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A Seminiferous Tubule Squash Technique for the Cytological Analysis of Spermatogenesis Using the Mouse Model
Published on: February 6, 2018
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p53-dependent programmed necrosis controls germ cell homeostasis during spermatogenesis
Francesco Napoletano1, Benjamin Gibert2, Keren Yacobi-Sharon3
1Laboratory of Biology and Modelling of the Cell, UMR5239 CNRS/Ecole Normale Supérieure de Lyon, INSERM U1210, UMS 3444 Biosciences Lyon Gerland, Université de Lyon, Lyon, France.
Plos Genetics
|September 26, 2017
Summary
The tumor suppressor p53 regulates programmed necrosis in fruit flies and mice. This discovery in spermatogenesis offers new models for treating apoptosis-resistant cancers.
Area of Science:
- Cell Biology
- Developmental Biology
- Genetics
Background:
- Regulated necrosis is crucial in diseases like stroke and heart attack.
- The physiological role of regulated necrosis is not fully understood.
- The tumor suppressor p53's role in necrosis is being investigated.
Purpose of the Study:
- To investigate the conserved role of p53 in regulating necrosis.
- To explore the function of p53-mediated necrosis in spermatogenesis.
- To establish Drosophila and mouse models for studying necrosis in cancer therapy.
Main Methods:
- Utilized Drosophila and mouse models of spermatogenesis.
- Investigated the role of p53 in spontaneous and induced germ cell necrosis.
- Examined the involvement of initiator caspase Dronc/Caspase 9 in p53-dependent necrosis.
Main Results:
- p53 is essential for programmed necrosis in Drosophila germ cells during spermatogenesis.
- This necrosis involves a non-catalytic function of Dronc/Caspase 9.
- p53-dependent necrosis prevents testicular hyperplasia in Drosophila and mediates heat-induced germ cell necrosis in mice.
Conclusions:
- p53 plays a conserved role in regulating necrosis across species, from invertebrates to vertebrates.
- Spermatogenesis in Drosophila and mice provides valuable models for studying necrosis.
- Identifying necrosis inducers could lead to new treatments for apoptosis-resistant cancers.
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