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m6A-mediated Cell-cell Communication Controls Planarian Regeneration

Cui, G.; Zhou, J.-Y.; Ge, X.-Y.; Sun, B.-F.; Song, G.-G.; Wang, X.; Wang, X.-Z.; Zhang, R.; Wang, H.; Jing, Q.; Zhao, Y.; Koziol, M.; Zeng, A.; Zhang, W.; Han, D.; Yang, Y.; Yang, Y.-G.

2021-07-29 molecular biology
10.1101/2021.07.29.454253 bioRxiv
Show abstract

Regeneration is the regrowth of damaged tissues or organs, a vital mechanism responding to damages from primitive organisms to higher mammals. Planarian possesses active whole-body regenerative capability owning to its vast reservoir of adult stem cells, neoblasts, thus provides an ideal model to delineate the underlying mechanisms for regeneration. N6-methyladenosine (m6A) regulates stem cell renewal and differentiation. However, how m6A controls regeneration at whole-organism level remains largely unknown. Here, we demonstrate that the depletion of m6A methyltransferase regulatory subunit wtap abolishes planarian regeneration, through regulating cell-cell communication and cell cycle. 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 m6A-modified transcripts grn/cdk9 (or cdk7) axis rescues the defective regeneration of planarian without wtap. Overall, our study reveals an indispensable role of m6A-dependent cell-cell communication essential for whole-organism regeneration.

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