What is the cause of osmosis? Typically, with my students of 14-16 years old (GCSE courses), I don't delve into the mechanism. It's the pattern that matters most at this stage. But as students progress to my IB biology course (16-18 years old) and explanation leans more on molecular details, the mechanism becomes more important.
In conjunction with the bigger pattern (i.e. water potential) what should we teach as the mechanistic cause?
Is it water dilution? Is it the number of free water particles? In 2013 Kramer and Myers published an article in Trends in Plant Science suggesting that it is neither. Not only that, but these alternative explanations have been repeated consistently in biology textbooks and classrooms for decades despite the real mechanism of osmosis being known for some time.
What if water dilution or number of free water particles are just simpler models that allow explanation without causing confusion with too many details?
Well, in my opinion, they are not. They aren't simpler models of more complex ones. They are alternative models. They're also not simpler, but more confusing. The model that Kramer and Myers explain is both better in terms of match (to reality) and range (how far the model can take students before it runs into problems).
A problem lies with how students often learn about the passage of molecules over a membrane.
Hydrophobic molecules can diffuse across, whereas hydrophilic molecules cannot. But what about water? They're hydrophilic too, being polar. It's often explained that water molecules can pass the membrane due to their small size, albeit at a slow rate.
What then of other small hydrophilic molecules? Ions (such as Na+) are ubiquitous in living organisms. They're smaller than water molecules. But they cannot pass unaided. We could add another caveat to save the exception; water molecules are found in such large quantities that the probabilities increase that a few will slip through.
But this is inconsistent with observation. Serious bouts of diarrhea (think cholera) can come on very quickly and depend on osmosis. The story of putting salt on slugs as an example of osmosis is often told, but in such situations it's visible that osmosis happens quickly.
When the tendrils of climbing plants are spiraling (circumnutating) in search of something to grab, they do so by pumping ions around their cells, controlling the movement of water, and thus which cells become plasmolysed and turgid. And it can happen quickly.
When watching paramecia excrete water with their contractile vacuoles, they seem to fill up pretty quickly too. This is all difficult to explain with a model that suggests that water diffuses through membranes slowly.
The model of 'free water' molecules is also problematic.
In this model explanation relies on the number of water molecules that are free to diffuse. When solute concentration is higher, more water molecules will be bound to solutes that cannot pass the membrane, therefore 'taking them out of the game'. Then, free water molecules diffuse to reach equilibrium across the membrane.
With this model we could predict that certain solutes would have a larger osmotic effect than others. Those that can bind more water molecules should cause a larger difference than those that bind less. For example, ribose should have a larger osmotic effect than deoxyribose (with one less hydroxyl group). But that's not what we observe.
Osmosis is colligative. It is not the solute that matters, but its concentration. As biology becomes more molecular at ages 16-18 years old, these things matter. We want our students to hold mental models that allow prediction. Can you understand, if you cannot predict?
Teaching osmosis with aquaporins
Normally osmosis is said to happen when there is a membrane, water, and a difference in solute concentration over the membrane. In the model in Kramer and Myers' paper however, osmosis also depends on the presence of aquaporins.
Immediately this is explanatory, as it means that osmosis only occurs in living systems. It won't occur in man made systems, such as with dialysis tubing, which filter by size.
The mechanism comes down to aquaporins repelling the solutes that approximate them through electrostatic interactions. This repulsion pushes them away from the membrane and into the water molecules behind them. The more solutes there are, the larger the effect of this repulsion. This explains the colligative property of osmosis. And explains why a concentration difference over the membrane is the difference that makes a difference.
The general movement away from the membrane favours the movement of water through the aquaporins towards the higher solute concentration.
Now the kidney makes so much more sense. Whereas textbooks refer to membranes of the nephron being 'permeable' or not to water, we can just say where aquaporins are located.
Rather than having exceptions for water, compared to other hydrophilic molecules, we can explain the movement of water due to the presence of aquaporins. This is much more parsimonious as it connects perfectly to the idea of the hydrophobicity of membranes, and the need for protein channels.
Rather than osmosis being fast at the visible macro level, but explained as slow at the micro level, now both can be explained consistently. Aquaporins, as protein channels, facilitate the diffusion of water across membranes, allowing movement to be rapid at the micro level.
With this model, no longer will students design osmosis experiments with dialysis tubing and get strange results. No longer will they uncomfortably accept that water follows different rules to other small hydrophobic molecules. No longer will they toil with 'free molecules' or the idea that to predict you need to know the configuration of the solute.
In all, by including aquaporins in our explanatory mechanism we get something simpler to understand and with better predictive power.
My books: Difference Maker | Biology Made Real, or my other posts.
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References
Kramer, E., and Myers, D. 2013. "Osmosis is not driven by water dilution." Trends in Plant Science 18(4) 195-197.