@article{oai:miyazaki-u.repo.nii.ac.jp:00001321,
 author = {剣持, 直哉 and Kenmochi, Naoya and Chakraborty, Anirban and Uechi, Tamayo and Higa, Sayomi and Torihara, Hidetsugu},
 issue = {1},
 journal = {PLoS ONE},
 month = {Jan},
 note = {Ribosome is responsible for protein synthesis in all organisms and ribosomal proteins （RPs） play important roles in the
formation of a functional ribosome. L11 was recently shown to regulate p53 activity through a direct binding with MDM2
and abrogating the MDM2-induced p53 degradation in response to ribosomal stress. However, the studies were performed
in cell lines and the significance of this tumor suppressor function of L11 has yet to be explored in animal models. To
investigate the effects of the deletion of L11 and its physiological relevance to p53 activity, we knocked down the rpl11
gene in zebrafish and analyzed the p53 response. Contrary to the cell line-based results, our data indicate that an L11
deficiency in a model organism activates the p53 pathway. The L11-deficient embryos （morphants） 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, thus correlating the morphological defects with
apparent cell death. A decrease in total abundance of genes involved in neural patterning of the brain was observed in the
morphants, suggesting a reduction in neural progenitor cells. Upregulation of the genes involved in the p53 pathway were
observed in the morphants. Simultaneous knockdown of the p53 gene rescued the developmental defects and apoptosis in
the morphants. These results suggest that ribosomal dysfunction due to the loss of L11 activates a p53-dependent
checkpoint response to prevent improper embryonic development.},
 pages = {e4152--e4152},
 title = {Loss of Ribosomal Protein L11 Affects Zebrafish Embryonic Development through a p53-Dependent Apoptotic Response},
 volume = {4},
 year = {2009},
 yomi = {ケンモチ, ナオヤ}
}