A Mechanistic Model of the Regulation of Division Timing by the Circadian Clock in Cyanobacteria
Copyright © 2020 Biophysical Society. Published by Elsevier Inc. All rights reserved..
The cyanobacterium Synechococcus elongatus possesses a circadian clock in the form of a group of proteins whose concentrations and phosphorylation states oscillate with daily periodicity under constant conditions. The circadian clock regulates the cell cycle such that the timing of the cell divisions is biased toward certain times during the circadian period, but the mechanism underlying this phenomenon remains unclear. Here, we propose a mechanism in which a protein limiting for division accumulates at a rate proportional to the cell volume growth and is modulated by the clock. This "modulated rate" model, in which the clock signal is integrated over time to affect division timing, differs fundamentally from the previously proposed "gating" concept, in which the clock is assumed to suppress divisions during a specific time window. We found that although both models can capture the single-cell statistics of division timing in S. elongatus, only the modulated rate model robustly places divisions away from darkness during changes in the environment. Moreover, within the framework of the modulated rate model, existing experiments on S. elongatus are consistent with the simple mechanism that division timing is regulated by the accumulation of a division limiting protein in a phase with genes whose activity peaks at dusk.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2020 |
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| Erschienen: |
2020 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:118 |
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| Enthalten in: |
Biophysical journal - 118(2020), 12 vom: 16. Juni, Seite 2905-2913 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Ho, Po-Yi [VerfasserIn] |
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| Links: |
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| Themen: |
Bacterial Proteins |
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| Anmerkungen: |
Date Completed 14.05.2021 Date Revised 17.06.2021 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.bpj.2020.04.038 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM310771005 |
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| 245 | 1 | 2 | |a A Mechanistic Model of the Regulation of Division Timing by the Circadian Clock in Cyanobacteria |
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| 500 | |a Date Revised 17.06.2021 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2020 Biophysical Society. Published by Elsevier Inc. All rights reserved. | ||
| 520 | |a The cyanobacterium Synechococcus elongatus possesses a circadian clock in the form of a group of proteins whose concentrations and phosphorylation states oscillate with daily periodicity under constant conditions. The circadian clock regulates the cell cycle such that the timing of the cell divisions is biased toward certain times during the circadian period, but the mechanism underlying this phenomenon remains unclear. Here, we propose a mechanism in which a protein limiting for division accumulates at a rate proportional to the cell volume growth and is modulated by the clock. This "modulated rate" model, in which the clock signal is integrated over time to affect division timing, differs fundamentally from the previously proposed "gating" concept, in which the clock is assumed to suppress divisions during a specific time window. We found that although both models can capture the single-cell statistics of division timing in S. elongatus, only the modulated rate model robustly places divisions away from darkness during changes in the environment. Moreover, within the framework of the modulated rate model, existing experiments on S. elongatus are consistent with the simple mechanism that division timing is regulated by the accumulation of a division limiting protein in a phase with genes whose activity peaks at dusk | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Research Support, U.S. Gov't, Non-P.H.S. | |
| 650 | 7 | |a Bacterial Proteins |2 NLM | |
| 700 | 1 | |a Martins, Bruno M C |e verfasserin |4 aut | |
| 700 | 1 | |a Amir, Ariel |e verfasserin |4 aut | |
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