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Uncovering Protein Mechanics in Physiology and Disease

Project description

Exploring the perturbations of titin mechanics

Playing a central role in cellular processes, proteins are now being engineered. What is known is that protein mechanics contribute to the function of biological systems. The question is how and whether alteration of protein mechanics can trigger disease, particularly in mechanical conditions such as cardiomyopathies. The ERC-funded ProtMechanics-Live project will build on unique expertise in protein mechanics and engineering, biophysics, biochemistry and cardiovascular biology. Its aim is to enable investigation of mechanical proteins in their functionally relevant, physiological context. Specifically, the project will apply first-of-their-kind tools to titin, the largest protein known. It will explore how perturbations of titin mechanics result in altered cardiomyocyte force generation, mechanosensing, mechanotransduction, differentiation and proliferation.

Objective

Protein mechanics is a key contributor to the form and function of biological systems by mechanisms that are just starting to be unraveled. An ensuing hypothesis is that alteration of protein mechanics can trigger disease, particularly in mechanical conditions such as cardiomyopathies in which primordial underlying molecular mechanisms remain elusive. Although tempting, this possibility has not been tested due to the absence of methods that can modulate the mechanics of proteins in vivo. My proposal aims to overcome technical barriers to scientific progress by establishing manipulation of protein mechanics in living cells and animals as a new research field. In aim 1, we will address current technological limitations through the generation of genetic, protein-engineering-based mechanical loss- and gain-of-function models to interfere acutely and reversibly with protein mechanics in living systems (mLOF and mGOF, respectively). We will apply these first-of-their-kind tools to the giant protein titin, a major contributor to the force-generating and sensing properties of cardiomyocytes with strong links with heart disease, and a workhorse protein that has been instrumental in the past to understand the biophysics of polypeptides under force. In aim 2, we will exploit cellular mLOF and mGOF to define how perturbations of titin mechanics result in altered cardiomyocyte force generation, mechanosensing, mechanotransduction, differentiation and proliferation. Leveraging on our cell studies, in aim 3 we will use murine mLOF and mGOF to shed light into the contribution of titin mechanics to the onset and progression of genetic and acquired cardiomyopathy. ProtMechanics-Live builds on our unique expertise in protein mechanics and engineering, biophysics, biochemistry and cardiovascular biology to enable investigation of mechanical proteins in their functionally relevant, physiological context

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Programme(s)

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Topic(s)

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Funding Scheme

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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

CENTRO NACIONAL DE INVESTIGACIONES CARDIOVASCULARES CARLOS III (F.S.P.)
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.

€ 2 000 000,00
Address
CALLE MELCHOR FERNANDEZ ALMAGRO 3
28029 Madrid
Spain

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Region
Comunidad de Madrid Comunidad de Madrid Madrid
Activity type
Research Organisations
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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.

€ 2 000 000,00

Beneficiaries (1)

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