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*
- Basic Helix-Loop-Helix Transcription Factors/genetics
- Basic Helix-Loop-Helix Transcription Factors/metabolism
- Biological Clocks/genetics*
- Body Patterning/genetics*
- Chromosomes, Artificial, Bacterial/genetics
- Embryo, Nonmammalian/metabolism
- Gene Expression Regulation, Developmental
- Genes, Reporter
- Nonsense Mediated mRNA Decay/genetics
- RNA Stability/genetics
- RNA, Messenger/genetics
- RNA, Messenger/metabolism
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- 28648842 Full text @ Dev. Biol.
Gallagher, T.L., Tietz, K.T., Morrow, Z.T., McCammon, J.M., Goldrich, M.L., Derr, N.L., Amacher, S.L. (2017) Pnrc2 regulates 3'UTR-mediated decay of segmentation clock-associated transcripts during zebrafish segmentation. Developmental Biology. 429(1):225-239.
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
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes