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Deciphering the starvation-induced effects on mitochondria phenotype

Grant number: 19/09732-0
Support type:Regular Research Grants
Duration: August 01, 2019 - July 31, 2021
Field of knowledge:Biological Sciences - Biochemistry - Metabolism and Bioenergetics
Principal Investigator:Fernanda Marques da Cunha
Grantee:Fernanda Marques da Cunha
Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

Energy metabolism is paramount for life and response to stress in eukaryotes, and mitochondria are key organelles not only for being the main site of ATP and intermediary metabolite synthesis, but also for acting as signaling platforms involved in the response to different stresses. Nutrient deprivation is one of the most ancient evolutionary pressures faced by living organisms and, in the nematode Caenorhabditis elegans, leads to increased life span and resistance to stress. Many molecular pathways are known to be necessary for the response to nutritional deprivation in C. elegans, but very few works aimed at studying the effects of nutrient deprivation on mitochondria activity and molecular composition. In a previous project, our group identified significant changes in C. elegans mitochondrial activity in response to nutrient deprivation. Moreover, those deprivation-related changes were blunted in mutants lacking a lysosomal lipase (LIPase-Like 5 enzyme; LIPL-5), suggesting that this protein controls mitochondrial response to nutrient deprivation. Thus, it is important to characterize the molecular changes induced by nutrient deprivation in C. elegans mitochondria, and identify the molecular pathways involved in the promotion of those changes. It is also important to understand the relation between LIPL-5 and mitochondria, investigating, for instance, whether the absence of LIPL-5 activates stress responses that ultimately impact on mitochondrial activity. Understanding the mitochondrial responses to nutrient deprivation as well as the molecular pathways that bring about those responses may pave the way for the identification of targets to modulate mitochondrial activity in pathologic situations. (AU)