The citric acid cycle, commonly referred to as the TCA cycle, generates metabolites and reducing equivalents (NADH and FADH2). This essentially describes the two salient functions of mitochondria described in most biochemistry textbooks: production of ATP, and the generation of intermediary metabolites. In his Nobel Lecture, Krebs stated, ‘that in some micro-organisms the cycle primarily supplies intermediates rather than energy, whilst in the animal and most other organisms it supplies both energy and intermediates’. Hans Krebs won the Nobel Prize in Physiology or Medicine in 1953 for his discovery of the citric acid cycle. This review is a brief account of recent work in mitochondria-dependent signaling in the historical framework of the early studies. Collectively these studies have established that mitochondria-dependent signaling has diverse physiological and pathophysiological outcomes. These include the release of metabolites, mitochondrial motility and dynamics, and interaction with other organelles such as endoplasmic reticulum in regulating signaling. In the past decade, multiple new modes of mitochondrial signaling have been discovered. It has also been shown that mitochondrial dysfunction causes induction of stress responses, bolstering the idea that mitochondria communicate their fitness to the rest of the cell. Within a few years, multiple other mitochondria-centric signaling mechanisms have been proposed, including release of reactive oxygen species and the scaffolding of signaling complexes on the outer mitochondrial membrane. Formerly viewed as sites of biosynthesis and bioenergy production, these double membrane organelles could now be thought of as regulators of signal transduction. ![]() ![]() Almost 20 years ago, the discovery that mitochondrial release of cytochrome c initiates a cascade that leads to cell death brought about a wholesale change in how cell biologists think of mitochondria.
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