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Article ; Online: FRET-Based Sorting of Live Cells Reveals Shifted Balance between PLK1 and CDK1 Activities During Checkpoint Recovery

Lorenzo Lafranchi / Erik Müllers / Dorothea Rutishauser / Arne Lindqvist

Cells, Vol 9, Iss 2126, p

2020 Volume 2126

Abstract: Cells recovering from the G2/M DNA damage checkpoint rely more on Aurora A-PLK1 signaling than cells progressing through an unperturbed G2 phase, but the reason for this discrepancy is not known. Here, we devised a method based on a FRET reporter for ... ...

Abstract	Cells recovering from the G2/M DNA damage checkpoint rely more on Aurora A-PLK1 signaling than cells progressing through an unperturbed G2 phase, but the reason for this discrepancy is not known. Here, we devised a method based on a FRET reporter for PLK1 activity to sort cells in distinct populations within G2 phase. We employed mass spectroscopy to characterize changes in protein levels through an unperturbed G2 phase and validated that ATAD2 levels decrease in a proteasome-dependent manner. Comparing unperturbed cells with cells recovering from DNA damage, we note that at similar PLK1 activities, recovering cells contain higher levels of Cyclin B1 and increased phosphorylation of CDK1 targets. The increased Cyclin B1 levels are due to continuous Cyclin B1 production during a DNA damage response and are sustained until mitosis. Whereas partial inhibition of PLK1 suppresses mitotic entry more efficiently when cells recover from a checkpoint, partial inhibition of CDK1 suppresses mitotic entry more efficiently in unperturbed cells. Our findings provide a resource for proteome changes during G2 phase, show that the mitotic entry network is rewired during a DNA damage response, and suggest that the bottleneck for mitotic entry shifts from CDK1 to PLK1 after DNA damage.
Keywords	G2 ; mitotic entry ; checkpoint recovery ; FRET ; PLK1 ; Cyclin B1 ; Biology (General) ; QH301-705.5
Subject code	612
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Author Correction

Savvas Raptis / Tomas Karlsson / Andris Vaivads / Craig Pollock / Ferdinand Plaschke / Andreas Johlander / Henriette Trollvik / Per-Arne Lindqvist

Nature Communications, Vol 13, Iss 1, Pp 1-

Downstream high-speed plasma jet generation as a direct consequence of shock reformation

2022 Volume 1

Keywords	Science ; Q
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Downstream high-speed plasma jet generation as a direct consequence of shock reformation

Savvas Rapitis / Tomas Karlsson / Andris Vaivads / Craig Pollock / Ferdinand Plaschke / Andreas Johlander / Henriette Trollvik / Per-Arne Lindqvist

Nature Communications, Vol 13, Iss 1, Pp 1-

2022 Volume 10

Abstract: Several mechanisms exist for formation of jets observed in Earth’s magnetosheath. Here, the authors show evidence of high-speed downstream flows generated at the Earth’s bow shock as a direct consequence of shock reformation, which is different than the ... ...

Abstract	Several mechanisms exist for formation of jets observed in Earth’s magnetosheath. Here, the authors show evidence of high-speed downstream flows generated at the Earth’s bow shock as a direct consequence of shock reformation, which is different than the proposed mechanisms.
Keywords	Science ; Q
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Electron Kinetic Entropy across Quasi-Perpendicular Shocks

Martin Lindberg / Andris Vaivads / Savvas Raptis / Per-Arne Lindqvist / Barbara L. Giles / Daniel Jonathan Gershman

Entropy, Vol 24, Iss 745, p

2022 Volume 745

Abstract: We use Magnetospheric Multiscale (MMS) data to study electron kinetic entropy per particle ... S ... e ... across Earth’ ...

