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Functional analysis of the c-myb proto-oncogene
H H Lin1, D C Sternfeld, S G Shinpock
1University of Tennessee Graduate School of Biomedical Sciences, Oak Ridge 37831-8080, USA.
Current Topics in Microbiology and Immunology
|January 1, 1996
Summary
Targeted mutagenesis of the c-myb proto-oncogene reveals its critical role in fetal liver erythropoiesis and myeloid progenitor development. Homozygous mutants exhibit embryonic lethality due to severe anemia and hematopoietic abnormalities.
Area of Science:
- Hematology
- Developmental Biology
- Oncogenes
Background:
- The c-myb proto-oncogene is essential for normal development.
- Its precise role in fetal hematopoiesis, particularly erythropoiesis, requires elucidation.
Purpose of the Study:
- To determine the biological function of the c-myb proto-oncogene using targeted mutagenesis in mice.
- To investigate the hematopoietic abnormalities in c-myb deficient fetal livers.
Main Methods:
- Targeted mutagenesis to create c-myb knockout mice.
- In vitro hematopoietic colony-forming cell assays.
- RT-PCR, Northern blot, and differential display analyses.
Main Results:
- Homozygous c-myb mutant fetuses die at 15.5 days gestation due to anemia, linked to impaired switch from yolk sac to fetal liver erythropoiesis.
- Reduced erythroid and dramatically reduced myeloid progenitors observed in mutant fetal livers.
- Differential gene expression identified, including novel genes, suggesting c-myb's regulatory role.
Conclusions:
- c-myb expression is critical for early hematopoietic progenitor proliferation and/or differentiation.
- Further analysis of c-myb mutant fetuses provides insight into hematopoiesis.
- Potential roles for novel genes in c-myb mediated hematopoiesis warrant investigation.