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. 2020 Aug 14;11(8):631. doi: 10.1038/s41419-020-02860-9

Fig. 8. Proposed model explaining Yap+/− phenotypes at postnatal and adult stages.

Fig. 8

Our results revealed the occurrence of a TAZ compensatory mechanism in postnatal Yap+/− retina, i.e., the decreased of Yap expression (red arrow) is accompanied by an increase of Taz expression (green arrow), that results in the upregulation of YAP/TAZ target gene expression. Our data suggest that this leads to prolonged proliferation of postnatal retinal progenitor cells, and that this phenotype may likely result from EGFR pathway potentiation. In the adult Yap+/− retina, the compensatory mechanism is no longer effective, and YAP/TAZ target genes expression is diminished. Under such conditions, one Yap allele deletion progressively leads to impaired Müller cell homoeostasis. We propose that this may, at least in part, contribute to impaired cone-specific visual cycle and therefore to the cone dystrophy observed in aged Yap+/− mice. RTKs Receptor tyrosine kinases. This figure was created with some schemas from ©BioRender—biorender.com.