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Analysis of Cell Cycle Position in Mammalian Cells
12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

Transmissible gastroenteritis virus infection induces cell cycle arrest at S and G2/M phases via p53-dependent

Li Ding1, Yong Huang, Meiling Dai

  • 1College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi 712100, PR China; College of Life Sciences, Hainan Normal University, Haikou, Hainan 571158, PR China.

Virus Research
|October 8, 2013
PubMed

Insights

Transmissible gastroenteritis virus (TGEV) infection causes host cells to arrest at the S and G2/M phases of the cell cycle, promoting viral replication. This cell cycle arrest is mediated by the p53 signaling pathway.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • The p53 signaling pathway is crucial for cell cycle regulation.
  • Previous studies indicated Transmissible gastroenteritis virus (TGEV) infection activates the p53 pathway.

Purpose of the Study:

  • To investigate TGEV infection's impact on host cell cycle progression.
  • To elucidate the role of p53 activation in TGEV-induced cell cycle changes.

Main Methods:

  • Utilized PK-15 and ST cells, both asynchronous and synchronized.
  • Analyzed cell cycle distribution, protein expression (p21, cyclins, PCNA), and viral replication.
  • Employed UV-inactivated TGEV and p53 signaling inhibition for mechanistic studies.

Main Results:

  • TGEV infection induced cell cycle arrest at S and G2/M phases.
  • Activated p53 pathway led to p21 accumulation and downregulation of key cell cycle proteins.
  • Inhibition of p53 signaling partially reversed TGEV-induced cell cycle arrest.
  • Viral replication was enhanced in cells arrested at S or G2/M phases.

Conclusions:

  • TGEV infection triggers S and G2/M phase arrest in host cells via p53 activation.
  • This cell cycle arrest creates a favorable environment for TGEV replication.
  • Understanding this interaction is key to controlling TGEV infections.
Keywords:
Cell cycle arrestTGEVVirus replicationp53 pathway

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