Pnrc2 regulates 3'UTR-mediated decay of segmentation clock-associated transcripts during zebrafish segmentation

Gallagher, T.L., Tietz, K.T., Morrow, Z.T., McCammon, J.M., Goldrich, M.L., Derr, N.L., Amacher, S.L.
Developmental Biology   429(1): 225-239 (Journal)
Registered Authors
Amacher, Sharon, Derr, Nicolas, Gallagher, Thomas, McCammon, Jasmine, Tietz, Kiel
Hes/her, RNA decay, Tortuga, cyclic expression, oscillations, somitogenesis
MeSH Terms
  • 3' Untranslated Regions/genetics*
  • Alleles
  • Animals
  • Basic Helix-Loop-Helix Transcription Factors/genetics
  • Basic Helix-Loop-Helix Transcription Factors/metabolism
  • Biological Clocks/genetics*
  • Body Patterning/genetics*
  • Chromosomes/genetics
  • Chromosomes, Artificial, Bacterial/genetics
  • Embryo, Nonmammalian/metabolism
  • Gene Expression Regulation, Developmental
  • Genes, Reporter
  • Mutation/genetics
  • Nonsense Mediated mRNA Decay/genetics
  • Phenotype
  • RNA Stability/genetics
  • RNA, Messenger/genetics
  • RNA, Messenger/metabolism
  • Trans-Activators/genetics
  • Trans-Activators/metabolism*
  • Zebrafish/embryology*
  • Zebrafish/genetics*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
  • Zygote/metabolism
28648842 Full text @ Dev. Biol.
Vertebrate segmentation is controlled by the segmentation clock, a molecular oscillator that regulates gene expression and cycles rapidly. The expression of many genes oscillates during segmentation, including hairy/Enhancer of split-related (her or Hes) genes, which encode transcriptional repressors that auto-inhibit their own expression, and deltaC (dlc), which encodes a Notch ligand. We previously identified the tortuga (tor) locus in a zebrafish forward genetic screen for genes involved in cyclic transcript regulation and showed that cyclic transcripts accumulate post-splicing in tor mutants. Here we show that cyclic mRNA accumulation in tor mutants is due to loss of pnrc2, which encodes a proline-rich nuclear receptor co-activator implicated in mRNA decay. Using an inducible in vivo reporter system to analyze transcript stability, we find that the her1 3'UTR confers Pnrc2-dependent instability to a heterologous transcript. her1 mRNA decay is Dicer-independent and likely employs a Pnrc2-Upf1-containing mRNA decay complex. Surprisingly, despite accumulation of cyclic transcripts in pnrc2-deficient embryos, we find that cyclic protein is expressed normally. Overall, we show that Pnrc2 promotes 3'UTR-mediated decay of developmentally-regulated segmentation clock transcripts and we uncover an additional post-transcriptional regulatory layer that ensures oscillatory protein expression in the absence of cyclic mRNA decay.
Genes / Markers
Figure Gallery
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes