Frankino PA et al. (2019) Cell Metab "Evolutionary Comeuppance: Mitochondrial Stress Awakens the Remnants of Ancient Bacterial Warfare."

Dillin A, Frankino PA, Moehle EA

[Cell Metab, 2019]

Mitochondria are organelles descended from an endosymbiosed bacterium, and many bacterial toxins impair mitochondria, likely as an echo of ancient bacterial warfare. However, the signal transduction pathways that translate mitochondrial dysfunction into a transcriptional program for detoxification have not been well understood. In this issue of Cell Metabolism, Mao etal. (2019) provide insight into how mitochondrial perturbations can activate both the mitochondrial unfolded protein response (UPR^mito) and detoxification response and, importantly, how these responses differentially affect organismal physiology under normal conditions or with pathogenic challenges.

Leiser SF et al. (2016) Worm "New insights into cell non-autonomous mechanisms of the C. elegans hypoxic response."

Leiser SF, Rossner R, Kaeberlein M

[Worm, 2016]

The hypoxic response is a well-studied and highly conserved biological response to low oxygen availability. First described more than 20 y ago, the traditional model for this response is that declining oxygen levels lead to stabilization of hypoxia-inducible transcription factors (HIFs), which then bind to hypoxia responsive elements (HREs) in target genes to mediate the transcriptional changes collectively known as the hypoxic response.(1,2) Recent work in C. elegans has forced a re-evaluation of this model by indicating that the worm HIF (HIF-1) can mediate effects in a cell non-autonomous fashion and, in at least one case, increase expression of an intestinal hypoxic response target gene in cells lacking HIF-1.