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Published on: January 29, 2020
HDAC activity is required during Xenopus tail regeneration
Ai-Sun Tseng1, Kátia Carneiro, Joan M Lemire
1Department of Developmental Biology, Center for Regenerative and Developmental Biology, Tufts University, Medford, Massachusetts, United States of America.
Plos One
|October 25, 2011
Summary
Histone deacetylase (HDAC) activity is crucial for early Xenopus tadpole tail regeneration. Inhibiting HDACs with Trichostatin A or valproic acid blocked regeneration, highlighting their role in appendage repair.
Area of Science:
- Developmental Biology
- Regenerative Medicine
- Epigenetics
Background:
- Complex organ regeneration is limited in vertebrates.
- The Xenopus tadpole tail regenerates after amputation, offering a model for study.
- Chromatin remodeling's role in in vivo organ regeneration is largely unknown.
Purpose of the Study:
- To investigate the role of histone deacetylase (HDAC) activity in Xenopus tadpole tail regeneration.
- To determine if chromatin remodeling is involved in complex appendage regeneration.
Main Methods:
- Utilized Xenopus tadpole tail amputation model.
- Administered HDAC inhibitors Trichostatin A (TSA) and valproic acid.
- Over-expressed wild-type Mad3 and a Mad3 mutant lacking the Sin3-interacting domain.
- Analyzed gene expression of Notch1 and BMP2.
Main Results:
- HDAC1 expression was detected during early regeneration (first two days).
- Pharmacological blockade of HDACs increased histone acetylation.
- HDAC inhibition by TSA or valproic acid specifically inhibited tail regeneration.
- Over-expression of Mad3 and its mutant also blocked regeneration, suggesting a complex with HDACs.
- HDAC inhibition led to aberrant expression of Notch1 and BMP2.
Conclusions:
- HDAC activity is essential for the early stages of Xenopus tail regeneration.
- HDACs, potentially in complex with Mad3, regulate key genes like Notch1 and BMP2 during regeneration.
- Modulation of histone acetylation is a critical factor in the regenerative repair of complex appendages.
