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Expression of v-src induces aberrant development and twinning in chimaeric mice
C A Boulter1, A Aguzzi, R L Williams
1Department of Genetics, University of Cambridge, UK.
Development (Cambridge, England)
|February 1, 1991
Summary
High levels of viral src (v-src) expression disrupt mouse embryonic development, causing death by day 9. This study reveals deregulated src proto-oncogene product activity
Area of Science:
- Developmental biology
- Molecular oncology
- Genetics
Background:
- The proto-oncogene c-src plays a critical role in cellular processes.
- Understanding its function in development is crucial for identifying disease mechanisms.
Purpose of the Study:
- To investigate the role of the src proto-oncogene in mouse development.
- To determine the consequences of deregulated src expression during embryogenesis.
Main Methods:
- Utilized embryonic stem (ES) cell lines with varying v-src tyrosine kinase activity.
- Generated chimaeric mice by introducing these ES cells.
- Observed developmental abnormalities in resulting embryos.
Main Results:
- Low-level v-src expression was compatible with normal embryogenesis.
- High-level v-src expression led to abnormal development and embryonic lethality by day 8-9 of gestation.
- Observed abnormalities included twin/multiple embryos, developmental arrest at the egg cylinder stage, and visceral yolk sac (VYS) expansion with endoderm hyperplasia.
Conclusions:
- Deregulated expression of the src proto-oncogene product induces significant developmental abnormalities during early mouse embryogenesis.
- This provides the first evidence linking aberrant src activity to embryonic developmental defects.