Abstract	We use Magnetospheric Multiscale (MMS) data to study electron kinetic entropy per particle <math xmlns="http://www.w3.org/1998/Math/MathML" display="inline"><semantics><msub><mi>S</mi><mi mathvariant="normal">e</mi></msub></semantics></math> across Earth’s quasi-perpendicular bow shock. We have selected 22 shock crossings covering a wide range of shock conditions. Measured distribution functions are calibrated and corrected for spacecraft potential, secondary electron contamination, lack of measurements at the lowest energies and electron density measurements based on plasma frequency measurements. All crossings display an increase in electron kinetic entropy across the shock <math xmlns="http://www.w3.org/1998/Math/MathML" display="inline"><semantics><mrow><mo>Δ</mo><msub><mi>S</mi><mi mathvariant="normal">e</mi></msub></mrow></semantics></math> being positive or zero within their error margin. There is a strong dependence of <math xmlns="http://www.w3.org/1998/Math/MathML" display="inline"><semantics><mrow><mo>Δ</mo><msub><mi>S</mi><mi mathvariant="normal">e</mi></msub></mrow></semantics></math> on the change in electron temperature, <math xmlns="http://www.w3.org/1998/Math/MathML" display="inline"><semantics><mrow><mo>Δ</mo><msub><mi>T</mi><mi mathvariant="normal">e</mi></msub></mrow></semantics></math> , and the upstream electron plasma beta, <math xmlns="http://www.w3.org/1998/Math/MathML" display="inline"><semantics><msub><mi>β</mi><mi mathvariant="normal">e</mi></msub></semantics></math> . Shocks with large <math xmlns="http://www.w3.org/1998/Math/MathML" ...<br />
Keywords	space plasma ; electron kinetic entropy ; quasi-perpendicular shock ; adiabatic index ; Science ; Q ; Astrophysics ; QB460-466 ; Physics ; QC1-999
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Mapping Metabolic Events in the Cancer Cell Cycle Reveals Arginine Catabolism in the Committed SG2M Phase

Irena Roci / Jeramie D. Watrous / Kim A. Lagerborg / Lorenzo Lafranchi / Arne Lindqvist / Mohit Jain / Roland Nilsson

Cell Reports, Vol 26, Iss 7, Pp 1691-1700.e

2019 Volume 5

Abstract: Summary: Alterations in cell-cycle regulation and cellular metabolism are associated with cancer transformation, and enzymes active in the committed cell-cycle phase may represent vulnerabilities of cancer cells. Here, we map metabolic events in the G1 ... ...

Abstract	Summary: Alterations in cell-cycle regulation and cellular metabolism are associated with cancer transformation, and enzymes active in the committed cell-cycle phase may represent vulnerabilities of cancer cells. Here, we map metabolic events in the G1 and SG2M phases by combining cell sorting with mass spectrometry-based isotope tracing, revealing hundreds of cell-cycle-associated metabolites. In particular, arginine uptake and ornithine synthesis are active during SG2M in transformed but not in normal cells, with the mitochondrial arginase 2 (ARG2) enzyme as a potential mechanism. While cancer cells exclusively use ARG2, normal epithelial cells synthesize ornithine via ornithine aminotransferase (OAT). Knockdown of ARG2 markedly reduces cancer cell growth and causes G2M arrest, while not inducing compensation via OAT. In human tumors, ARG2 is highly expressed in specific tumor types, including basal-like breast tumors. This study sheds light on the interplay between metabolism and cell cycle and identifies ARG2 as a potential metabolic target. : Here, Roci et al. map metabolic events in the G1 and SG2M cell cycle phases, and show that arginase 2 (ARG2) is critical for cancer cell progression through SG2M. As proliferating cells are vulnerable during SG2M phase, metabolic enzymes active during this phase are potential targets for cancer chemotherapy. Keywords: isotope tracing, mass spectrometry, cancer metabolism, ornithine, polyamines, arginase 2, ARG2, OAT, basal-like breast cancer
Keywords	Biology (General) ; QH301-705.5
Language	English
Publishing date	2019-02-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: DNA Replication Determines Timing of Mitosis by Restricting CDK1 and PLK1 Activation

Lemmens, Bennie / Arne Lindqvist / Helfrid Hochegger / Jiri Bartek / Joan Sala-Gaston / Karen Akopyan / Nadia Hegarat

Molecular cell. 2018 July 05, v. 71, no. 1

2018

Abstract: To maintain genome stability, cells need to replicate their DNA before dividing. Upon completion of bulk DNA synthesis, the mitotic kinases CDK1 and PLK1 become active and drive entry into mitosis. Here, we have tested the hypothesis that DNA replication ...

