Caspase-3 and caspase-9 mediate developmental apoptosis in the mouse olfactory system

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Catherine M Cowan1, A Jane Roskams

  • 1Department of Zoology, University of British Columbia, Vancouver, British Columbia, V6T 1Z4, Canada.

The Journal of Comparative Neurology
|May 25, 2004
PubMed

Insights

Caspase-3 and caspase-9 are crucial for programmed cell death in developing olfactory receptor neurons (ORNs). Blocking these caspases in mice leads to an expanded ORN population and abnormal olfactory bulb development, including ectopic OBs.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cell Biology

Background:

  • Neuronal apoptosis is essential for tissue development, primarily mediated by caspases.
  • Caspase-3 and -9 are known to drive olfactory receptor neuron (ORN) apoptosis in adult mice after olfactory bulb (OB) ablation.

Purpose of the Study:

  • To investigate the role of caspase-3 and -9 in early embryonic development of ORNs.
  • To determine the consequences of caspase deficiency on ORN populations and olfactory bulb formation.

Main Methods:

  • Analysis of caspase-3 and -9 expression in developing mouse olfactory systems.
  • Generation and analysis of mice lacking both caspase-3 and -9.
  • Histological examination of ORN populations and olfactory bulb structure in wild-type and null mice.

Main Results:

  • Caspase-3 and -9 are expressed in outgrowing ORN axons during early embryonic development.
  • Mice lacking both caspases exhibit a failure of developmental ORN apoptosis, leading to an expanded ORN population.
  • Caspase-3 deficiency can result in abnormal olfactory bulb development, including the formation of ectopic OBs.

Conclusions:

  • Caspase-3 and -9 play a critical role in regulating ORN numbers during embryonic development.
  • Disruption of caspase-mediated apoptosis in ORNs has significant implications for olfactory system architecture and function.

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