University of Manchester, UK

A physiologist notes the similarities between animal and plant electricity.

Almost all organisms run on electricity. As an undergraduate, I was intrigued by the fact that the long, single cells of the freshwater plant Nitella are nearly identical to those of single nerve fibres. These plant cells generate slow action potentials that are similar to those of human or animal nerves. But the electrical components that span plant and animal membranes — the ion channels and transporter proteins — are usually quite different, as are some of the ions they transport.

Earlier this year, however, two researchers in Italy found that a single mutation can turn an important transport protein from a component that is compatible with animal electrical systems into one that is appropriate for plants. They studied the protein CLC-5, which is abundant in the intracellular vesicles of kidney cells. There, it exchanges chloride ions for protons, and in so doing regulates the vesicles' acid content (G. Zifarelli and M. Pusch EMBO J. 28, 175–182; 2009).

The researchers knew that CLC-5 resembled the plant transporter atCLCa, but they had no idea how closely. In plant vacuoles, which are formed by the fusion of several vesicles, atCLCa exchanges not chloride but nitrate ions for protons. The difference is vital: nitrate is necessary for plants to grow and is stored in the vacuoles of root and shoot cells, whereas chloride has a very different role. It is needed for photosynthesis and for the opening and closing of stomata, which matters mostly in the leaves.

Merely substituting one serine amino acid in CLC-5 with a proline changed the protein from a chloride transporter into a nitrate transporter. I find this fascinating because it provides an even more striking example of the similarities that animals and plants can share, even though their biologies are generally very different.

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University of Oxford, UK

A physiologist discusses matters close to the heart.

This time last year my father was suffering from congestive heart failure. He became increasingly frail, slowing down like an unwound clockspring until, in February, his heart simply stopped.

As a physiologist, I had some idea of his condition, but I did not then realize how close it was to my own research area.

In 1983, ATP-sensitive potassium (K-ATP) channels were found in the heart. These channels are gated pores that control potassium fluxes across the cell membrane. However, their precise role in the heart was unclear.

One year later, I discovered that these channels are central to the mechanism by which glucose stimulates insulin secretion from the pancreas. Unravelling the role of K-ATP channels in diabetes, and the way in which channel structure influences function, has been an all-consuming passion for me ever since.

To my surprise, it now turns out that these channels also play a role in heart failure. Heart failure is usually caused by narrowing of the arteries, which increases the pressure against which the heart has to pump, making it work harder. Eventually, it fails.

Recently, Andre Terzic of the Mayo Clinic in Rochester, Minnesota, and his group showed that K-ATP channels confer protection against heart failure (S. Yamada et al. J. Physiol. Lond. published online doi:10.1113/jphysiol.2006.119511; 2006). In normal mice, cardiac K-ATP channels open in response to an increased pressure load, reducing stress on the heart. Mice lacking K-ATP channels rapidly develop heart failure and die.

In the pancreas, K-ATP-channel activity is finely balanced: too much causes diabetes and too little hyperinsulinism. But in the heart, as this paper shows, opening is almost always beneficial.

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