sunshine. Presentations covered a broad
range of contemporary cell-cycle topics, ranging from
regulation of DNA replication and mitosis to DNA damage
recognition and checkpoint control.},
Key = {fds141051}
}
@article{fds141052,
Author = {SB Haase and M Winey and SI Reed},
Title = {Multi-step control of spindle pole body duplication by
cyclin-dependent kinase.},
Journal = {Nature cell biology, England},
Volume = {3},
Number = {1},
Pages = {38-42},
Year = {2001},
Month = {January},
Keywords = {Cell Cycle • Cell Transformation, Neoplastic •
Centrosome • Cyclin B • Cyclin-Dependent Kinases
• Cyclins • Mitosis • Mitotic Spindle
Apparatus • Saccharomyces cerevisiae Proteins* •
Yeasts • enzymology* • genetics • genetics*
• metabolism • metabolism* •
physiology*},
Abstract = {Organelles called centrosomes in metazoans or spindle pole
bodies (SPBs) in yeast direct the assembly of a bipolar
spindle that is essential for faithful segregation of
chromosomes during mitosis. Abnormal accumulation of
multiple centrosomes leads to genome instability, and has
been observed in both tumour cells and cells with targeted
mutations in tumour-suppressor genes. The defects that lead
to centrosome amplification are not understood. We have
recapitulated the multiple-centrosome phenotype in budding
yeast by disrupting the activity of specific
cyclin-dependent kinase (CDK) complexes. Our observations
are reminiscent of mechanisms that govern DNA replication,
and show that specific cyclin/CDK activities function both
to promote SPB duplication and to prevent SPB
reduplication.},
Key = {fds141052}
}
@article{fds17348,
Author = {S.B. Haase and M. Winey and S. I Reed},
Title = {Multi-step control of spindle pole body duplication by
cyclin-dependent kinase},
Journal = {Nature Cell Biology},
Volume = {3},
Number = {1},
Pages = {599-607},
Year = {2001},
Abstract = {Organelles called centrosomes in metazoans or spindle pole
bodies (SPBs) in yeast direct the assembly of a bipolar
spindle that is essential for faithful segregation of
chromosomes during mitosis. Abnormal accumulation of
multiple centrosomes leads to genome instability, and has
been observed in both tumour cells and cells with targeted
mutations in tumour-suppressor genes. The defects that lead
to centrosome amplification are not understood. We have
recapitulated the multiple-centrosome phenotype in budding
yeast by disrupting the activity of specific
cyclin-dependent kinase (CDK) complexes. Our observations
are reminiscent of mechanisms that govern DNA replication,
and show that specific cyclin/CDK activities function both
to promote SPB duplication and to prevent SPB
reduplication.},
Key = {fds17348}
}
@article{fds17349,
Author = {S.B. Haase and D. J. Clarke},
Title = {A Festival of Cell Cycle Controls},
Journal = {Trends in Cell Biology},
Volume = {11},
Number = {11},
Pages = {445-446},
Year = {2001},
Abstract = {The second biennial Salk Cell Cycle meeting convened on 22
June 2001 in San Diego, California. Organized by Tony Hunter
and Susan Forsburg of the Salk Institute, the five-day
conference was highlighted by enlightening science and
plenty of San Diego sunshine. Presentations covered a broad
range of contemporary cell-cycle topics, ranging from
regulation of DNA replication and mitosis to DNA damage
recognition and checkpoint control.},
Key = {fds17349}
}
@article{fds141053,
Author = {J Kiely and SB Haase and P Russell and J Leatherwood},
Title = {Functions of fission yeast orp2 in DNA replication and
checkpoint control.},
Journal = {Genetics, UNITED STATES},
Volume = {154},
Number = {2},
Pages = {599-607},
Year = {2000},
Month = {February},
Keywords = {Base Sequence • Cell Cycle • DNA Primers •
DNA Replication • DNA-Binding Proteins • Genes,
Essential • Mutagenesis • Origin Recognition
Complex • Plasmids • Schizosaccharomyces •
Schizosaccharomyces pombe Proteins* • Thymidine Kinase
• cytology • genetics • genetics* •
physiology*},
Abstract = {orp2 is an essential gene of the fission yeast
Schizosaccharomyces pombe with 22% identity to budding yeast
ORC2. We isolated temperature-sensitive alleles of orp2
using a novel plasmid shuffle based on selection against
thymidine kinase. Cells bearing the temperature-sensitive
allele orp2-2 fail to complete DNA replication at a
restrictive temperature and undergo cell cycle arrest. Cell
cycle arrest depends on the checkpoint genes rad1 and rad3.
