TRIM71 reactivation enhances the mitotic and hair cell–forming potential of cochlear supporting cells

Xiao Jun Li, Charles Morgan, Prathamesh T. Nadar-Ponniah, Waldemar Kolanus, Angelika Doetzlhofer*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Cochlear hair cell loss is a leading cause of deafness in humans. Neighboring supporting cells have some capacity to regenerate hair cells. However, their regenerative potential sharply declines as supporting cells undergo maturation (postnatal day 5 in mice). We recently reported that reactivation of the RNA-binding protein LIN28B restores the hair cell–regenerative potential of P5 cochlear supporting cells. Here, we identify the LIN28B target Trim71 as a novel and equally potent enhancer of supporting cell plasticity. TRIM71 is a critical regulator of stem cell behavior and cell reprogramming; however, its role in cell regeneration is poorly understood. Employing an organoid-based assay, we show that TRIM71 re-expression increases the mitotic and hair cell–forming potential of P5 cochlear supporting cells by facilitating their de-differentiation into progenitor-like cells. Our mechanistic work indicates that TRIM71's RNA-binding activity is essential for such ability, and our transcriptomic analysis identifies gene modules that are linked to TRIM71 and LIN28B-mediated supporting cell reprogramming. Furthermore, our study uncovers that the TRIM71-LIN28B target Hmga2 is essential for supporting cell self-renewal and hair cell formation.

Original languageEnglish
Article numbere56562
JournalEMBO Reports
Issue number9
StatePublished - 6 Sep 2023
Externally publishedYes


  • Lin28b
  • Trim71
  • cochlea
  • hair cell regeneration
  • supporting cell reprogramming


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