TY - JOUR
T1 - The mitochondrial intermembrane space-facing proteins Mcp2 and Tgl2 are involved in yeast lipid metabolism
AU - Odendall, Fenja
AU - Backes, Sandra
AU - Tatsuta, Takashi
AU - Weill, Uri
AU - Schuldiner, Maya
AU - Langer, Thomas
AU - Herrmann, Johannes M.
AU - Rapaport, Doron
AU - Dimmer, Kai Stefan
N1 - We thank E. Kracker for technical assistance and the students Johannes Heimgärtner and Sabrina Eschbach for their help during their internships. This research was funded by the German Research Foundation (DFG) through GRK2364 and DI1386/2-1 to K.S.D. K.S.D. was additionally supported by the PROFILplus program of the Faculty of Medicine of the University of Tübingen. Collaborative work in the D.R., M.S., T.L., and J.M.H. labs was supported by a DFG DIP program (mitobalance 117516). D.R. and M.S. are supported by a German–Israeli Foundation (GIF) grant (Grant I-1458-412.13/2018). M.S. is an incumbent of the Dr. Gilbert Omenn and Martha Darling Professorial Chair in Molecular Genetics.
PY - 2019/9/30
Y1 - 2019/9/30
N2 - Mitochondria are unique organelles harboring two distinct membranes, the mitochondrial inner and outer membrane (MIM and MOM, respectively). Mitochondria comprise only a subset of metabolic pathways for the synthesis of membrane lipids; therefore most lipid species and their precursors have to be imported from other cellular compartments. One such import process is mediated by the ER mitochondria encounter structure (ERMES) complex. Both mitochondrial membranes surround the hydrophilic intermembrane space (IMS). Therefore, additional systems are required that shuttle lipids between the MIM and MOM. Recently, we identified the IMS protein Mcp2 as a high-copy suppressor for cells that lack a functional ERMES complex. To understand better how mitochondria facilitate transport and biogenesis of lipids, we searched for genetic interactions of this suppressor. We found that MCP2 has a negative genetic interaction with the gene TGL2 encoding a neutral lipid hydrolase. We show that this lipase is located in the intermembrane space of the mitochondrion and is imported via the Mia40 disulfide relay system. Furthermore, we show a positive genetic interaction of double deletion of MCP2 and PSD1, the gene encoding the enzyme that synthesizes the major amount of cellular phosphatidylethanolamine. Finally, we demonstrate that the nucleotide-binding motifs of the predicted atypical kinase Mcp2 are required for its proper function. Taken together, our data suggest that Mcp2 is involved in mitochondrial lipid metabolism and an increase of this involvement by overexpression suppresses loss of ERMES.
AB - Mitochondria are unique organelles harboring two distinct membranes, the mitochondrial inner and outer membrane (MIM and MOM, respectively). Mitochondria comprise only a subset of metabolic pathways for the synthesis of membrane lipids; therefore most lipid species and their precursors have to be imported from other cellular compartments. One such import process is mediated by the ER mitochondria encounter structure (ERMES) complex. Both mitochondrial membranes surround the hydrophilic intermembrane space (IMS). Therefore, additional systems are required that shuttle lipids between the MIM and MOM. Recently, we identified the IMS protein Mcp2 as a high-copy suppressor for cells that lack a functional ERMES complex. To understand better how mitochondria facilitate transport and biogenesis of lipids, we searched for genetic interactions of this suppressor. We found that MCP2 has a negative genetic interaction with the gene TGL2 encoding a neutral lipid hydrolase. We show that this lipase is located in the intermembrane space of the mitochondrion and is imported via the Mia40 disulfide relay system. Furthermore, we show a positive genetic interaction of double deletion of MCP2 and PSD1, the gene encoding the enzyme that synthesizes the major amount of cellular phosphatidylethanolamine. Finally, we demonstrate that the nucleotide-binding motifs of the predicted atypical kinase Mcp2 are required for its proper function. Taken together, our data suggest that Mcp2 is involved in mitochondrial lipid metabolism and an increase of this involvement by overexpression suppresses loss of ERMES.
UR - http://www.scopus.com/inward/record.url?scp=85072791142&partnerID=8YFLogxK
U2 - 10.1091/mbc.E19-03-0166
DO - 10.1091/mbc.E19-03-0166
M3 - مقالة
SN - 1059-1524
VL - 30
SP - 2681
EP - 2694
JO - Molecular Biology of the Cell
JF - Molecular Biology of the Cell
IS - 21
ER -