Figure 6. STS induces mitochondrial biogenesis.

(A) Fold change in the expression of genes used as markers for mitochondrial biogenesis following STS compared to AL conditions. Measurements by real-time quantitative PCR were corrected with rp49 expression as in [26]. The genes used were tfam, master regulator of mitochondrial biogenesis; CG13096 and CG10664, cox4; CG17280, cox6A. Note that the induction observed was dependent on NF-κB since it was not observed when both Toll-Dif and the Imd-Relish pathway were deficient (Dif-Key) (B) AMP gene expression is induced upon starvation. Fold-change in Diptericin (black bars) or Drosomycin (white bars) expression in wild type (Wn) or rel flies following STS. Induction of AMPs implies that NF-κB signalling is robustly activated following STS. In all cases in (A) and (B) mean expression levels (±s.e.) from three independent experiments are shown. (C) Putative mode of regulation of NO expression in Drosophila. NO is synthesised via overlapping and interconnected pathways. The main component of this mode is achieved through the direct upregulation of NOS mediated by the NF-κB protein Relish after infection by Gram-negative bacteria. NO can then upregulate the IMD pathway in a positive feedback loop. A second (minor) component of this would be the direct (NF-κB-independent) production of NO as an antimicrobial agent against Gram-negative bacteria. Finally, STS-mediated NO expression is catalysed by two-independent means. Principally through the up-regulation of Relish, leading to NOS upregulation as described above, or secondly, in a NOS-independent fashion. In this case starvation-induced NF-κB (either Relish and/or Dif) upregulation leads to CCO upregulation and NOS-independent NO production.