Abstract
Originally Lipid droplets (LDs) were considered as being droplets for lipid storage only. Increasing evidence, however, demonstrates that LDs fulfill a pleiotropy of additional functions. Among them is the modulation of protein as well as lipid homeostasis. Under unfavorable pro-oxidative conditions, proteins can form aggregates which may exceed the overall proteolytic capacity of the proteasome. After stress termination LDs can adjust and support the removal of these aggregates. Additionally, LDs interact with mitochondria, specifically take over certain proteins and thus prevent apoptosis. LDs, which are loaded with these harmful proteins, are subsequently eliminated via lipophagy. Recently it was demonstrated that this autophagic process is a modulator of longevity. LDs do not only eliminate potentially dangerous proteins, but they are also able to prevent lipotoxicity by storing specific lipids. In the present study we used the model organism Saccharomyces cerevisiae to compare the proteome as well as lipidome of mitochondria and LDs under different conditions: replicative aging, stress and apoptosis. In this context we found an accumulation of proteins at LDs, supporting the role of LDs in proteostasis. Additionally, the composition of main lipid classes such as phosphatidylcholines, phosphatidylethanolamines, phosphatidylinositols, phosphatidylglycerols, triacylglycerols, ceramides, phosphatidic acids and ergosterol of LDs and mitochondria changed during stress conditions and aging.
Highlights
Among many theories of aging the most prominent is the BFree Radical Theory of Aging^ (FRTA) which is probably the most cited theory in this field
We demonstrated that specific mitochondrial proteins such as mammalian BAX and BCL-XL, as well as Mmi1 (Bischof et al 2017) and Erg6 in yeast cells are transferred from mitochondria to Lipid droplets (LDs)
Only scarce knowledge is available on the number of proteins that can shuttle from mitochondria to LDs
Summary
Among many theories of aging the most prominent is the BFree Radical Theory of Aging^ (FRTA) which is probably the most cited theory in this field. Similar proteins include Ybh and Mmi among many others (Braun et al 2006; Buttner et al 2011) Some of these proteins induce changes in and at mitochondria that include fragmentation of the mitochondrial network, mitochondrial outer membrane permeabilization, calcium influx and cyctochrome c release. Bcl-XL blocks the permeabilization of the mitochondrial outer membrane, which is initiated by the oligomerization of BAX and BAK (Dlugosz et al 2006) This oligomerization is a prerequisite for cytochrome c release from mitochondria which initiates a caspase cascade that can be blocked by IAPs (inhibitor of apoptosis proteins) (Yang and Li 2000)
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