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Fluxes of water through aquaporin 9 weaken membrane-cytoskeleton anchorage and promote formation of membrane protrusions.

Karlsson T, Bolshakova A, Magalhães MA, Loitto VM, Magnusson KE.

PLoS One. 2013;8(4):e59901.

Division of Medical Microbiology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linkoping University, Linkoping, Sweden.

 

 

Abstract

 

All modes of cell migration require rapid rearrangements of cell shape, allowing the cell to navigate within narrow spaces in an extracellular matrix. Thus, a highly flexible membrane and a dynamic cytoskeleton are crucial for rapid cell migration. Cytoskeleton dynamics and tension also play instrumental roles in the formation of different specialized cell membrane protrusions, viz. lamellipodia, filopodia, and membrane blebs. The flux ofwater through membrane-anchored water channels, known as aquaporins (AQPs) has recently been implicated in the regulation of cell motility, and here we provide novel evidence for the role of AQP9 in the development of various forms of membrane protrusion. Using multiple imaging techniques and cellular models we show that: (i) AQP9 induced and accumulated in filopodia, (ii) AQP9-associated filopodial extensions preceded actin polymerization, which was in turn crucial for their stability and dynamics, and (iii) minute, local reductions in osmolarity immediately initiated small dynamic bleb-like protrusions, the size of which correlated with the reduction in osmotic pressure. Based on this, we present a model for AQP9-induced membrane protrusion, where the interplay of water fluxes through AQP9 and actin dynamics regulate the cellular protrusive and motile activity of cells.

 

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Additional information

The formation of membrane protrusions enable cellular shape changes, which are pivotal for directional cell motility. Such processes require major cytoskeletal rearrangements, where filamentous actin reorganize into various patterns based on shape, location and volume of the specific membrane protrusion. Today there are several lines of evidence showing that the expression of membrane-spanning water channels, known as aquaporins (AQPs), promote cell migration. It is suggested that an increase in the rate of membrane protrusion formation underlies AQP-induced increases in cell migration. We have recently shown that AQP9, overexpressed in fibroblasts, dramatically induce the formation of numerous thin and long membrane extensions known as filopodia. Here, we have further addressed filopodial formation by visualizing the formation of AQP9-induced membrane extension together with various cytoskeletal components in live cells. We show that highly dynamic membrane structures like filopodia, lamellipodia and blebs form specifically at locations with high AQP9 accumulation. Subsequent stabilization of the membrane protrusions require a tight interplay with the actin cytoskeleton. Moreover, we now provide a hypothetical working model for such AQP9-induced membrane protrusions and cytoskeleton dynamics.

 

Figure Legend

Ag1518 fibroblast expressing GFP-AQP9, VivaTome-based confocal section, presented in Rainbow scale to clearly visualize intensity differences corresponding to local, filopodia-associated AQP9 expression.

 

Fluxes of Water through Aquaporin 9 Weaken Me