The inhibition of Cg2076, the GHITM homologue in neurons of Drosophila Melanogaster can be rescued by Buffy

Growth hormone-inducible transmembrane protein (GHITM) is an inner mitochondrial membrane protein that contains the Bax inhibitor-1 motif and is implicated in the regulation of mitochondrial morphology and especially cristae structure. The downregulation of GHITM results in fragmented mitochondria and the release of cytochrome c, while its upregulation delays the release of cytochrome c. We inhibited CG2076 the Drosophila GHITM homologue in the neurons using RNA interference and analysed the phenotypic consequences of this mitochondrial protein. The directed expression of GHITM-RNAi in neurons under the control of the Dopa decarboxylase (Ddc) transgene results in shortened lifespan and impaired climbing ability. The co-expression of Buffy, the only anti-apoptotic B cell lymphoma 2 (Bcl-2) protein in Drosophila, along with GHITM-RNAi results in suppression of the shortened lifespan and premature age-dependent loss in climbing ability.