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Sci Rep. 2015 Nov 24;5:16816. doi: 10.1038/srep16816.

Loss of Polo ameliorates APP-induced Alzheimer's disease-like symptoms in Drosophila.

Author information

1
Institute of Intervention Vessel, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai 200092, China.
2
School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai 200092, P.R. China.

Abstract

The amyloid precursor protein (APP) has been implicated in the pathogenesis of Alzheimer's disease (AD). Despite extensive studies, little is known about the regulation of APP's functions in vivo. Here we report that expression of human APP in Drosophila, in the same temporal-spatial pattern as its homolog APPL, induced morphological defects in wings and larval NMJ, larva and adult locomotion dysfunctions, male choice disorder and lifespan shortening. To identify additional genes that modulate APP functions, we performed a genetic screen and found that loss of Polo, a key regulator of cell cycle, partially suppressed APP-induced morphological and behavioral defects in larval and adult stages. Finally, we showed that eye-specific expression of APP induced retina degeneration and cell cycle re-entry, both phenotypes were mildly ameliorated by loss of Polo. These results suggest Polo is an important in vivo regulator of the pathological functions of APP, and provide insight into the role of cell cycle re-entry in AD pathogenesis.

PMID:
26597721
PMCID:
PMC4657023
DOI:
10.1038/srep16816
[Indexed for MEDLINE]
Free PMC Article

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