Differential oxidation of protein-tyrosine phosphatases during zebrafish caudal fin regeneration
- Wu, W., Hale, A.J., Lemeer, S., den Hertog, J.
- Scientific Reports 7: 8460 (Journal)
- Registered Authors
- den Hertog, Jeroen, Lemeer, Simone
- Phosphorylases, Self-renewal
- MeSH Terms
- Amino Acid Motifs/genetics
- Amino Acid Sequence
- Amputation, Surgical
- Animal Fins/physiology*
- Animal Fins/surgery
- Multigene Family/genetics
- Protein Tyrosine Phosphatases/genetics
- Protein Tyrosine Phosphatases/metabolism*
- Sequence Homology, Amino Acid
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- 28814789 Full text @ Sci. Rep.
Wu, W., Hale, A.J., Lemeer, S., den Hertog, J. (2017) Differential oxidation of protein-tyrosine phosphatases during zebrafish caudal fin regeneration. Scientific Reports. 7:8460.
Zebrafish have the capacity to regenerate lost tissues and organs. Amputation of the caudal fin results in a rapid, transient increase in H2O2 levels emanating from the wound margin, which is essential for regeneration, because quenching of reactive oxygen species blocks regeneration. Protein-tyrosine phosphatases (PTPs) have a central role in cell signalling and are susceptible to oxidation, which results in transient inactivation of their catalytic activity. We hypothesized that PTPs may become oxidized in response to amputation of the caudal fin. Using the oxidized PTP-specific (ox-PTP) antibody and liquid chromatography-mass spectrometry, we identified 33 PTPs in adult zebrafish fin clips of the total of 44 PTPs that can theoretically be detected based on sequence conservation. Of these 33 PTPs, 8 were significantly more oxidized 40 min after caudal fin amputation. Surprisingly, Shp2, one of the PTPs that were oxidized in response to caudal fin amputation, was required for caudal fin regeneration. In contrast, Rptpα, which was not oxidized upon amputation, was dispensable for caudal fin regeneration. Our results demonstrate that PTPs are differentially oxidized in response to caudal fin amputation and that there is a differential requirement for PTPs in regeneration.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes