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. 2015 Sep 14;10(9):e0137691. doi: 10.1371/journal.pone.0137691

Fig 1. CBP is a genetic modifier of Aβ42 mediated neurodegeneration in the Drosophila eye.

Fig 1

(A) In comparison to the wild-type compound eye comprising of nearly 800 ommatidia of unit eyes, (C) misexpression of Aβ42 in the differentiating photoreceptor neurons of the developing eye using GMR-Gal4 driver (GMR> Aβ42) results in a strong neurodegenerative phenotype of highly reduced eye, glazed appearance and ommatidial fusion. (E, F) Misexpression of full length CBP with Aβ42 in the developing eye (GMR> Aβ42 +CBP FL) results in a significant rescue of the neurodegeneration in ~20% (22/112) flies as seen in (C) GMR> Aβ42 alone. (G) Reducing CBP function by misexpression of CBP RNAi (GMR> Aβ42 +CBP RNAi) results in a strong neurodegenerative phenotype in nearly all the hatched flies. Levels of CBP in (B) wild-type, (D) GMR> Aβ42, (F) GMR> Aβ42 +CBP FL, (H) GMR> Aβ42+ CBP RNAi eye imaginal disc. Note that CBP levels are reduced in GMR> Aβ42 background as compared to the wild-type eye imaginal disc. The orientation of all imaginal discs is identical with posterior to the left and dorsal up. Magnification of all eye imaginal discs is 20X, and adult eyes is 10X.