Even when checkpoint functions are wild type, the orp2-2
mutation causes high rates of chromosome and plasmid loss.
These phenotypes support the idea that Orp2 is a replication
initiation factor. Selective spore germination allowed
analysis of orp2 deletion mutants. These experiments showed
that in the absence of orp2 function, cells proceed into
mitosis despite a lack of DNA replication. This suggests
either that the Orp2 protein is a part of the checkpoint
machinery or more likely that DNA replication initiation is
required to induce the replication checkpoint
signal.},
Key = {fds141053}
}
@article{fds17347,
Author = {J. Kiely and S. B. Haase and P. Russell and J.
Leatherwood},
Title = {Functions of fission yeast Orp2 in DNA replication and
checkpoint control},
Journal = {Genetics},
Number = {154},
Pages = {599-607},
Year = {2000},
Abstract = {orp2 is an essential gene of the fission yeast
Schizosaccharomyces pombe with 22% identity to budding yeast
ORC2. We isolated temperature-sensitive alleles of orp2
using a novel plasmid shuffle based on selection against
thymidine kinase. Cells bearing the temperature-sensitive
allele orp2-2 fail to complete DNA replication at a
restrictive temperature and undergo cell cycle arrest. Cell
cycle arrest depends on the checkpoint genes rad1 and rad3.
Even when checkpoint functions are wild type, the orp2-2
mutation causes high rates of chromosome and plasmid loss.
These phenotypes support the idea that Orp2 is a replication
initiation factor. Selective spore germination allowed
analysis of orp2 deletion mutants. These experiments showed
that in the absence of orp2 function, cells proceed into
mitosis despite a lack of DNA replication. This suggests
either that the Orp2 protein is a part of the checkpoint
machinery or more likely that DNA replication initiation is
required to induce the replication checkpoint
signal.},
Key = {fds17347}
}
@article{fds141054,
Author = {SB Haase and SI Reed},
Title = {Evidence that a free-running oscillator drives G1 events in
the budding yeast cell cycle.},
Journal = {Nature, ENGLAND},
Volume = {401},
Number = {6751},
Pages = {394-7},
Year = {1999},
Month = {September},
Keywords = {CDC28 Protein Kinase, S cerevisiae • Cyclin B •
Cyclin-Dependent Kinases • Cyclins • DNA
Replication • DNA, Fungal • Fungal Proteins •
G1 Phase • Mitotic Spindle Apparatus • Periodicity
• Saccharomycetales • Transcription, Genetic
• biosynthesis • genetics • metabolism •
physiology • physiology*},
Abstract = {In yeast and somatic cells, mechanisms ensure cell-cycle
events are initiated only when preceding events have been
completed. In contrast, interruption of specific cell-cycle
processes in early embryonic cells of many organisms does
not affect the timing of subsequent events, indicating that
cell-cycle events are triggered by a free-running cell-cycle
oscillator. Here we present evidence for an independent
cell-cycle oscillator in the budding yeast Saccharomyces
cerevisiae. We observed periodic activation of events
normally restricted to the G1 phase of the cell cycle, in
cells lacking mitotic cyclin-dependent kinase activities
that are essential for cell-cycle progression. As in
embryonic cells, G1 events cycled on schedule, in the
absence of S phase or mitosis, with a period similar to the
cell-cycle time of wild-type cells. Oscillations of similar
periodicity were observed in cells responding to mating
pheromone in the absence of G1 cyclin (Cln)- and mitotic
cyclin (Clb)-associated kinase activity, indicating that the
oscillator may function independently of cyclin-dependent
