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Cited by 9Circadian rhythm and melatoninRNA Research and SplicingCircular RNAs in diseases

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Critical role of deadenylation in regulating poly(A) rhythms and circadian gene expression

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Yao, Xiangyu, Kojima, Shihoko, Chen, Jing·2020·PLOS Computational Biology
DOI 10.1371/journal.pcbi.1007842PMC PMC7205317

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Abstract

The mammalian circadian clock is deeply rooted in rhythmic regulation of gene expression. Rhythmic transcriptional control mediated by the circadian transcription factors is thought to be the main driver of mammalian circadian gene expression. However, mounting evidence has demonstrated the importance of rhythmic post-transcriptional controls, and it remains unclear how the transcriptional and post-transcriptional mechanisms collectively control rhythmic gene expression. In mouse liver, hundreds of genes were found to exhibit rhythmicity in poly(A) tail length, and the poly(A) rhythms are strongly correlated with the protein expression rhythms. To understand the role of rhythmic poly(A) regulation in circadian gene expression, we constructed a parsimonious model that depicts rhythmic control imposed upon basic mRNA expression and poly(A) regulation processes, including transcription, deadenylation, polyadenylation, and degradation. The model results reveal the rhythmicity in deadenylation as the strongest contributor to the rhythmicity in poly(A) tail length and the rhythmicity in the abundance of the mRNA subpopulation with long poly(A) tails (a rough proxy for mRNA translatability). In line with this finding, the model further shows that the experimentally observed distinct peak phases in the expression of deadenylases, regardless of other rhythmic controls, can robustly cluster the rhythmic mRNAs by their peak phases in poly(A) tail length and abundance of the long-tailed subpopulation. This provides a potential mechanism to synchronize the phases of target gene expression regulated by the same deadenylases. Our findings highlight the critical role of rhythmic deadenylation in regulating poly(A) rhythms and circadian gene expression.

