Multiple ribosomal proteins are expressed at high levels in developing zebrafish endoderm and are required for normal exocrine pancreas development
- Authors
- Provost, E., Weier, C.A., and Leach, S.D.
- ID
- ZDB-PUB-130702-2
- Date
- 2013
- Source
- Zebrafish 10(2): 161-169 (Journal)
- Registered Authors
- Leach, Steven D.
- Keywords
- none
- MeSH Terms
-
- Animals
- Embryo, Nonmammalian/embryology
- Embryo, Nonmammalian/metabolism
- Gene Expression Regulation, Developmental*
- In Situ Hybridization
- Larva/genetics
- Larva/metabolism
- Microscopy, Confocal
- Organ Specificity
- Organogenesis
- Pancreas, Exocrine/embryology*
- Pancreas, Exocrine/growth & development
- Pancreas, Exocrine/metabolism
- Polymerase Chain Reaction
- Ribosomal Proteins/genetics*
- Ribosomal Proteins/metabolism
- Zebrafish/embryology
- Zebrafish/genetics*
- Zebrafish/metabolism
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- PubMed
- 23697888 Full text @ Zebrafish
Ribosomal protein L (rpl) genes are essential for assembly of the 60S subunit of the eukaryotic ribosome and may also carry out additional extra-ribosomal functions. We have identified a common expression pattern for rpl genes in developing zebrafish larvae. After initially widespread expression in early embryos, the expression of multiple rpl genes becomes increasingly restricted to the endoderm. With respect to the pancreas, rpl genes are highly expressed in ptf1a-expressing pancreatic progenitors at 48 hpf, suggesting possible functional roles in pancreatic morphogenesis and/or differentiation. Utilizing two available mutant lines, rpl23ahi2582 and rpl6hi3655b, we found that ptf1a-expressing pancreatic progenitors fail to properly expand in embryos homozygous for either of these genes. In addition to these durable homozygous phenotypes, we also demonstrated recoverable delays in ptf1a-expressing pancreatic progenitor expansion in rpl23ahi2582 and rpl6hi3655b heterozygotes. Disruptions in ribosome assembly are generally understood to initiate a p53-dependent cellular stress response. However, concomitant p53 knockdown was unable to rescue normal pancreatic progenitor expansion in either rpl23ahi2582 or rpl6hi3655b mutant embryos, suggesting required and p53-independent roles for rpl23a and rpl6 in pancreas development.