Our skin and mucous membranes are protected by epithelial cells, which form a barrier that defends the body from the outside environment. This barrier function relies on specialized structures called junctions that hold cells together and regulate the exchange of substances between them.
Researchers at the University of Geneva (UNIGE), in collaboration with the National University of Singapore (NUS) and the Institute of Physical Chemistry (IPC) in Göttingen, investigated the role of a specific protein called gamma-actin in shaping the structure and mechanical properties of epithelial cells and their junctions. Their findings, published in Nature Communications, uncover a mechanism of interdependence between different forms of the cytoskeletal proteins actin and myosin. The study also highlights gamma-actin’s critical role in maintaining cell membrane stiffness and controlling the movement of junctional proteins – factors that may help explain certain forms of hearing loss.
Essential Role of Epithelium
The epithelium is a tissue of fundamental importance, that covers the surface of the body and lines the interior of many organs. Composed of tightly bound epithelial cells, it plays a crucial protective role against external aggressions, such as pathogens. This function relies to a large extent on the presence of “adherens” and “tight junctions,” veritable protein locks linking neighboring cells and ensuring tissue tightness. Tight junctions regulate the passage of molecules in and out of organs. For example, they facilitate nutrient absorption in the intestine and help filter substances in the kidneys.
The laboratory of Sandra Citi, Associate Professor in the Department of Molecular and Cellular Biology at the UNIGE Faculty of Science, is interested in how tight junctions interact with the cytoskeleton – the internal framework of cells – to regulate cell architecture, as well as the various functions performed by the epithelium.
Exploring Gamma-Actin’s Impact on Hearing
In this recent study, the researcher and her team analyzed the role of gamma-actin – one of the components of the cytoskeleton – in the organization of junctions between cells, and discovered that in its absence another form of actin, beta-actin, is produced in greater quantities, and this is linked to an increase in a specific form of myosin. “These changes make the apical membrane – the top of the cell – less stiff and certain constituents of the tight junctions more mobile, without however affecting the barrier formed by these junctions,” explains Marine Maupérin, postdoctoral fellow in the Department of Molecular and Cellular Biology at the UNIGE Faculty of Science and first author of the study.
Key Insights into Gamma-Actin and Hearing Loss
Gamma-actin therefore confers increased rigidity to the apical membrane, forming a network of filaments that is stronger and stiffer than that made up of beta-actin filaments. “This result is particularly interesting because the stiffness of the apical membrane is essential for auditory function,” explains Sandra Citi, who led this research.
Indeed, gamma-actin-deficient mice show altered architecture of the apical surface of epithelial cells and progressive hearing loss. A stiffer cortical membrane may be required to withstand the constant mechanical stimuli to which the hair cells lining the inner ear are exposed. A deeper investigation into the role of gamma-actin in maintaining cell integrity could thus help to understand the pathologies of hearing loss, for example.
Reference: “A feedback circuitry involving γ-actin, β-actin and nonmuscle myosin-2 A controls tight junction and apical cortex mechanics” by Marine Maupérin, Yuze Sun, Thomas Glandorf, Tabea Anne Oswald, Niklas Klatt, Burkhard Geil, Annick Mutero-Maeda, Isabelle Méan, Lionel Jond, Andreas Janshoff, Jie Yan and Sandra Citi, 13 March 2025, Nature Communications.
DOI: 10.1038/s41467-025-57428-y
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3 Comments
Hi, interesting reading but I doubt it will help a person who’s born deaf but I can still hear with a hearing aid in one ear. Once it’s out of my ear, then I have a blissful sleep 😴 nothing wakes me up unless it’s very loud. My late mother contracted German Measles (in Austria!) A dead nerve.
I’m too old now and I got used to it at a tender age of nearly 76 in April.🤭 My hearing hardly changes judging from all the tests I’ve had over the years. I’m due for one soon. I hated the moulds that went in too deep making me sound hollow so I asked them to make it shorter so that air can get around ear. Unusual it may sound it’s perfect for me. 😄
A lot of people I know won’t wear hearing aids because they had normal hearing but what they don’t realise to fix sound to their liking, the should keep going back until sound is right for them.
I absolutely hate comperterised artificial sound and I always had the same tone before stupid computers arrived. It threw me and I hold back because of this. One sound in a quiet office then once outside, too loud and terrible sound.
I thought I’d write and tell you how it was for me all these years. I can’t do without my hearing aid, not nice when people have to shout.
I need for you to break it down so I can understand, is their anything that I can do reverse hearing loss by what you are saying , is their away for my to relax or stop the stiffness down in my ear where their is hearing loss ?
Readers of this promotional piece should know that mice genetically modified to completely lack gamma-actin (the protein you’ve never heard of) have normal hearing. Here’s the reference:
Sundby LJ, Hawbaker KM, Powers J, Southern WM, Johnson EE, Patrinostro X, Perrin BJ, Ervasti JM. The complete absence of cytoplasmic γ-actin results in no discernible phenotype in mice or primary fibroblasts. FEBS J. 2025 Mar 20. doi: 10.1111/febs.70075. Epub ahead of print. PMID: 40109120.