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Ribosomal biogenesis genes play an essential and p53-independent role in pancreas development

ABSTRACT: Analysis of transcriptional profiles in Sbds(ATG) MO-injected embryos with and without coinjection of p53(ATG) MO. We identified a large number of changes in transcript abundance associated with loss of Sbds. Among the 24,278 annotated zebrafish genes in the platform, 4,892 significantly differentially expressed genes were identified.

ORGANISM(S): Danio rerio

PROVIDER: GSE39399 | GEO | 2012/07/17

SECONDARY ACCESSION(S): PRJNA170775

REPOSITORIES: GEO

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Ribosomal biogenesis genes play an essential and p53-independent role in pancreas development

Project description:Analysis of transcriptional profiles in Sbds(ATG) MO-injected embryos with and without coinjection of p53(ATG) MO. We identified a large number of changes in transcript abundance associated with loss of Sbds. Among the 24,278 annotated zebrafish genes in the platform, 4,892 significantly differentially expressed genes were identified. Embryos were carefully staged at 24 hpf and RNA was extracted from approximately 50 embryos per condition in Trizol, followed by purification using RNA miniprep columns (Qiagen). Four independent experiments were extracted. cDNA microarrays were performed at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins Microarray Core Facility using 4x44K Zebrafish gene expression microarray slides (Agilent, Santa Clara, CA).

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Ribosomal biogenesis genes play an essential and p53-independent role in zebrafish pancreas development.

Project description:Mutations in the human Shwachman-Bodian-Diamond syndrome (SBDS) gene cause defective ribosome assembly and are associated with exocrine pancreatic insufficiency, chronic neutropenia and skeletal defects. However, the mechanism underlying these phenotypes remains unclear. Here we show that knockdown of the zebrafish sbds ortholog fully recapitulates the spectrum of developmental abnormalities observed in the human syndrome, and further implicate impaired proliferation of ptf1a-expressing pancreatic progenitor cells as the basis for the observed pancreatic phenotype. It is thought that diseases of ribosome assembly share a p53-dependent mechanism. However, loss of p53 did not rescue the developmental defects associated with loss of zebrafish sbds. To clarify the molecular mechanisms underlying the observed organogenesis defects, we performed transcriptional profiling to identify candidate downstream mediators of the sbds phenotype. Among transcripts displaying differential expression, functional group analysis revealed marked enrichment of genes related to ribosome biogenesis, rRNA processing and translational initiation. Among these, ribosomal protein L3 (rpl3) and pescadillo (pes) were selected for additional analysis. Similar to knockdown of sbds, knockdown or mutation of either rpl3 or pes resulted in impaired expansion of pancreatic progenitor cells. The pancreatic phenotypes observed in rpl3- and pes-deficient embryos were also independent of p53. Together, these data suggest novel p53-independent roles for ribosomal biogenesis genes in zebrafish pancreas development.

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