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Overexpression of the chromosome 21 transcription factor Ets2 induces neuronal apoptosis

E J Wolvetang1, O M Bradfield, T Hatzistavrou

  • 1Monash Institute of Reproduction and Development, Monash University, Monash Medical Center, 246 Clayton Road, 3168 Clayton, Australia. ernst.wolvetang@med.monash.edu.au

Neurobiology of Disease
|December 18, 2003
PubMed

Insights

Overexpression of the transcription factor Ets2 in neurons contributes to increased apoptosis, a cell death process implicated in Down syndrome (trisomy 21). This finding suggests ETS2 as a potential factor in neuronal cell death associated with Down syndrome.

Area of Science:

  • Neuroscience
  • Genetics
  • Cell Biology

Background:

  • Neurons in Down syndrome (trisomy 21) exhibit elevated apoptosis rates in vitro.
  • The specific genes on chromosome 21 responsible for this increased neuronal cell death are not fully understood.

Purpose of the Study:

  • To investigate the role of the transcription factor Ets2, located on chromosome 21 and overexpressed in Down syndrome, in neuronal apoptosis.

Main Methods:

  • Examined Ets2 expression in neurons.
  • Utilized primary neuronal cultures from Ets2 transgenic (tg) mice.
  • Assessed apoptosis rates and caspase-3 activation.

Main Results:

  • Ets2 is expressed in neurons.
  • Moderate overexpression of Ets2 in primary neuronal cultures from Ets2 tg mice resulted in increased apoptosis.
  • This increased apoptosis involved the activation of caspase-3.

Conclusions:

  • Overexpression of ETS2 may be a contributing factor to the elevated rate of neuronal apoptosis observed in Down syndrome.
  • ETS2's role in apoptosis warrants further investigation in the context of Down syndrome neuropathology.

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