Loss of Ribosomal Protein L11 Affects Zebrafish Embryonic Development through a p53-Dependent Apoptotic Response
Author Information
Author(s): Anirban Chakraborty, Tamayo Uechi, Sayomi Higa, Hidetsugu Torihara, Naoya Kenmochi
Primary Institution: Frontier Science Research Center, University of Miyazaki, Miyazaki, Japan
Hypothesis
The deletion of L11 and its physiological relevance to p53 activity in zebrafish will activate the p53 pathway.
Conclusion
L11 deficiency activates a p53-dependent checkpoint response that prevents proper embryonic development in zebrafish.
Supporting Evidence
- L11-deficient embryos displayed developmental abnormalities primarily in the brain, leading to embryonic lethality within 6–7 days post fertilization.
- Extensive apoptosis was observed in the head region of the morphants, correlating morphological defects with apparent cell death.
- Simultaneous knockdown of the p53 gene rescued the developmental defects and apoptosis in the morphants.
Takeaway
When zebrafish don't have enough of a protein called L11, it causes problems in their brain development and makes them die early because their cells are dying.
Methodology
The researchers knocked down the rpl11 gene in zebrafish using Morpholino antisense oligonucleotides and analyzed the resulting phenotypes.
Limitations
The study primarily focuses on the effects in zebrafish, which may not fully translate to other species.
Participant Demographics
Zebrafish embryos were used in the study.
Digital Object Identifier (DOI)
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