Tiny channels provide corridors of communication between adult stem cells and their differentiated neighbours, a study has found. The finding could be an important step towards determining how to control the development of adult stem-cell identity, but there's a catch — it was discovered in the planarian flatworm Schmidtea mediterranea.

The flatworms, best known for their regenerative prowess and cross-eyed charm, maintain a supply of stem cells to regrow tissue lost to anything from daily wear-and-tear to full decapitation. And, although it seems a long way to travel along the evolutionary tree, there are reasons to think planarians make a good model for human stem cells, says regeneration biologist and planarian researcher Alejandro Sánchez Alvarado at the University of Utah School of Medicine in Salt Lake City. He belives that the basic principles uncovered in planarians will translate to human cells, although the finer details may differ.

Even biologists who don't study the worms agree. “Work in planarians and other lower organisms always gives us hints regarding human stem cells,” says Shinya Yamanaka, a stem-cell researcher at Kyoto University in Japan.

Biologists Néstor Oviedo and Michael Levin of the Forsyth Institute in Boston, Massachusetts, studied channels known as gap junctions that permit the passage of small molecules and ions between cells. When S. mediterranea was manipulated so that it did not express a key gap-junction protein, thus preventing communication between cells, it lost its regenerative capabilities and its reservoir of stem cells (N. J. Oviedo and M. Levin Development 134, 3121–3131; 2007).

This fits with the findings of studies in human embryonic stem cells, says Alice Pébay, a biologist at the University of Melbourne, Australia. Previous work has shown that chemically induced closure of gap junctions can slow human embryonic stem-cell growth. But, notes Pébay, Ovideo and Levin were able to use a technique to reduce expression of the gap-junction proteins — something that would be very difficult to do in human embryonic stem cells.

Nevertheless, technical challenges to planarian research remain. For example, reducing expression of an S. mediterranea gene is straightforward, but techniques for over-expressing planarian genes are still rudimentary, says Levin.