RESEARCH
Our lab aims to understand how changes in mitochondria ultrastructure and dynamics impact cell function and metabolism. The identification of key players, the study of the dynamic interactions, and the definition of molecular mechanisms are our main interest.
MITOCHONDRIAL COMPLEXOMIC CHANGES IN PHYSIOLOGY AND PATHOLOGY
Mitochondria adaptation to cellular requirements likely requires the reorganization of the mitochondrial protein complexes. However, the complexes dynamics in conditions such as metabolic switch are poorly described. Our interest is to identify these changes and understand the relevance in pathological contexts such as cancer and stemness.
ATAD3 PROTEIN FAMILY: IMPLICATIONS FOR CANCER AND STEMNESS
ATAD3A is a mitochondrial protein whose involvement in mitochondrial cristae biogenesis and mitoribosome stability have been recently described in our lab (under revision). Still the role of the other member, ATAD3B, is still unknown. Our results indicate that its expression change cellular metabolism by regulating mitochondrial function, which is in line with the expression pattern of ATAB3B in tumoral and pluripotent cells. Current research in our lab wants to reveal the function and molecular mechanism that mediate ATAD3B impact on mitochondrial function.
OPTIMIZING MITOCHONDRIAL TRANSLATION TO BYPASS ALS-MITO DYSREGULATION
During ALS, the protein TDP-43 mislocalizes into mitochondria, an event that is accompanied by alteration in mitochondrial ultrastructure, respiratory supercomplexes deficiency, and impaired respiratory capacity. The molecular mechanism underlying this phenotype is still under study; however, it has been shown that TDP-43 can bind mtDNA-derived transcripts. This project wants to address whether optimizing mitochondrial ultrastructure accompanied by increased mitochondrial translation ameliorates TDP-43-induced mitochondrial dysfunction