| 論文作者 |
Cui, GS; Zhou, JY; Ge, XY; Sun, BF; Song, GG; Wang, X; Wang, XZ; Zhang, R; Wang, HL; Jing, Q; Koziol, MJ; Zhao, YL; Zeng, A; Zhang, WQ; Han, DL; Yang, YG; Yang, Y |
| 摘要 |
Regeneration is the regrowth of damaged tissues or organs, a vital process in response to damages from primitive organisms to higher mammals. Planarian possesses active whole-body regenerative capability owing to its vast reservoir of adult stem cells, neoblasts, providing an ideal model to delineate the underlying mechanisms for regeneration. RNA N-6-methyladenosine (m(6)A) modification participates in many biological processes, including stem cell self-renewal and differentiation, in particular the regeneration of haematopoietic stem cells and axons. However, how m(6)A controls regeneration at the whole-organism level remains largely unknown. Here, we demonstrate that the depletion of m(6)A methyltransferase regulatory subunit wtap abolishes planarian regeneration, potentially through regulating genes related to cell-cell communication and cell cycle. Single-cell RNA-seq (scRNA-seq) analysis unveils that the wtap knockdown induces a unique type of neural progenitor-like cells (NP-like cells), characterized by specific expression of the cell-cell communication ligand grn. Intriguingly, the depletion of m(6)A-modified transcripts grn, cdk9 or cdk7 partially rescues the defective regeneration of planarian caused by wtap knockdown. Overall, our study reveals an indispensable role of m(6)A modification in regulating whole-organism regeneration. |
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