Abstract	To maintain genome stability, cells need to replicate their DNA before dividing. Upon completion of bulk DNA synthesis, the mitotic kinases CDK1 and PLK1 become active and drive entry into mitosis. Here, we have tested the hypothesis that DNA replication determines the timing of mitotic kinase activation. Using an optimized double-degron system, together with kinase inhibitors to enforce tight inhibition of key proteins, we find that human cells unable to initiate DNA replication prematurely enter mitosis. Preventing DNA replication licensing and/or firing causes prompt activation of CDK1 and PLK1 in S phase. In the presence of DNA replication, inhibition of CHK1 and p38 leads to premature activation of mitotic kinases, which induces severe replication stress. Our results demonstrate that, rather than merely a cell cycle output, DNA replication is an integral signaling component that restricts activation of mitotic kinases. DNA replication thus functions as a brake that determines cell cycle duration.
Keywords	DNA ; DNA replication ; enzyme inhibitors ; genome ; humans ; interphase ; mitosis ; phosphotransferases (kinases) ; proteins
Language	English
Dates of publication	2018-0705
Size	p. 117-128.e3.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2018.05.026
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: The human long non-coding RNA gene RMRP has pleiotropic effects and regulates cell-cycle progression at G2

Svetlana Vakkilainen / Tiina Skoog / Elisabet Einarsdottir / Anna Middleton / Minna Pekkinen / Tiina Öhman / Shintaro Katayama / Kaarel Krjutškov / Panu E. Kovanen / Markku Varjosalo / Arne Lindqvist / Juha Kere / Outi Mäkitie

Scientific Reports, Vol 9, Iss 1, Pp 1-

2019 Volume 9

Abstract: Abstract RMRP was the first non-coding nuclear RNA gene implicated in a disease. Its mutations cause cartilage-hair hypoplasia (CHH), an autosomal recessive skeletal dysplasia with growth failure, immunodeficiency, and a high risk for malignancies. This ... ...

Abstract	Abstract RMRP was the first non-coding nuclear RNA gene implicated in a disease. Its mutations cause cartilage-hair hypoplasia (CHH), an autosomal recessive skeletal dysplasia with growth failure, immunodeficiency, and a high risk for malignancies. This study aimed to gain further insight into the role of RNA Component of Mitochondrial RNA Processing Endoribonuclease (RMRP) in cellular physiology and disease pathogenesis. We combined transcriptome analysis with single-cell analysis using fibroblasts from CHH patients and healthy controls. To directly assess cell cycle progression, we followed CHH fibroblasts by pulse-labeling and time-lapse microscopy. Transcriptome analysis identified 35 significantly upregulated and 130 downregulated genes in CHH fibroblasts. The downregulated genes were significantly connected to the cell cycle. Multiple other pathways, involving regulation of apoptosis, bone and cartilage formation, and lymphocyte function, were also affected, as well as PI3K-Akt signaling. Cell-cycle studies indicated that the CHH cells were delayed specifically in the passage from G2 phase to mitosis. Our findings expand the mechanistic understanding of CHH, indicate possible pathways for therapeutic intervention and add to the limited understanding of the functions of RMRP.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2019-09-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Loss of CSL Unlocks a Hypoxic Response and Enhanced Tumor Growth Potential in Breast Cancer Cells

Eike-Benjamin Braune / Yat Long Tsoi / Yee Peng Phoon / Sebastian Landor / Helena Silva Cascales / Daniel Ramsköld / Qiaolin Deng / Arne Lindqvist / Xiaojun Lian / Cecilia Sahlgren / Shao-Bo Jin / Urban Lendahl

Stem Cell Reports, Vol 6, Iss 5, Pp 643-

2016 Volume 651

Abstract: Notch signaling is an important regulator of stem cell differentiation. All canonical Notch signaling is transmitted through the DNA-binding protein CSL, and hyperactivated Notch signaling is associated with tumor development; thus it may be anticipated ... ...

