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Last of known genes identified in complex obesity syndrome

BS-related mutations seem to disrupt the scaffolding upon which cilia are built, but others may cause ciliary dysfunction in other ways, perhaps preventing or misdirecting the shuttling of materials along the cilia.

By searching a database of cilia-related genes compiled by comparing three species' genomes -- a bacterium, a plant, and a human [see May 15, 2004, news release] -- the researchers found three possibilities in the right region of chromosome 3. Next, they determined the genetic sequences of those three genes in four families with BBS. One of the genes, ARL6, had a different, critical mutation in each of the families, the researchers found.

"ARL6 is the first member of its larger gene family to be tied to any disease," says Katsanis. "While not much is known about ARL6 specifically, we know quite a bit about its relatives, so we know which regions of ARL6 are crucial for the protein's correct function. The mutations in these families wouldn't let the protein work properly."

ARL6 is a member of a class of proteins that bind GTP, or guanosine triphosphate -- a class given the obvious title of GTP-binding proteins. GTP-binding is a critical step in a wide variety of signaling "cascades" that pass along messages and instructions inside cells -- such as to open or close the cell's entry points or to trigger relocation of "freight" within the cell.

"That this type of molecule could cause BBS is particularly intriguing," says Katsanis.

In additional experiments using the worm C. elegans, the researchers proved that ARL6 normally functions only in cilia, suggesting it might relay specific signals in that part of the cell. The next step is to figure out exactly what those signals might be.

"We don't know what its message is, but because we know that it binds GTP, we have some ideas of where to start looking," says Katsanis.


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Contact: Joanna Downer
jdowner1@jhmi.edu
410-614-5105
Johns Hopkins Medical Institutions
15-Aug-2004


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