functional Mg2+ transporter. However, later work by Chubanov et al. (2004) clearly showed that TRPM7 is required for TRPM6 activity and that the results of Voets et al. are explained by the expression of TRPM7 in the experimental cell line used by Voets et al. in their experiments. Whether TRPM6 is functional by itself is yet to be determined. The predicted TM topology of the TPRM6 and TRPM7 proteins has been adapted from Nadler et al. (2001), Runnels et al. (2001) and Montell et al. (2002), this figure shows the computer predicted membrane topology of the TRPM6 and TRPM7 proteins in Homo sapiens. At this time, the topology shown should be considered a tentative hypothesis. The TM domains are shown in light blue, the pore loop in purple, the TRP motif in red and the kinase domain in green. The orientation in the membrane and the positions of the N- and C-termini are indicated and the figure is not drawn to scale. The conclusions of the Voets et al. (2004) paper are probably incorrect in attributing the Mg2+ dependent currents to TRPM7 alone, and their kinetic data are likely to reflect the combined TRPM7/ TRPM6 channel. The report presents a robust collection of data consistent with a channel-like activity passing Mg2+, based on both electrophysiological techniques and also mag-fura 2 to determine changes in cytoplasmic free Mg2+. Paracellular transport Claudins allow for Mg2+ transport via the paracellular pathway; that is, it mediates the transport of the ion through the tight junctions between cells that form an epithelial cell layer. In particular, Claudin-16 allows the selective reuptake of Mg2+ in the human kidney. Some patients with mutations in the CLDN19 gene also have altered magnesium transport. The gene Claudin-16 was cloned by Simon et al. (1999), but only after a series of reports described the Mg2+ flux itself with no gene or protein. The expression pattern of the gene was determined by RT-PCR, and was shown to be very tightly confined to a continuous region of the kidney tubule running from the medullary thick descending limb to the distal convoluted tubule. This localisation was consistent with the earlier reports for the location of Mg2+ re-uptake by the kidney. Following the cloning, mutations in the gene were identified in patients with familial hypomagnesaemia with hypercalciuria and nephrocalcinosis, strengthening the links between the gene and the uptake of Mg2+. Plants The current knowledge