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Cse1l is essential for early embryonic growth and development.
T K Bera1, J Bera, U Brinkmann
1Laboratory of Molecular Biology, Clinical Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Molecular and Cellular Biology
|September 21, 2001
Summary
The CSE1L gene is crucial for early embryonic development in mice. Homozygous knockout mice lacking functional CSE1L die before birth, indicating its essential role in embryogenesis.
Area of Science:
- Molecular Biology
- Developmental Biology
- Genetics
Background:
- CSE1L, a homolog of yeast chromosome segregation gene CSE1, functions as a nuclear transport factor.
- CSE1 and CSE1L are known to be essential in yeast and mammalian cell cultures.
- Previous studies indicated CSE1L's role in proliferation and apoptosis.
Purpose of the Study:
- To determine if CSE1L is essential in vivo.
- To investigate potential compensation mechanisms for CSE1L absence.
- To analyze the tissue- and development-specific expression of murine CSE1L (Cse1l).
Main Methods:
- Cloned the murine CSE1L gene (Cse1l).
- Analyzed Cse1l expression across embryonic and adult stages.
- Generated Cse1l knockout mice using embryonic stem cells.
- Interbred heterozygous Cse1l mice to assess homozygous phenotype.
Main Results:
- Cse1l expression was detected from embryonic day 7.0 (E7.0) through adulthood, with high levels in proliferating tissues.
- Heterozygous Cse1l mice were normal and fertile.
- No homozygous Cse1l knockout pups were born from heterozygous interbreeding.
- Homozygous mutant embryos showed disorganization and degeneration by E5.5.
Conclusions:
- CSE1L is essential for early embryonic development in mice.
- Homozygous deficiency of Cse1l leads to an embryonically lethal phenotype.
- Cse1l plays a critical role in early embryogenesis, with no apparent compensation mechanisms.