Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.jgg.2012.07.007
Title: Ribosome Biogenesis Factor Bms1-like Is Essential for Liver Development in Zebrafish
Authors: Wang, Y.
Luo, Y.
Hong, Y. 
Peng, J.
Lo, L. 
Keywords: Bms1-like
Digestive organ development
Liver development
Ribosome biogenesis
Zebrafish
Issue Date: 20-Sep-2012
Citation: Wang, Y., Luo, Y., Hong, Y., Peng, J., Lo, L. (2012-09-20). Ribosome Biogenesis Factor Bms1-like Is Essential for Liver Development in Zebrafish. Journal of Genetics and Genomics 39 (9) : 451-462. ScholarBank@NUS Repository. https://doi.org/10.1016/j.jgg.2012.07.007
Abstract: Ribosome biogenesis in the nucleolus requires numerous nucleolar proteins and small non-coding RNAs. Among them is ribosome biogenesis factor Bms1, which is highly conserved from yeast to human. In yeast, Bms1 initiates ribosome biogenesis through recruiting Rcl1 to pre-ribosomes. However, little is known about the biological function of Bms1 in vertebrates. Here we report that Bms1 plays an essential role in zebrafish liver development. We identified a zebrafish bms1lsq163 mutant which carries a T to A mutation in the gene bms1-like (bms1l). This mutation results in L152 to Q152 substitution in a GTPase motif in Bms1l. Surprisingly, bms1lsq163 mutation confers hypoplasia specifically in the liver, exocrine pancreas and intestine after 3 days post-fertilization (dpf). Consistent with the bms1lsq163 mutant phenotypes, whole-mount in situ hybridization (WISH) on wild type embryos showed that bms1l transcripts are abundant in the entire digestive tract and its accessory organs. Immunostaining for phospho-Histone 3 (P-H3) and TUNEL assay revealed that impairment of hepatoblast proliferation rather than cell apoptosis is one of the consequences of bms1lsq163 giving rise to an under-developed liver. Therefore, our findings demonstrate that Bms1l is necessary for zebrafish liver development. © 2012.
Source Title: Journal of Genetics and Genomics
URI: http://scholarbank.nus.edu.sg/handle/10635/101600
ISSN: 16738527
DOI: 10.1016/j.jgg.2012.07.007
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