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Increase in ER-mitochondria contacts and mitochondrial fusion are hallmarks of mitochondrial activation during embryogenesis

ABSTRACT: Increase in ER-mitochondria contacts and mitochondrial fusion are hallmarks of mitochondrial activation during embryogenesis

PROVIDER: PRJNA1111056 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29007855.fastq.gz	Fastqsanger.gz
	SRR29007856.fastq.gz	Fastqsanger.gz
	SRR29007857.fastq.gz	Fastqsanger.gz
	SRR29007858.fastq.gz	Fastqsanger.gz
	SRR29007859.fastq.gz	Fastqsanger.gz

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Increase in ER-mitochondria contacts and mitochondrial fusion are hallmarks of mitochondrial activation during embryogenesis

Project description:Mitochondrial energy production is essential for development, yet the mechanisms underlying the continuous increase in mitochondrial activity during embryogenesis remain elusive. Using zebrafish as a model system for vertebrate development, we identify two sequentially acting mechanisms that could contribute to the rise in mitochondrial activity: an increased association between mitochondria and the endoplasmic reticulum (ER) at early stages, followed by the fusion of mitochondria leading to their elongated morphology at later embryonic stages. By comprehensively profiling mitochondrial activity, abundance, morphology, metabolome, proteome and phospho-proteome as well as respiratory chain enzymatic activity, we find that the increase in mitochondrial activity during embryogenesis does not require mitochondrial biogenesis, is not limited by metabolic substrates at early stages, and occurs under steady levels of respiratory chain complexes and enzymatic activities. Instead, our analyses pinpoint a previously unexplored increase in mitochondrial-ER association during early stages in combination with changes in mitochondrial morphology at later stages as possible contributors to the rise in mitochondrial activity during embryogenesis. Overall, our systematic profiling of the molecular and morphological changes to mitochondria during embryogenesis provides a valuable resource for further studying mitochondrial function during embryogenesis.

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Regulation of endoplasmic reticulum-mitochondria contacts and mitochondrial dynamics by Sel1L-Hrd1 ERAD during thermogenesis

Project description:Organelles such as endoplasmic reticulum (ER) and mitochondria interact with each other at specialized domains on the ER known as mitochondria-associated membranes (MAMs). Here, using three-dimensional high-resolution imaging techniques, we show that the Sel1LHrd1 protein complex, the most conserved branch of ER-associated protein degradation (ERAD), exerts a profound impact on ER-mitochondria contacts and mitochondrial dynamics, at least in part, by regulating the turnover and hence the abundance of the MAM protein sigma receptor 1 (SigmaR1). Sel1L or Hrd1 deficiency in brown adipocytes impairs dynamic interaction between ER and mitochondria, leading to the formation of pleomorphic “megamitochondria” and, in some cases with penetrating ER tubule(s), in response to acute cold challenge. Mice with ERAD deficiency are cold sensitive and exhibit mitochondrial dysfunction in brown adipocytes. Mechanistically, endogenous SigmaR1 is targeted for proteasomal degradation by Sel1L-Hrd1 ERAD, whose accumulation in ERAD-deficient cells leads to mitofusin 2 (Mfn2) oligomerization, thereby linking ERAD to mitochondrial dynamics. Our study identifies Sel1L-Hrd1 ERAD as a critical determinant of ER-mitochondria contacts, thereby regulating mitochondrial dynamics and thermogenesis.

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Mitochondria-Rough-ER Contacts in The Liver Regulate Systemic Lipid Homeostasis

Project description:Contacts between organelles create microdomains that play major roles in regulating key intracellular activities and signaling pathways, but whether they also regulate systemic functions remains unknown. Here, we report the ultrastructural organization and dynamics of the inter-organellar contact established by rough-Endoplasmic Reticulum closely wrapped around the mitochondria (wrappER). To elucidate the in vivo function of this contact, mouse liver fractions enriched in wrappER-associated-mitochondria are analyzed by transcriptomics, proteomics and lipidomics. The biochemical signature of the wrappER points to a role in the biogenesis of very-low-density lipoproteins (VLDL). Altering wrappER-mitochondria contacts curtails VLDL secretion and increases hepatic fatty acids, lipid droplets and neutral lipid content. Conversely, acute liver-specific ablation of Mttp, the most upstream regulator of VLDL biogenesis, recapitulates this hepatic dyslipidemia phenotype and promotes remodelling of the wrappER-mitochondria contact. The discovery that liver wrappER-mitochondria contacts participate in VLDL biology suggests an involvement of inter-organelle contacts in systemic lipid homeostasis.

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Regulation of endoplasmic reticulum-mitochondria contacts and mitochondrial dynamics by Sel1L-Hrd1 ERAD during thermogenesis

Project description:Regulation of endoplasmic reticulum-mitochondria contacts and mitochondrial dynamics by Sel1L-Hrd1 ERAD during thermogenesis

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Project description:Contacts between organelles create microdomains that play major roles in regulating key intracellular activities and signaling pathways, but whether they also directly regulate systemic cellular activities, remains unknown. Here, we report the ultrastructural organization and dynamics of a new type of inter-organelle contact which is formed by rough-Endoplasmic Reticulum that is closely wrapped around the mitochondrion (wrappER). To elucidate the in vivo function of this inter-organelle association, mouse liver fractions enriched in wrappER-associated-mitochondria were analyzed in parallel by transcriptomics, proteomics, and lipidomics. The biochemical signature of the wrappER points to an unexpected role in the biogenesis of very-low-density lipoproteins (VLDLs). Altering wrappER-mitochondria contacts curtails liver VLDL secretion and increases hepatic fatty acids, lipid droplets and neutral lipid content. Conversely, acute liver-specific ablation of Mttp, the most upstream regulator of VLDL biogenesis, mirrors this hepatic dyslipidemia phenotype and promotes remodelling of the wrappER-mitochondria contact. The participation of liver wrappER-mitochondria contacts in VLDL biology reveals a role of inter-organelle contacts in systemic lipid homeostasis.

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