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Yeast As a Chassis for Developing Functional Assays to Study Human P53

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Actin nucleation by a transcription co-factor that links cytoskeletal events with the p53 response

Amanda S Coutts1, Louise Weston, Nicholas B La Thangue

  • 1Medical Sciences Division, University of Oxford, Oxford, UK.

Cell Cycle (Georgetown, Tex.)
|April 8, 2010
PubMed

Insights

JMY protein regulates cell motility and invasion through cytoplasmic functions, contrasting its nuclear role in the p53 DNA damage response. Aberrant JMY regulation contributes to cancer development.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Tumorigenesis involves complex mechanisms integrating cell motility, invasion, and nuclear events.
  • The tumor suppressor p53 is a key DNA damage-responsive transcription factor.
  • JMY functions as a transcription co-factor in the nucleus during the p53 response, interacting with p300 and Mdm2.

Purpose of the Study:

  • To investigate the role of JMY in integrating cell motility and invasion with nuclear events.
  • To explore the cytoplasmic functions of JMY in regulating cell motility and invasion.
  • To understand how JMY connects cytoskeletal events with the DNA damage response.

Main Methods:

  • Review of recent studies on JMY's function.
  • Analysis of JMY's interaction with p53, p300, and Mdm2.
  • Investigation of JMY's influence on cadherin expression and actin nucleation.

Main Results:

  • JMY has an unexpected cytoplasmic role in regulating cell motility and invasion.
  • JMY controls cell motility and invasion by influencing cadherin expression and actin nucleation.
  • JMY acts as a transcription co-factor in the nucleus, driving the p53 response to DNA damage.

Conclusions:

  • JMY connects cell motility and invasion with the p53 response.
  • Aberrant regulation of JMY significantly contributes to tumorigenesis.
  • JMY integrates cytoskeletal events and cellular motility with the DNA damage response.

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