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Reconciling conflicting models for global control of cell-cycle transcription.

ABSTRACT: Models for the control of global cell-cycle transcription have advanced from a CDK-APC/C oscillator, a transcription factor (TF) network, to coupled CDK-APC/C and TF networks. Nonetheless, current models were challenged by a recent study that concluded that the cell-cycle transcriptional program is primarily controlled by a CDK-APC/C oscillator in budding yeast. Here we report an analysis of the transcriptome dynamics in cyclin mutant cells that were not queried in the previous study. We find that B-cyclin oscillation is not essential for control of phase-specific transcription. Using a mathematical model, we demonstrate that the function of network TFs can be retained in the face of significant reductions in transcript levels. Finally, we show that cells arrested at mitotic exit with non-oscillating levels of B-cyclins continue to cycle transcriptionally. Taken together, these findings support a critical role of a TF network and a requirement for CDK activities that need not be periodic.

SUBMITTER: Cho CY

PROVIDER: S-EPMC5638368 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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Reconciling conflicting models for global control of cell-cycle transcription.

Cho Chun-Yi CY Motta Francis C FC Kelliher Christina M CM Deckard Anastasia A Haase Steven B SB

Cell cycle (Georgetown, Tex.) 20170921 20

Models for the control of global cell-cycle transcription have advanced from a CDK-APC/C oscillator, a transcription factor (TF) network, to coupled CDK-APC/C and TF networks. Nonetheless, current models were challenged by a recent study that concluded that the cell-cycle transcriptional program is primarily controlled by a CDK-APC/C oscillator in budding yeast. Here we report an analysis of the transcriptome dynamics in cyclin mutant cells that were not queried in the previous study. We find th ...[more]

PMID: 28934013

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Project description:Background/objectivesPhysiological evidence indicates that high-protein diets reduce caloric intake and increase thermogenic response, which may prevent weight gain and regain after weight loss. Clinical trials have shown such effects, whereas observational cohort studies suggest an association between greater protein intake and weight gain. In both types of studies the results are based on average weight changes, and show considerable diversity in both directions. This study investigates whether the discrepancy in the evidence could be due to recruitment of overweight and obese individuals into clinical trials.Subjects/methodsData were available from the European Diet, Obesity and Genes (DiOGenes) post-weight-loss weight-maintenance trial and the Danish Diet, Cancer and Health (DCH) cohort. Participants of the DCH cohort were matched with participants from the DiOGenes trial on gender, diet, and body characteristics. Different subsets of the DCH-participants, comparable with the trial participants, were analyzed for weight maintenance according to the randomization status (high or low protein) of the matched trial participants.ResultsTrial participants were generally heavier, had larger waist circumference and larger fat mass than the participants in the entire DCH cohort. A better weight maintenance in the high-protein group compared to the low protein group was observed in the subgroups of the DCH cohort matching body characteristics of the trial participants.ConclusionThis modified observational study, minimized the differences between the RCT and observational data with regard to dietary intake, participant characteristics and statistical analysis. Compared with low protein diet the high protein diet was associated with better weight maintenance when individuals with greater body mass index and waist circumference were analyzed. Selecting subsets of large-scale observational cohort studies with similar characteristics as participants in clinical trials may reconcile the otherwise conflicting results.

Dataset Information

Reconciling conflicting models for global control of cell-cycle transcription.

Publications

Reconciling conflicting models for global control of cell-cycle transcription.

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