Rbf and healthy ageing in Drosophila: interactionswith parkin, Buffy and Debcl

A. Hasan and B.E. Staveley
Published June 13, 2024
Genet. Mol. Res. 23 (2): gmr19282
DOI http://dx.doi.org/10.4238/gmr19282

About the authors
A. Hasan and B.E. Staveley

Corresponding author
Brian E. Staveley
E-mail: bestave@mun.ca


Mitochondrial health depends upon proteins that counteract dysfunction generated by cellular stress due to impairment of essential cellular pathways. The expression of the Bcl-2 family genes, the E3 ubiquitin ligase encoding, parkin, and the transcription regulator gene, Rbf/Rb, play significant roles in mitochondrial and cellular survival. Under conditions of extreme cellular stress, mitochondria can act to promote apoptosis. The overexpression of Rbf in the dopaminergic neurons of Drosophila directed by Ddc-Gal4 can result in flies with a reduced median lifespan and impaired climbing ability over time: a well-established Drosophila model of Parkinson Disease (PD). The inhibition of Rbf can lead to a premature reduction in locomotor ability compared to control. The overexpression of Rbf can rescue the neurodegenerative phenotypes induced due to the loss of function of parkin. The expression of the pro-cell survival Bcl-2 family member Buffy and inhibition of the anti-apoptotic Debcl can rescue the longevity and impaired locomotor ability over time observed in a model of PD induced by Rbf-RNAi. Overall, the alteration of expression of Rbf in selected neurons can produce a novel model of PD in Drosophila; the directed expression of Buffy acts to protect to counteract the Rbf-RNAiinduced deficits in lifespan and climbing ability.

Key Words: Drosophila melanogaster; Aging; Climbing Ability; Mitochondria; Drosophila model of Parkinson disease

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