ZFIN ID: ZDB-PUB-051101-2
tortuga refines Notch pathway gene expression in the zebrafish presomitic mesoderm at the post-transcriptional level
Dill, K.K., and Amacher, S.L.
Date: 2005
Source: Developmental Biology   287(2): 225-236 (Journal)
Registered Authors: Amacher, Sharon, Dill, Kariena
Keywords: Somite, Segmentation clock, her1, her7, deltaC, deltaD, Cyclic genes
MeSH Terms:
  • Animals
  • Basic Helix-Loop-Helix Transcription Factors/genetics
  • Basic Helix-Loop-Helix Transcription Factors/metabolism
  • Body Patterning
  • Embryo, Nonmammalian/metabolism
  • Gene Expression Regulation, Developmental*
  • In Situ Hybridization
  • Intracellular Signaling Peptides and Proteins
  • Membrane Proteins/genetics
  • Membrane Proteins/metabolism
  • Mesoderm/metabolism*
  • Muscle Fibers, Skeletal/metabolism
  • Muscle Fibers, Skeletal/ultrastructure
  • Muscle, Skeletal/cytology
  • Muscle, Skeletal/embryology
  • Muscle, Skeletal/metabolism
  • Mutation
  • Nerve Tissue Proteins/genetics
  • Nerve Tissue Proteins/metabolism
  • RNA, Messenger/metabolism
  • Receptors, Notch/metabolism*
  • Signal Transduction
  • Somites/cytology
  • Somites/metabolism
  • Transcription Factors/genetics
  • Transcription Factors/metabolism
  • Zebrafish/embryology
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
PubMed: 16236276 Full text @ Dev. Biol.
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ABSTRACT
We have identified the zebrafish tortuga (tor) gene by an ENU-induced mutation that disrupts the presomitic mesoderm (PSM) expression of Notch pathway genes. In tor mutants, Notch pathway gene expression persists in regions of the PSM where expression is normally off in wild type embryos. The expression of hairy/Enhancer of split-related 1 (her1) is affected first, followed by the delta genes deltaC and deltaD, and finally, by another hairy/Enhancer of split-related gene, her7. In situ hybridization with intron-specific probes for her1 and deltaC indicates that transcriptional bursts of expression are normal in tor mutants, suggesting that tor normally functions to refine her1 and deltaC message levels downstream of transcription. Despite the striking defects in Notch pathway gene expression, somite boundaries form normally in tor mutant embryos, although somitic mesoderm defects are apparent later, when cells mature to form muscle fibers. Thus, while the function of Notch pathway genes is required for proper somite formation, the tor mutant phenotype suggests that precise oscillations of Notch pathway transcripts are not essential for establishing segmental pattern in the presomitic mesoderm.
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