High impact information on gft

• Distinct protein degradation mechanisms mediated by Cul1 and Cul3 controlling Ci stability in Drosophila eye development [1].
• In posterior cells, Ci degradation is controlled by a mechanism that requires the activity of Cul3, another member of the Cullin family [1].
• We further show that neddylated Cul1 and Cul3 are unstable - as suggested by the evidence that Nedd8 promotes the instability of both cullins - and that the unneddylatable forms of cullins are stable [2].
• Cullin-3 regulates pattern formation, external sensory organ development and cell survival during Drosophila development [3].
• Perturbation of Cullin-3 function has pleiotropic effects during development, including defects in external sensory organ development, pattern formation and cell growth and survival [3].

Biological context of gft

• The diverse nature of Cullin-3 phenotypes highlights the importance of targeted proteolysis during Drosophila development [3].
• Cul3 mutant neurons are defective in terminal morphogenesis of neurites [4].

Anatomical context of gft

• Requirement of Cul3 for axonal arborization and dendritic elaboration in Drosophila mushroom body neurons [4].
• Together, Cul3 plays an essential role in both axonal arborization and proper elaboration of dendrites and may require neddylation for its proper function [4].

Regulatory relationships of gft

• Loss of Cullin-3 function in eye discs but not other imaginal discs promotes cell-autonomous accumulation of Ci155 [3].

Other interactions of gft

• The 35C3 QTL localizes to a 200-kb interval with 15 genes, including three genes for which mutations exist (reduced (rd), guftagu (gft) and ms(2)35Ci) [5].

References