kinase dynamics. We also show that Clb-associated kinase
activity is essential for ensuring dependencies by
preventing the initiation of new G1 events when cell-cycle
progression is delayed.},
Key = {fds141054}
}
@article{fds17345,
Author = {S. B. Haase and S. I. Reed},
Title = {Evidence that a free-running oscillator drives G1 events in
the budding yeast cell cycle},
Journal = {Nature},
Number = {401},
Pages = {394-397},
Year = {1999},
Abstract = {In yeast and somatic cells, mechanisms ensure cell-cycle
events are initiated only when preceding events have been
completed. In contrast, interruption of specific cell-cycle
processes in early embryonic cells of many organisms does
not affect the timing of subsequent events, indicating that
cell-cycle events are triggered by a free-running cell-cycle
oscillator. Here we present evidence for an independent
cell-cycle oscillator in the budding yeast Saccharomyces
cerevisiae. We observed periodic activation of events
normally restricted to the G1 phase of the cell cycle, in
cells lacking mitotic cyclin-dependent kinase activities
that are essential for cell-cycle progression. As in
embryonic cells, G1 events cycled on schedule, in the
absence of S phase or mitosis, with a period similar to the
cell-cycle time of wild-type cells. Oscillations of similar
periodicity were observed in cells responding to mating
pheromone in the absence of G1 cyclin (Cln)- and mitotic
cyclin (Clb)-associated kinase activity, indicating that the
oscillator may function independently of cyclin-dependent
kinase dynamics. We also show that Clb-associated kinase
activity is essential for ensuring dependencies by
preventing the initiation of new G1 events when cell-cycle
progression is delayed.},
Key = {fds17345}
}
@article{fds141055,
Author = {SB Haase and DJ Lew},
Title = {Flow cytometric analysis of DNA content in budding
yeast.},
Journal = {Methods in enzymology, UNITED STATES},
Volume = {283},
Pages = {322-32},
Year = {1997},
Keywords = {Animals • Artifacts • Cell Cycle* • DNA
• DNA, Fungal • DNA, Mitochondrial • Flow
Cytometry • Fluorescent Dyes • Indicators and
Reagents • Mammals • Microscopy, Fluorescence
• Propidium • Saccharomyces cerevisiae •
Software • analysis* • cytology* •
methods},
Key = {fds141055}
}
@article{fds141056,
Author = {SB Haase and SS Heinzel and MP Calos},
Title = {Transcription inhibits the replication of autonomously
replicating plasmids in human cells.},
Journal = {Molecular and cellular biology, UNITED STATES},
Volume = {14},
Number = {4},
Pages = {2516-24},
Year = {1994},
Month = {April},
Keywords = {Actins • Cell Line • Chromosomes, Human •
Cytomegalovirus • DNA • DNA Replication* •
DNA, Viral • Enhancer Elements (Genetics) • Genes,
Immediate-Early* • Humans • Kidney • Plasmids
• Promoter Regions (Genetics) • Restriction
Mapping • Terminator Regions (Genetics) •
Tetracycline • Transcription, Genetic* •
biosynthesis • drug effects • genetics •
genetics* • metabolism* • pharmacology},
Abstract = {This study addresses the effect of transcription on
replication, using a system based on autonomously
replicating plasmids in human cells. We added
transcriptional elements from the human cytomegalovirus
promoter/enhancer and the human beta-actin promoter to
autonomously replicating plasmids based on human sequences
and found that the transcriptional elements inhibited
plasmid replication. Furthermore, conditional inhibition of
plasmid replication was demonstrated by using a
tetracycline-responsive promoter. We found that replication
activity of plasmids carrying this promoter was inversely