Abstract	Notch signaling is an important regulator of stem cell differentiation. All canonical Notch signaling is transmitted through the DNA-binding protein CSL, and hyperactivated Notch signaling is associated with tumor development; thus it may be anticipated that CSL deficiency should reduce tumor growth. In contrast, we report that genetic removal of CSL in breast tumor cells caused accelerated growth of xenografted tumors. Loss of CSL unleashed a hypoxic response during normoxic conditions, manifested by stabilization of the HIF1α protein and acquisition of a polyploid giant-cell, cancer stem cell-like, phenotype. At the transcriptome level, loss of CSL upregulated more than 1,750 genes and less than 3% of those genes were part of the Notch transcriptional signature. Collectively, this suggests that CSL exerts functions beyond serving as the central node in the Notch signaling cascade and reveals a role for CSL in tumorigenesis and regulation of the cellular hypoxic response.
Keywords	breast cancer ; Notch signaling ; xenograft ; transcriptome ; mitosis ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2016-05-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cyclin B1-Cdk1 activation continues after centrosome separation to control mitotic progression.

Arne Lindqvist / Wouter van Zon / Christina Karlsson Rosenthal / Rob M F Wolthuis

PLoS Biology, Vol 5, Iss 5, p e

2007 Volume 123

Abstract: Activation of cyclin B1-cyclin-dependent kinase 1 (Cdk1), triggered by a positive feedback loop at the end of G2, is the key event that initiates mitotic entry. In metaphase, anaphase-promoting complex/cyclosome-dependent destruction of cyclin B1 ... ...

Abstract	Activation of cyclin B1-cyclin-dependent kinase 1 (Cdk1), triggered by a positive feedback loop at the end of G2, is the key event that initiates mitotic entry. In metaphase, anaphase-promoting complex/cyclosome-dependent destruction of cyclin B1 inactivates Cdk1 again, allowing mitotic exit and cell division. Several models describe Cdk1 activation kinetics in mitosis, but experimental data on how the activation proceeds in mitotic cells have largely been lacking. We use a novel approach to determine the temporal development of cyclin B1-Cdk1 activity in single cells. By quantifying both dephosphorylation of Cdk1 and phosphorylation of the Cdk1 target anaphase-promoting complex/cyclosome 3, we disclose how cyclin B1-Cdk1 continues to be activated after centrosome separation. Importantly, we discovered that cytoplasmic cyclin B1-Cdk1 activity can be maintained even when cyclin B1 translocates to the nucleus in prophase. These experimental data are fitted into a model describing cyclin B1-Cdk1 activation in human cells, revealing a striking resemblance to a bistable circuit. In line with the observed kinetics, cyclin B1-Cdk1 levels required to enter mitosis are lower than the amount of cyclin B1-Cdk1 needed for mitotic progression. We propose that gradually increasing cyclin B1-Cdk1 activity after centrosome separation is critical to coordinate mitotic progression.
Keywords	Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2007-05-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Assessing Kinetics from Fixed Cells Reveals Activation of the Mitotic Entry Network at the S/G2 Transition

Akopyan, Karen / AdrianÂ T. Saurin / Arne Lindqvist / Danielle A.A. Hollman / Elvira Hukasova / Erik MÃ¼llers / GeertÂ J.P.L. Kops / Helena SilvaÂ Cascales / Himjyot Jaiswal / RenÃ©Â H. Medema

Molecular cell. 2014 Mar. 06, v. 53

2014

Abstract: During the cell cycle, DNA duplication in S phase must occur before a cell divides in mitosis. In the intervening G2 phase, mitotic inducers accumulate, which eventually leads to a switch-like rise in mitotic kinase activity that triggers mitotic entry. ... ...

Abstract	During the cell cycle, DNA duplication in S phase must occur before a cell divides in mitosis. In the intervening G2 phase, mitotic inducers accumulate, which eventually leads to a switch-like rise in mitotic kinase activity that triggers mitotic entry. However, when and how activation of the signaling network that promotes the transition to mitosis occurs remains unclear. We have developed a system to reduce cell-cell variation and increase accuracy ofÂ fluorescence quantification in single cells. This allows us to use immunofluorescence of endogenous marker proteins to assess kinetics from fixed cells. We find that mitotic phosphorylations initially occur at the completion of S phase, showing that activation of the mitotic entry network does not depend on protein accumulation through G2. Our data show insights into how mitotic entry is linked to the completion of S phase and forms a quantitative resource for mathematical models of the human cell cycle.
Keywords	DNA ; fluorescence ; fluorescent antibody technique ; humans ; interphase ; mathematical models ; mitosis ; proteins
Language	English
Dates of publication	2014-0306
Size	p. 843-853.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2014.01.031
Database	NAL-Catalogue (AGRICOLA)

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