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Time resolved DIA MS analysis of FZO1 depletion in s. cerevisiae

ABSTRACT: Mitochondrial biogenesis and inheritance must be carefully regulated alongside cell division to ensure proper mitochondrial function and cell survival. The dynamics of the mitochondrial network, including fusion and fission, play a crucial role in mitochondrial inheritance by facilitating the distribution and quality control of mitochondria. Here, we investigate the consequences of impaired mitochondrial fusion through depletion of Fzo1, which is essential for mitochondrial outer membrane fusion in s. cerevisiae. We use the AID (auxin-induced degron) system, which enables induced protein degradation and monitor changes in the proteome up to 21 hours after depletion.

INSTRUMENT(S):

ORGANISM(S): Saccharomyces Cerevisiae (baker's Yeast)

TISSUE(S): Cell Suspension Culture

SUBMITTER: Bianca Lemke

LAB HEAD: Jennifer C. Ewald

PROVIDER: PXD063340 | Pride | 2026-03-27

REPOSITORIES: Pride

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			Action	DRS
	20240122_LC05_BL_Lisa_fzo1_Rep1_DIA_1.raw	Raw
	20240122_LC05_BL_Lisa_fzo1_Rep1_DIA_10.raw	Raw
	20240122_LC05_BL_Lisa_fzo1_Rep1_DIA_2.raw	Raw
	20240122_LC05_BL_Lisa_fzo1_Rep1_DIA_3.raw	Raw
	20240122_LC05_BL_Lisa_fzo1_Rep1_DIA_4.raw	Raw

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Project description:Mitochondria are highly dynamic organelles undergoing fusion, fission and degradation. Although mitochondria are known to be essential for cellular metabolism, it is not fully understood how mitochondrial dynamics affect cellular metabolism. We previously identified a mouse gene, transmembrane protein 135 (TMEM135) that plays a role in the regulation of mitochondrial dynamics. Mice with mutant Tmem135 (Tmem135FUN025/FUN025) show accelerated aging phenotypes and age-related pathologies in the retina including the retinal pigment epithelium (RPE). We also generated a transgenic mouse line globally overexpressing the Tmem135 gene (Tmem135 TG). In several tissues and cells that we studied such as the retina, heart and fibroblast cells, we observed that the Tmem135 mutation causes elongated mitochondria, while over-expression of Tmem135 results in fragmented mitochondria. These unique mouse models allow us to test how abnormal mitochondrial dynamics affect metabolic signatures of tissues and cells. In this study, we identified metabolic changes in primary RPE cell cultures as well as tissues isolated from Tmem135FUN025/FUN025 mice (fusion > fission) and Tmem135 TG mice (fusion < fission) using nuclear magnetic resonance (NMR) spectroscopy. Metabolomics analysis revealed a tissue-dependent response to alterations to Tmem135 whereby, significant metabolic changes were observed in heart in both mutant and TG mice as compared to WT while negligible effects were observed in cerebellum and hippocampus. We also observed changes in Tmem135FUN025/FUN025 and Tmem135 TG RPE cells associated with osmosis, glucose metabolism and phospholipid metabolism. Significant depletion of NAD+ was detected in both Tmem135FUN025/FUN025 and Tmem135 TG RPE cells, indicating that imbalance in mitochondrial dynamics to both directions lowers the cellular NAD+ level. Thus, we have identified metabolomic changes associated with imbalanced mitochondrial dynamics in heart tissue and RPE cells which can likely lead to functional abnormalities.

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Time resolved DIA MS analysis of FZO1 depletion in s. cerevisiae

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