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Fig 1 Overview of the study. (A) Schematic diagram of the model. The model describes four processes that control the poly(A) tail length and mRNA abundance: transcription, degradation, cytoplasmic deadenylation and polyadenylation. The rhythmicities of the four processes, i.e., amplitude and phase, are presumably controlled by the core clock mechanism (shaded molecular circuit), which is not explicitly included in the model. (B) Work flow of the study. Numeric simulations of the ODE model using different sets of input parameters (sampled according to Table 1, S1 Fig) generate the output quantities. The input parameters and output quantities are analyzed through the global parameter sensitivity analysis to quantify the impact of each parameter on each output quantity over the global parameter space.
Fig 1 Overview of the study. (A) Schematic diagram of the model. The model describes four processes that control the poly(A) tail length and mRNA abundance: transcription, degradation, cytoplasmic deadenylation and polyadenylation. The rhythmicities of the four processes, i.e., amplitude and phase, are presumably controlled by the core clock mechanism (shaded molecular circuit), which is not explicitly included in the model. (B) Work flow of the study. Numeric simulations of the ODE model using different sets of input parameters (sampled according to Table 1, S1 Fig) generate the output quantities. The input parameters and output quantities are analyzed through the global parameter sensitivity analysis to quantify the impact of each parameter on each output quantity over the global parameter space.CC BY · PubMed Central
Fig 2 Rhythmicities of poly(A) tail length and long-tailed mRNA abundance are strongly controlled by rhythmic deadenylation. (A) Scatter plot of the peak phases of input processes versus the peak phases of L/S ratio (i.e., poly(A) length metric). (B) Sobol indices for the peak phase of L/S ratio. (C) Scatter plot of the peak phases of input processes versus the peak phases of L+S (i.e., total mRNA abundance). (D) Sobol indices for the peak phase of L+S. (E) Scatter plot of the peak phases of input processes versus the peak phases of L (i.e., long-tailed mRNA abundance). (F) Sobol indices for the peak phase of L. (A, C, E) Each scatter plot shows 10,000 data points randomly chosen from the original simulations for the sake of visual clarity. (B, D, F) Bars with “S” on top: single Sobol indices. Bars with “T” on top: total Sobol indices. Mean values of the Sobol indices are shown, because the variances are too small for clear visualization (S2 Fig).
Fig 2 Rhythmicities of poly(A) tail length and long-tailed mRNA abundance are strongly controlled by rhythmic deadenylation. (A) Scatter plot of the peak phases of input processes versus the peak phases of L/S ratio (i.e., poly(A) length metric). (B) Sobol indices for the peak phase of L/S ratio. (C) Scatter plot of the peak phases of input processes versus the peak phases of L+S (i.e., total mRNA abundance). (D) Sobol indices for the peak phase of L+S. (E) Scatter plot of the peak phases of input processes versus the peak phases of L (i.e., long-tailed mRNA abundance). (F) Sobol indices for the peak phase of L. (A, C, E) Each scatter plot shows 10,000 data points randomly chosen from the original simulations for the sake of visual clarity. (B, D, F) Bars with “S” on top: single Sobol indices. Bars with “T” on top: total Sobol indices. Mean values of the Sobol indices are shown, because the variances are too small for clear visualization (S2 Fig).CC BY · PubMed Central
Fig 3 Distinct peak phases in deadenylases cluster transcripts by their peak phases of poly(A) tail length and long-tailed mRNA abundance. (i) Transcription, degradation, deadenylation and polyadenylation phases evenly distributed around the clock. (ii) Transcription phases within three narrow windows at ZT 0, 8, and 16. Degradation, deadenylation and polyadenylation phases evenly distributed around the clock. (iii) Degradation phases within three narrow windows at ZT 0, 8, and 16. Transcription, deadenylation and polyadenylation phases evenly distributed around the clock. (iv) Deadenylation phases within three narrow windows at ZT 0, 8, and 16. Transcription, degradation and polyadenylation phases evenly distributed around the clock. (v) Polyadenylation phases within three narrow windows at ZT 0, 8, and 16. Transcription, degradation and deadenylation phases evenly distributed around the clock. (vi) Peak phases of transcription follow transcriptome data reported by [13]. Deadenylation phases within three narrow windows at ZT 2, 5, and 13, and polyadenylation phases within one narrow windows at ZT 3.5, based on the data from [29], while degradation phases evenly distributed around the clock. Mean rates and relative amplitudes follow Table 1 and S1 Fig.
Fig 3 Distinct peak phases in deadenylases cluster transcripts by their peak phases of poly(A) tail length and long-tailed mRNA abundance. (i) Transcription, degradation, deadenylation and polyadenylation phases evenly distributed around the clock. (ii) Transcription phases within three narrow windows at ZT 0, 8, and 16. Degradation, deadenylation and polyadenylation phases evenly distributed around the clock. (iii) Degradation phases within three narrow windows at ZT 0, 8, and 16. Transcription, deadenylation and polyadenylation phases evenly distributed around the clock. (iv) Deadenylation phases within three narrow windows at ZT 0, 8, and 16. Transcription, degradation and polyadenylation phases evenly distributed around the clock. (v) Polyadenylation phases within three narrow windows at ZT 0, 8, and 16. Transcription, degradation and deadenylation phases evenly distributed around the clock. (vi) Peak phases of transcription follow transcriptome data reported by [13]. Deadenylation phases within three narrow windows at ZT 2, 5, and 13, and polyadenylation phases within one narrow windows at ZT 3.5, based on the data from [29], while degradation phases evenly distributed around the clock. Mean rates and relative amplitudes follow Table 1 and S1 Fig.CC BY · PubMed Central
Fig 4 Factors distinguishing between Class I and Class II PAR mRNAs. (A) Characteristics of Class I and Class II PAR mRNAs. (B) Sobol indices for the amplitude of L+S (i.e., total mRNA abundance). Bars with “S” on top: single Sobol indices. Bars with “T” on top: total Sobol indices. (C) Distributions of mean mRNA degradation rates for the two classes. (D) Distributions of peak phase differences between transcription and degradation for the two classes. (E) Distributions of relative amplitudes of transcription for the two classes. (F) Distributions of relative amplitudes of degradation for the two classes. (G) Distribution of mean deadenylation rates for the two classes. Results in (C-G) from 100,000 simulations with parameters randomly sampled according to Table 1. Parameter sets with ≥0.2 relative amplitude in both L+S and L/S ratio are defined as Class I, while those with <0.2 relative amplitude in L+S and ≥0.2 relative amplitude in L/S ratio are defined as Class II.
Fig 4 Factors distinguishing between Class I and Class II PAR mRNAs. (A) Characteristics of Class I and Class II PAR mRNAs. (B) Sobol indices for the amplitude of L+S (i.e., total mRNA abundance). Bars with “S” on top: single Sobol indices. Bars with “T” on top: total Sobol indices. (C) Distributions of mean mRNA degradation rates for the two classes. (D) Distributions of peak phase differences between transcription and degradation for the two classes. (E) Distributions of relative amplitudes of transcription for the two classes. (F) Distributions of relative amplitudes of degradation for the two classes. (G) Distribution of mean deadenylation rates for the two classes. Results in (C-G) from 100,000 simulations with parameters randomly sampled according to Table 1. Parameter sets with ≥0.2 relative amplitude in both L+S and L/S ratio are defined as Class I, while those with <0.2 relative amplitude in L+S and ≥0.2 relative amplitude in L/S ratio are defined as Class II.CC BY · PubMed Central
Fig 5 Factors distinguishing between Class III and Class IV PAR mRNAs. (A) Characteristics of Class III and the hypothetical Class IV mRNAs. (B) Sobol indices for the amplitude of L+S (i.e., total mRNA abundance) for the model without rhythmic transcription. Bars with “S” on top: single Sobol indices. Bars with “T” on top: total Sobol indices. (C) Distributions of mean mRNA degradation rates for the two classes. (D) Distributions of relative amplitudes of degradation for the two classes. (E) Distributions of peak phase differences (i) between deadenylation and degradation, (ii) between polyadenylation and degradation, and (iii) between deadenylation and polyadenylation for the two classes. Results in (C-E) from 100,000 simulations with parameters randomly sampled according to Table 1, but without rhythmic transcription (Atrsc = 0). Parameter sets with ≥0.2 relative amplitude in L/S ratio and <0.2 relative amplitude in L+S are defined as Class III, while those with and ≥0.2 relative amplitude in both L/S ratio and L+S are defined as Class IV.
Fig 5 Factors distinguishing between Class III and Class IV PAR mRNAs. (A) Characteristics of Class III and the hypothetical Class IV mRNAs. (B) Sobol indices for the amplitude of L+S (i.e., total mRNA abundance) for the model without rhythmic transcription. Bars with “S” on top: single Sobol indices. Bars with “T” on top: total Sobol indices. (C) Distributions of mean mRNA degradation rates for the two classes. (D) Distributions of relative amplitudes of degradation for the two classes. (E) Distributions of peak phase differences (i) between deadenylation and degradation, (ii) between polyadenylation and degradation, and (iii) between deadenylation and polyadenylation for the two classes. Results in (C-E) from 100,000 simulations with parameters randomly sampled according to Table 1, but without rhythmic transcription (Atrsc = 0). Parameter sets with ≥0.2 relative amplitude in L/S ratio and <0.2 relative amplitude in L+S are defined as Class III, while those with and ≥0.2 relative amplitude in both L/S ratio and L+S are defined as Class IV.CC BY · PubMed Central

