munication structure created by two immune cells. According to the theory, this communication activates immune cells to fight invaders. Swat had hypothesized that DLGH1 might help move structures to one side of an immune cell for creation of the synapse.

As expected, loss of DLGH1 proved fatal for mice during or shortly after birth. While examining the mice, Swat and co-author Thaddeus Stappenbeck, M.D., Ph.D., assistant professor of pathology and immunology and of molecular biology and pharmacology, noticed that many had swollen kidneys.

"We didn't think the kidney problems were what was killing them, but we were told to go to Jeff Miner for expert advice on what was happening," Swat says. "That's the beauty of Washington University--that it's so easy to collaborate across different research specialties."

With help from other colleagues, Swat, Miner, and graduate student Zhen Mahoney were able to arrange for video microscopy of mouse ureters in action. These revealed that peristalsis, the normal pulse-like contraction that squeezes the ureter at one point while opening it up at the next point in the tube, had been disabled.

"We saw that peristalsis had been replaced by a vertical, non-squeezing motion that went down the ureter but propelled very little urine through it," Swat says.

A closer look at the musculature surrounding the ureter revealed why. Normally the ureter is surrounded by two layers of smooth muscle: an outer, longitudinal sheath where the muscles cells are oriented along the path of the ureter; and an inner, circular layer where the cells form rings around the tube of the ureter.

"In mutant mice, the longitudinal muscle is fine, but the circular muscle is either missing or has become longitudinal," Miner says.

Swat and Miner are planning to collaborate with geneticists to see if functional obstruction in humans can be linked to alterations in DLGH1, a possibility Swa
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