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. 2015 May 23;138(7):1801–1816. doi: 10.1093/brain/awv132

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© The Author (2015). Published by Oxford University Press on behalf of the Guarantors of Brain.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits non-commercial reuse, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Lack of iPLA2-VIA gene activity leads to reduced survival and locomotor deficits. (A) Schematic of the Drosophila iPLA2-VIA gene, showing the position of the P-element insertion (arrowhead). The iPLA2-VIA gene has four main transcripts: iPLA2-VIA-RB, iPLA2-VIA-RC, iPLA2-VIA-RD and iPLA2-VIA-RA (FlyBase). The position of the primers has been previously shown (Malhotra et al., 2009). (B) RT-PCR analysis of iPLA2-VIA^−/− flies shows that there is no mRNA expression of the iPLA2-VIA gene compared with w¹¹¹⁸ control flies. The end products of the RT-PCR reaction were run on an agarose gel. RP49 is an internal control gene and is expressed in both the iPLA2-VIA^−/− and control w¹¹¹⁸ flies. (C) iPLA2-VIA^−/− flies display an age-dependent reduction in climbing ability compared with w¹¹¹⁸ controls (n = 45 flies per genotype, three repeats per genotype, P < 0.05). Climbing ability is expressed as a perfomance index (PI) over time in days (d). (D) Female flies lacking both iPLA2-VIA genes (iPLA2-VIA⁻^/⁻) have a significantly reduced lifespan compared with w¹¹¹⁸ control flies (P < 0.0001). Furthermore female flies lacking only one iPLA2-VIA gene (iPLA2-VIA^+/⁻; n = 150 flies per genotype) do not display a reduction in lifespan. (E) Ubiquitous downregulation of iPLA2-VIA activity using sRNAi (UAS-iPLA2-VIA-RNAi) driven by Act5c-Gal4 (Act5c-Gal4 > UAS-iPLA2-VIA-RNAi) results in an age-dependent reduction in climbing ability compared with control UAS-iPLA2-VIA-RNAi flies (P < 0.05; n = 45 flies per genotype, three repeats each). (F) Knockdown of iPLA2-VIA activity using iPLA2-VIA sRNAi (UAS-iPLA2-VIA-RNAi) driven ubiquitously by Act5c-Gal4 (Act5c-Gal4 > UAS-iPLA2-VIA-RNAi) results in a decrease in lifespan compared with control non-expressing UAS-iPLA2-VIA-RNAi flies (P < 0.0001) or driver Act5c-Gal4 flies (P < 0.0001), similar to that seen with the null mutant flies (iPLA2-VIA^−/−; n = 150 flies per genotype). (G) Knockdown of iPLA2-VIA activity using sRNAi (UAS-iPLA2-VIA-RNAi) driven in the fly nervous system using the elav-Gal4 driver results in a decrease in lifespan compared with control non-expressing UAS-iPLA2-VIA-RNAi flies (P < 0.0001), or driver elav-Gal4 (P < 0.0001; n = 150 flies per genotype), similar to that seen with the null mutant flies (iPLA2-VIA^−/−).