Mutation in utp15 Disrupts Vascular Patterning in Zebrafish Embryos
Author Information
Author(s): Mouillesseaux Kevin, Chen Jau-Nian
Primary Institution: University of California Los Angeles
Hypothesis
The study investigates the role of utp15 in vascular patterning during zebrafish embryogenesis.
Conclusion
Utp15 deficiency leads to significant vascular defects and increased apoptosis in zebrafish embryos, mediated by p53.
Supporting Evidence
- LA1908 mutants show massive apoptosis during early embryogenesis.
- Overexpression of wild type utp15 mRNA suppresses mutant phenotypes.
- Blocking p53 activity rescues vascular abnormalities in LA1908 mutants.
Takeaway
When zebrafish embryos have a mutation in a gene called utp15, they have trouble forming blood vessels and many of their cells die, which is linked to a protein called p53.
Methodology
The researchers used a forward genetic screen in zebrafish to identify the LA1908 mutant and performed genetic mapping and sequencing to analyze the mutation.
Limitations
The study primarily focuses on a single mutation and its effects, which may not represent broader genetic interactions.
Participant Demographics
Zebrafish embryos were used as the model organism.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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