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Metadata

Authors
Yao, X., Kojima, S., & Chen, J.
Affiliations
Virginia Tech (US)
Corresponding author
Chen, Jing
ORCID
Venue
PLOS Computational Biology
Publisher
Public Library of Science (PLoS)
Published
2020-04-27
Volume
16
Issue
4
Pages
e1007842
ISSN
  • 1553-734X (ISSN-L)
  • 1553-7358
DOI
10.1371/journal.pcbi.1007842
PMC
PMC7205317
OpenAlex
W3018942718
Cited by
9
References
6
Citations by year
2026: 2 · 2025: 1 · 2024: 1 · 2022: 1 · 2021: 3 · 2020: 1
FWCI
0.64
Type
journal article
Language
en
Update notices
Open access
Licence
Locations
  • PLoS Computational Biology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Figshare (submittedVersion, cc-by)
  • VTechWorks (Virginia Tech) (submittedVersion, cc-by)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Circular RNAs in diseases
Keywords
deadenylation, poly(A) tail length, circadian gene expression, circadian clock, post-transcriptional regulation, mRNA degradation, polyadenylation, deadenylase, phase synchronization, mouse liver
MeSH terms
Adenine, Animals, Computer Simulation, Gene Expression Regulation, Liver, Models, Genetic, Poly A, RNA, Messenger, Computational Biology, Polyadenylation, Mice, Circadian Clocks

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Yao, X., Kojima, S., & Chen, J. (2020). Critical role of deadenylation in regulating poly(A) rhythms and circadian gene expression. PLOS Computational Biology. https://doi.org/10.1371/journal.pcbi.1007842