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The sox2 expressing (sox2 + ) progenitors in adult mammalian inner ear lose the capacity to regenerate while progenitors in the zebrafish lateral line are able to proliferate and regenerate damaged HCs throughout lifetime. To mimic the HC damage in mammals, we have established a zebrafish severe injury model to eliminate both progenitors and HCs. The  atoh1a  expressing ( atoh1a  + ) HC precursors were the main population that survived post severe injury, and gained sox2 expression to initiate progenitor regeneration. In response to severe injury,  yap  was activated to upregulate  lin28a  transcription. Severe-injury-induced progenitor regeneration was disabled in  lin28a  or  yap  mutants. In contrary, overexpression of  lin28a  initiated the recovery of sox2 +  progenitors. Mechanistically, microRNA  let7  acted downstream of  lin28a  to activate Wnt pathway for promoting regeneration. Our findings that lin28a is necessary and sufficient to regenerate the exhausted sox2 +  progenitors shed light on restoration of progenitors to initiate HC regeneration in mammals.

Yap-lin28a axis targets let7-Wnt pathway to restore progenitors for initiating regeneration