scholarly journals Regulation of a transcription factor network by Cdk1 coordinates late cell cycle gene expression

2014 ◽  
Vol 33 (9) ◽  
pp. 1044-1060 ◽  
Author(s):  
B. D. Landry ◽  
C. E. Mapa ◽  
H. E. Arsenault ◽  
K. E. Poti ◽  
J. A. Benanti
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Transcription Factor ◽  
Cell Cycle Gene ◽  
Transcription Factor Network ◽  
Cell Cycle Gene Expression

scholarly journals A toxin-antitoxin system associated transcription factor of Caulobacter crescentus can influence cell cycle-regulated gene expression during the SOS response

2020 ◽  
Author(s):  
Koyel Ghosh ◽  
Kamilla Ankær Brejndal ◽  
Clare L. Kirkpatrick
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Dna Damage ◽  
Transcription Factor ◽  
Caulobacter Crescentus ◽  
Sos Response ◽  
Cell Cycle Gene ◽  
Regulated Gene Expression ◽  
Cell Cycle Gene Expression

AbstractToxin-antitoxin (TA) systems are widespread in bacterial chromosomes but their functions remain enigmatic. Although many are transcriptionally upregulated by stress conditions, it is unclear what role they play in cellular responses to stress and to what extent the role of a given TA system homologue varies between different bacterial species. In this work we investigate the role of the DNA damage-inducible TA system HigBA of Caulobacter crescentus in the SOS response and discover that in addition to the toxin HigB affecting cell cycle gene expression through inhibition of the master regulator CtrA, HigBA possesses a transcription factor third component, HigC, which both auto-regulates the TA system and acts independently of it. Through HigC, the system exerts downstream effects on antibiotic (ciprofloxacin) resistance and cell cycle gene expression. HigB and HigC had inverse effects on cell cycle gene regulation, with HigB reducing and HigC increasing the expression of CtrA-dependent promoters. Neither HigBA nor HigC had any effect on formation of persister cells in response to ciprofloxacin. Rather, their role in the SOS response appears to be as transcriptional and post-transcriptional regulators of cell cycle-dependent gene expression, transmitting the status of the SOS response as a regulatory input into the cell cycle control network via CtrA.ImportanceAlmost all bacteria respond to DNA damage by upregulating a set of genes that helps them to repair and recover from the damage, known as the SOS response. The set of genes induced during the SOS response varies between species, but frequently includes toxin-antitoxin systems. However, it is unknown what the consequence of inducing these systems is, and whether they provide any benefit to the cells. We show here that the DNA damage-induced TA system HigBA of the asymmetrically dividing bacterium Caulobacter crescentus affects the cell cycle regulation of this bacterium. HigBA also has a transcription factor encoded immediately downstream of it, named here HigC, which controls expression of the TA system and potentially other genes as well. Therefore, this work identifies a new role for TA systems in the DNA damage response, distinct from non-specific stress tolerance mechanisms which had been proposed previously.

scholarly journals Tissue-specific actions of Pax6 on proliferation-differentiation balance in the developing forebrain are Foxg1-dependent

2018 ◽  
Author(s):  
Idoia Quintana-Urzainqui ◽  
Zrinko Kozić ◽  
Soham Mitra ◽  
Tian Tian ◽  
Martine Manuel ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Transcription Factor ◽  
Transcriptional Regulation ◽  
Transcription Factors ◽  
Cell Cycle Gene ◽  
Tissue Specific ◽  
Proliferation And Differentiation ◽  
Multiple Regions ◽  
Cell Cycle Gene Expression

SummaryDifferences in the growth and maturation of diverse forebrain tissues depends on region-specific transcriptional regulation. Individual transcription factors act simultaneously in multiple regions that develop very differently, raising questions about the extent to which their actions vary regionally. We found that the transcription factor Pax6 affects the transcriptomes and the balance between proliferation and differentiation in opposite directions in murine diencephalon versus cortex. We tested several possible mechanisms to explain Pax6’s tissue-specific actions and found that the presence of the transcription factor Foxg1 in cortex but not diencephalon was most influential. We found that Foxg1 is responsible for many of the differences in cell cycle gene expression between diencephalon and cortex. In cortex lacking Foxg1, Pax6’s action on the balance of proliferation versus differentiation became diencephalon-like. Our findings reveal a mechanism for generating regional forebrain diversity in which the actions of one transcription factor completely reverse the actions of another.

Ethanol alters cell cycle gene expression in human embryonic stem cells

2016 ◽  
Vol 01 (03) ◽  
pp. 201-208 ◽  
Author(s):  
Malini Krishnamoorthy ◽  
Brian Gerwe ◽  
Jamie Heimburg-Molinaro ◽  
Rachel Nash ◽  
Jagan Arumugham ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Human Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Cell Cycle Gene ◽  
Cell Cycle Gene Expression

scholarly journals Altered Cell Cycle Gene Expression and Apoptosis in Post-Implantation Dog Parthenotes

PLoS ONE ◽  
2012 ◽  
Vol 7 (8) ◽  
pp. e41256 ◽  
Author(s):  
Jung Eun Park ◽  
Min Jung Kim ◽  
Seung Kwon Ha ◽  
So Gun Hong ◽  
Hyun Ju Oh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Cell Cycle Gene ◽  
Altered Cell ◽  
Post Implantation ◽  
Cell Cycle Gene Expression

scholarly journals Global Analysis of Host Cell Gene Expression Late during Cytomegalovirus Infection Reveals Extensive Dysregulation of Cell Cycle Gene Expression and Induction of Pseudomitosis Independent of US28 Function

2004 ◽  
Vol 78 (21) ◽  
pp. 11988-12011 ◽  
Author(s):  
Laura Hertel ◽  
Edward S. Mocarski
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Dna Replication ◽  
Host Cell ◽  
Small Gtpases ◽  
Global Changes ◽  
Cell Cycle Gene ◽  
Gene Products ◽  
Cell Gene ◽  
Cell Cycle Gene Expression

ABSTRACT Replication of human cytomegalovirus (CMV) depends on host cell gene products working in conjunction with viral functions and leads to a dramatic dysregulation of cell cycle gene expression. Comprehensive transcriptional profiling was used to identify pathways most dramatically modulated by CMV at late times during infection and to determine the extent to which expression of the viral chemokine receptor US28 contributed to modulating cellular gene expression. Cells infected with the AD169 strain of virus or a fully replication competent US28-deficient derivative (RV101) were profiled throughout the late phase of infection (50, 72, and 98 h postinfection). Although sensitive statistical analysis showed striking global changes in transcript levels in infected cells compared to uninfected cells, the expression of US28 did not contribute to these alterations. CMV infection resulted in lower levels of transcripts encoding cytoskeletal, extracellular matrix, and adhesion proteins, together with small GTPases and apoptosis regulators, and in higher levels of transcripts encoding cell cycle, DNA replication, energy production, and inflammation-related gene products. Surprisingly, a large number of cellular transcripts encoding mitosis-related proteins were upmodulated at late times in infection, and these were associated with the formation of abnormal mitotic spindles and the appearance of pseudomitotic cells. These data extend our understanding of how broadly CMV alters the regulation of host cell cycle gene products and highlight the establishment of a mitosis-like environment in the absence of cellular DNA replication as important for viral replication and maturation.

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