correlated with promoter activity. Replication activity was
partially restored on plasmids when a transcriptional
termination sequence was placed directly downstream of the
promoter element. Transcriptional activity of the promoters
and the efficacy of the terminator sequence were confirmed
by using steady-state RNA analysis. These experiments
suggest that transcription inhibits DNA replication on these
plasmids and that the degree of inhibition is dependent on
transcription strength. The possible significance of these
results for chromosomal DNA replication are
discussed.},
Key = {fds141056}
}
@article{fds141057,
Author = {SB Haase and MP Calos},
Title = {Replication control of autonomously replicating human
sequences.},
Journal = {Nucleic acids research, ENGLAND},
Volume = {19},
Number = {18},
Pages = {5053-8},
Year = {1991},
Month = {September},
Keywords = {Bromodeoxyuridine • Cell Line • Centrifugation,
Density Gradient • DNA • DNA Replication* •
Genetic Vectors • Herpesvirus 4, Human • Humans
• Plasmids* • Repetitive Sequences, Nucleic Acid
• S Phase • Transfection • genetics •
isolation & purification},
Abstract = {Three autonomously replicating plasmids carrying human
genomic DNA and a vector derived from Epstein-Barr virus
were studied by density labelling to determine the number of
times per cell cycle these plasmids replicate in human
cells. Each of the plasmids replicated semi-conservatively
once per cell cycle. The results suggest that these human
autonomously replicating sequences undergo replication
following the same controls as chromosomal DNA and represent
a good model system for studying chromosomal replication. We
also determined the time within the S phase of the cell
cycle that three of the plasmids replicate. Centromeric
alpha sequences, which normally replicate late in S phase
when in their chromosomal context, were found to replicate
earlier when they mediate replication on an extrachromosomal
vector. Reproducible patterns of replication within S phase
were found for the plasmids, suggesting that the mechanism
specifying time of replication may be subject to
experimental analysis with this system.},
Key = {fds141057}
}
@article{fds141058,
Author = {PJ Krysan and SB Haase and MP Calos},
Title = {Isolation of human sequences that replicate autonomously in
human cells.},
Journal = {Molecular and cellular biology, UNITED STATES},
Volume = {9},
Number = {3},
Pages = {1026-33},
Year = {1989},
Month = {March},
Keywords = {Base Sequence • Cell Nucleus • Cloning, Molecular
• DNA Replication* • Genes* • Genetic Markers
• Genetic Vectors • Herpesvirus 4, Human •
Humans • Plasmids • Replicon • genetics
• metabolism},
Abstract = {We have isolated a heterogeneous collection of human genomic
sequences which replicate autonomously when introduced into
human cells. The novel strategy for the isolation of these
sequences involved cloning random human DNA fragments into a
defective Epstein-Barr virus vector. This vector alone was
unable to replicate in human cells, but appeared to provide
for the nuclear retention of linked DNA. The human sequences
persist in a long-term replication assay (greater than 2
months) in the presence of the viral nuclear retention
sequences. Using a short-term (4-day) assay, we showed that
the human sequences are able to replicate in the absence of
all viral sequences. The plasmids bearing human sequences
were shown to replicate based on the persistence of
MboI-sensitive plasmid DNA in the long-term assay and the
appearance of DpnI-resistant DNA in the short-term assay.
