The Best Toenail-Fungus-Treatments

For more than a century, physicians have recognized this curious syndrome in which people have, to varying degrees, abnormal growth of fingernails, toenails, and knee caps, or patellae. At the extreme, people with NPS have no knee caps or nails whatsoever. Some 50 years ago, physicians linked kidney problems, often severe enough to require transplants, to the syndrome. Last year, investigators also noticed that people with the syndrome frequently have the eye disorder glaucoma.

Scientists have been puzzled by this odd collection of symptoms and have even pondered whether more than one gene must be involved. At the Society for Developmental Biology meeting last week in Palo Alto, Calif., Johnson, who works at the University of Texas M.D. Anderson Cancer Center in Houston, explained how the findings on his mutant mice strongly indicate that a single gene is behind NPS. Some of his team's results are also described in the May Nature Genetics.

Tumors of the nailbed, such as melanoma, glomus tumor or squamous cell carcinoma, can result in nail plate destruction and lifting of the nail plate, as seen in this case. A longitudinal split in the nail plate and involvement proximal to the neoplastic lesion would be unusual.

The gene's link to NPS grew stronger when the researchers realized that the human version of Lmx1b maps to the exact region of chromosome 9 where the syndrome's mutant gene is thought to reside. Finally, working with a research team led by Brendan Lee of Baylor College of Medicine in Houston, Johnson's group found that three people with NPS harbor mutations in the gene and their unaffected parents do not.

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Curiously, it takes mutations in both copies of Lmx1b to produce symptoms in mice, although a defect in just one is sufficient to cause NPS in people. The amount of transcription factor produced may be crucial to the human disorder, which could explain why people with similar mutations are afflicted to different degrees, says Johnson.

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