Mitochondrial retrograde signalling Sample Clauses

Mitochondrial retrograde signalling. As discussed above, the nuclear genome plays a crucial role in the regulation of mitochondrial structure and function. The nucleus, therefore, must efficiently communicate with the mitochondria, ensuring a constant flow of information – this process is referred to as nucleus-to-mitochondria ‘anterograde signalling’. In the early 1990s, pioneering work by the Butow laboratory also led to the identification of a mitochondria- to-nucleus communication pathway referred to as ‘retrograde signalling’ (Liao and Xxxxx, 1993; Xxxxx and Xxxxxxxx, 2004). Research carried out on the mitochondrial retrograde signalling pathway suggests that dysfunctional mitochondria communicate with the nucleus
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Mitochondrial retrograde signalling. MtDNA damage or the presence of mutations in mtDNA can lead to mitochondrial dysfunction, including a bioenergetic deficit due to functional changes in respiratory chain complexes. Mitochondria can relay this information back to the nucleus via a retrograde signalling pathway, which will elicit an anterograde response, acting to repair the damage or induce cell death (Xxxxxx et al., 2010). Recently, studies have also been carried out in Drosophila, in order to uncover more details regarding the mechanisms of retrograde pathways which are activated upon mitochondrial dysfunction (Xxxxxx et al., 2005; Xxxx et al., 2006; Xxxxxx et al., 2012). Downregulation of Complex IV (COX) subunit Va (CoVa) in the developing Drosophila retina, activates a retrograde pathway specifically involving AMP-activated protein kinase and tumor- suppressor protein p53 (Xxxxxx et al., 2010). Activated p53 will transcriptionally activate archipelago, an F-box protein which will in turn ubiquitinylate Cyclin E, resulting in proteasomal degredation and a block in the cell cycle from G1 to S phase (Xxxxxx et al., 2010; Xxxxxx et al., 2012). However, cell viability is maintained, suggesting that the retrograde signal acts to alter the metabolic state whilst favouring cell survival. Indeed, disruption of ETC genes has been reported to extend lifespan, via a retrograde signal, in Drosophila (Xxxxxxxx et al., 2009; Xxx et al., 2011) and xxxx (Xxx et al., 2005; Dell'xxxxxxx et al., 2007; Xxxxxxxx and Xxxxxx, 2008). Furthermore, studies in mammalian cells also identified an additional retrograde response, which was termed the mitochondrial unfolded protein response (UPRmt). In a healthy mitochondrion, mitochondrial chaperones localised in the mitochondrial matrix act to regulate protein import and folding of proteins and complex assembly, whilst proteases in the matrix and inner membrane degrade any misfolded proteins (Tatsuta and Xxxxxx, 2008). However, several disruptions in the mitochondrial environment, such as mutations in assembly proteins, harsh environmental conditions or high levels of reactive oxygen species (ROS), might lead to the accumulation of unfolded or misfolded proteins, triggering a UPRmt (Xxxxxx and Xxx, 2010). This stress response induces an upregulation of nuclear encoded mitochondrial chaperones and proteases (Xxxxxxxx et al., 1996; Xxxx et al., 2002). The UPRmt response has also been shown to be activated upon mitochondrial stress caused by mtDNA depletion, downregula...
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