The human sequences were shown to be responsible for the
replication activity and may represent authentic human
origins of replication.},
Key = {fds141058}
}
@article{fds141050,
Author = {SB Haase and SI Reed},
Title = {Improved flow cytometric analysis of the budding yeast cell
cycle.},
Journal = {Cell cycle (Georgetown, Tex.), United States},
Volume = {1},
Number = {2},
Pages = {132-6},
Keywords = {Cell Cycle • Cell Division • Coloring Agents
• Flow Cytometry • Fluorescent Dyes* •
Organic Chemicals • Propidium • Saccharomyces
cerevisiae • cytology* • metabolism •
methods*},
Abstract = {The budding yeast, Saccharomyces cerevisiae has been a
remarkably useful model system for the study of eukaryotic
cell cycle regulation. Flow cytometric analysis of DNA
content in budding yeast has become a standard tool for the
analysis of cell cycle progression. However, popular
protocols utilizing the DNA binding dye, propidium iodide,
suffer from a number of drawbacks that confound accurate
analysis by flow cytometry. Here we show the utility of the
DNA binding dye, SYTOX Green, in the cell cycle analysis of
yeast. Samples analyzed using SYTOX Green exhibited better
coefficients of variation, improved linearity between DNA
content and fluorescence, and decreased peak drift
associated with changes in dye concentration, growth
conditions or cell size.},
Key = {fds141050}
}
@article{fds141059,
Author = {SB Haase and SS Heinzel and PJ Krysan and MP Calos},
Title = {Improved EBV shuttle vectors.},
Journal = {Mutation research, NETHERLANDS},
Volume = {220},
Number = {2-3},
Pages = {125-32},
Keywords = {Cells, Cultured • DNA Replication • Genetic
Vectors* • Herpesvirus 4, Human • Humans •
Mutagenicity Tests • Recombination, Genetic •
Selection (Genetics) • Transfection • Virus
Replication • genetics* • methods*},
Abstract = {Shuttle vectors based on Epstein-Barr virus (EBV) replicate
autonomously in the nuclei of human cells. These vectors
represent reasonable models for chromosomes, have low
background mutation frequencies, and have been useful for
studying induced mutation in human cells. Two improvements
in the EBV vector system are discussed. Attempts are
described to increase vector copy number per cell by using a
limited period of replication driven by the simian virus 40
(SV40) origin of replication. Isolation of human sequences
that can replace the viral origin of replication in
providing for autonomous replication of the vectors is also
described. These improvements are leading toward shuttle
vectors that are more efficient and more closely resemble
authentic chromosomes.},
Key = {fds141059}
}
%% Papers Submitted
@article{fds141067,
Author = {David A. Orlando and Charles Y. Lin and Allister Bernard and Jean Y.
Wang and Joshua E. S. Socolar and Edwin S. Iversen and Alexander J.
Hartemink and Steven B. Haase},
Title = {Global control of cell cycle transcription by coupled CDK
and network oscillators},
Journal = {Nature},
Year = {2007},
Month = {August},
Abstract = {A significant fraction of the Saccharomyces cerevisiae
genome is transcribed periodically during the cell division
cycle1, 2, suggesting that properly timed gene expression is
important for regulating cell cycle events. Genomic analyses
of transcription factor localization and expression dynamics
suggest that a network of sequentially expressed
transcription factors could control the temporal program of
transcription during the cell cycle3. However, directed
studies interrogating small numbers of genes indicate that
their periodic transcription is governed by the activity of
cyclin-dependent kinases (CDKs)4. To determine the extent to
which the global cell cycle transcription program is
controlled by cyclin/CDK complexes, we examined genome-wide
transcription dynamics in budding yeast mutant cells that do
not express S-phase and mitotic cyclins. Here we show that a
significant fraction of periodic genes were aberrantly
expressed in the cyclin mutant. Surprisingly, although cells
lacking cyclins are blocked at the G1/S border, nearly 70%
of periodic genes continued to be expressed periodically and
on schedule. Our findings reveal that while CDKs play a role
in the regulation of cell cycle transcription, they are not
solely responsible for establishing the global periodic
transcription program. We propose that periodic
transcription is an emergent property of a transcription
factor network that can function as a cell cycle oscillator
independent of, and in tandem with, the CDK
oscillator.},
Key = {fds141067}
}
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