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EGFR signalling talks to mitochondria through contact sites

Project description

Mitochondrial contact sites with cell membranes and EGFR signalling

Contact sites between cellular organelles create microdomains with specific signalling as an additional layer of regulation. The EU-funded EGFRtoMITO project is working under the hypothesis that the interface comprising the plasma membrane (PM), the endoplasmic reticulum (ER) and the mitochondria represents a functional unit where direct cross-communication between epidermal growth factor receptor (EGFR) signalling and mitochondria takes place. Previously, the project partners showed that EGFR internalisation via non-clathrin endocytosis results in receptor degradation and signal extinction while leading to the formation of contact sites between the PM, the ER and the mitochondria, where EGF-dependent localised Ca2+ signalling occurs. The hypothesis verification will shed light on the impact of EGFR signalling on cellular functions newly linked to this pathway and possibly affecting cellular energetics and metabolism.

Objective

The integration of distinct internalization routes is crucial to determine the fate of plasma membrane (PM) receptors and the output of their signalling pathways. Contact sites between cellular organelles adds a further layer of regulation by creating microdomains that favour different signalling and metabolic pathways. These regulatory mechanisms are relevant to the epidermal growth factor receptor (EGFR). We found that EGFR internalization through non-clathrin endocytosis (NCE) leads primarily to receptor degradation and signal extinction, while clathrin-mediated endocytosis (CME) is mainly involved in EGFR recycling and sustaining signalling. Notably, internalization via NCE involves the formation of contact sites between the PM, the endoplasmic reticulum (ER) and the mitochondria, where EGF-dependent localized Ca2+ signalling occurs.
The founding hypothesis of this proposal is that the PM-ER-mitochondrial interface could represent a functional unit where direct cross-communication between EGFR signalling and mitochondria takes place. To investigate this hypothesis, we will use a three-tiered strategy aimed at elucidating:
1. the EGFR-dependent signalling that leads to NCE-ER-mitochondrial contact site formation and to local Ca2+ release, and the role of these contacts in EGFR endocytosis, signalling and fate;
2. the crosstalk between EGFR signalling and mitochondrial function at the PM-ER-mitochondrial interface by analysing the impact of EGFR-NCE on mitochondrial physiology and metabolism;
3. the relevance of NCE-ER-mitochondrial crosstalk to EGF-dependent cell physiological responses, e.g. migration, proliferation and differentiation, by exploiting isogenic cell derivatives from embryonic/pluripotent stem cells or ex vivo organoid cultures.
The verification of this hypothesis will expand our understanding of the impact of EGFR signalling on cellular functions not previously linked to this pathway and possibly impinging on cellular energetics and metabolism.

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Topic(s)

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ERC-COG - Consolidator Grant

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Call for proposal

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(opens in new window) ERC-2020-COG

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Host institution

UNIVERSITA DEGLI STUDI DI MILANO
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 920 062,50
Address
Via Festa Del Perdono 7
20122 Milano
Italy

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Region
Nord-Ovest Lombardia Milano
Activity type
Higher or Secondary Education Establishments
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 920 062,50

Beneficiaries (2)

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