https://orcid.org/0000-0002-7828-8118
Figures & data
Figure 1. TUBGCP4 plays essential roles in early embryo development and retina homeostasis. (A) Two copies of Tubgcp4 are sufficient for embryo viability and normal retinal function. GCP4, TUBGCP4; PE, phosphatidylethanolamine. (B) Haploinsufficiency of TUBGCP4 affects TUBGRC/γ-TuRC assembly, disrupts autophagy homeostasis, and leads to photoreceptor degeneration. (C) Homozygous mutation of Tubgcp4 results in early embryonic lethality owing to abnormal spindle assembly. ATG7 can interact with either ATG3 or TUBGCP4 through its N-terminal domain (NTD). When Tubgcp4 is knocked out, ATG3 interacts with ATG7 to promote lipidation of LC3B and autophagy. Thus, TUBGCP4 can inhibit autophagy by competing with ATG3 to interact with ATG7, and interfere with lipidation of LC3B. TUBGCP4 regulates autophagy through an ATG3-TUBGCP4-ATG7-LC3B pathway, which plays key roles in maintaining retina homeostasis in a dose-dependent manner.
