Lipid-protein interactions: Lessons learned from stress.
Biological membranes are essential for normal function and regulation of cells, forming a physical barrier between extracellular and intracellular space and cellular compartments. These physical barriers are subject to mechanical stresses. As a consequence, nature has developed proteins that are able to transpose mechanical stimuli into meaningful intracellular signals. These proteins, termed Mechanosensitive (MS) proteins provide a variety of roles in response to these stimuli. In prokaryotes these proteins form transmembrane spanning channels that function as osmotically activated nanovalves to prevent cell lysis by hypoosmotic shock. In eukaryotes, the function of MS proteins is more diverse and includes physiological processes such as touch, pain and hearing. The transmembrane portion of these channels is influenced by the physical properties such as charge, shape, thickness and stiffness of the lipid bilayer surrounding it, as well as the bilayer pressure profile. In this review we provide an overview of the progress to date on advances in our understanding of the intimate biophysical and chemical interactions between the lipid bilayer and mechanosensitive membrane channels, focusing on current progress in both eukaryotic and prokaryotic systems. These advances are of importance due to the increasing evidence of the role the MS channels play in disease, such as xerocytosis, muscular dystrophy and cardiac hypertrophy. Moreover, insights gained from lipid-protein interactions of MS channels are likely relevant not only to this class of membrane proteins, but other bilayer embedded proteins as well. This article is part of a Special Issue entitled: Lipid-protein interactions.
Menzies Health Institute Queensland and School of Pharmacy, Griffith University, Gold Coast Campus, QLD 4222, Australia.
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Battle
Victor Chang Cardiac Research Institute, Darlinghurst, NSW 2010, Australia.
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Ridone
Victor Chang Cardiac Research Institute, Darlinghurst, NSW 2010, Australia; St Vincent's Clinical School, University of New South Wales, Darlinghurst, NSW, Australia.
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Bavi
Victor Chang Cardiac Research Institute, Darlinghurst, NSW 2010, Australia.
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Nakayama
Victor Chang Cardiac Research Institute, Darlinghurst, NSW 2010, Australia; School of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW 2308, Australia.
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Nikolaev
Victor Chang Cardiac Research Institute, Darlinghurst, NSW 2010, Australia; St Vincent's Clinical School, University of New South Wales, Darlinghurst, NSW, Australia. Electronic address: bmartinac@victorchang.edu.au.
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Martinac
D000818:Animals; D002462:Cell Membrane / Q000737:chemistry / Q000378:metabolism*; D006801:Humans; D008051:Lipid Bilayers / Q000737:chemistry / Q000378:metabolism; D040542:Mechanotransduction, Cellular; D008563:Membrane Lipids / Q000737:chemistry / Q000378:metabolism*; D008565:Membrane Proteins / Q000737:chemistry / Q000378:metabolism*; D008958:Models, Molecular; D011485:Protein Binding; D017434:Protein Structure, Tertiary
D008051:Lipid Bilayers; D008563:Membrane Lipids; D008565:Membrane Proteins
Computer modeling; EPR; FRET/FLIM; Liposome; Mechanosensitive channel; Patch fluorometry