Ribosome Biogenesis Factor Bms1-like Is Essential for Liver Development in Zebrafish
- Authors
- Wang, Y., Luo, Y., Hong, Y., Peng, J., and Lo, L.
- ID
- ZDB-PUB-121010-24
- Date
- 2012
- Source
- Journal of genetics and genomics = Yi chuan xue bao 39(9): 451-462 (Journal)
- Registered Authors
- Peng, Jinrong
- Keywords
- liver development, digestive organ development, ribosome biogenesis, Bms1-like, zebrafish
- MeSH Terms
-
- Animals
- Cell Proliferation
- Embryo, Nonmammalian/metabolism
- GTP Phosphohydrolases/genetics*
- Humans
- In Situ Hybridization
- Liver/growth & development*
- Liver/metabolism
- Liver/pathology
- Mutation
- Ribosomes/genetics
- Ribosomes/metabolism
- Zebrafish/growth & development*
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- PubMed
- 23021545 Full text @ J. Genet. Genomics
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.