Linking YAP to Müller Glia Quiescence Exit in the Degenerative Retina - Sorbonne Université Access content directly
Journal Articles Cell Reports Year : 2019

Linking YAP to Müller Glia Quiescence Exit in the Degenerative Retina

Abstract

Contrasting with fish or amphibian, retinal regeneration from Müller glia is largely limited in mammals. In our quest toward the identification of molecular cues that may boost their stemness potential, we investigated the involvement of the Hippo pathway effector YAP (Yes-associated protein), which is upregulated in Müller cells following retinal injury. Conditional Yap deletion in mouse Müller cells prevents cell-cycle gene upregulation that normally accompanies reactive gliosis upon photoreceptor cell death. We further show that, in Xenopus, a species endowed with efficient regenerative capacity, YAP is required for their injury-dependent proliferative response. In the mouse retina, where Müller cells do not spontaneously proliferate, YAP overactivation is sufficient to induce their reprogramming into highly proliferative cells. Overall, we unravel a pivotal role for YAP in tuning Müller cell proliferative response to injury and highlight a YAP-EGFR (epidermal growth factor receptor) axis by which Müller cells exit their quiescence state, a critical step toward regeneration.
Fichier principal
Vignette du fichier
1-s2.0-S2211124719305108-main.pdf (4.9 Mo) Télécharger le fichier
Origin : Publication funded by an institution
Loading...

Dates and versions

hal-02136721 , version 1 (22-05-2019)

Identifiers

Cite

Annaïg Hamon, Diana García-García, Divya Ail, Juliette Bitard, Albert Chesneau, et al.. Linking YAP to Müller Glia Quiescence Exit in the Degenerative Retina. Cell Reports, 2019, 27 (6), pp.1712-1725.e6. ⟨10.1016/j.celrep.2019.04.045⟩. ⟨hal-02136721⟩
110 View
163 Download

Altmetric

Share

Gmail Facebook X LinkedIn More