They believe the major finding will give researchers a better understanding of what causes the brain disorder which disrupts reading and writing skills.
It is now hoped that follow-up research will also lead to the discovery of treatments which could help children susceptible to dyslexia.
The discovery was made by a team from the Department of Psychological Medicine, Wales College of Medicine.
They carried out analysis of 300 families from Wales and the West of England where at least one child suffered from the disorder.
The research team led by Professor Julie Williams and Professor Michael O'Donovan will now continue their study in order to discover more about the gene called "KIAA0319".
The research will focus on discovering exactly how the gene works within the brain to disrupt reading and writing skills.
Professor Williams said: "This is a major breakthrough and the first study to identify one gene which contributes to susceptibility to the common form of dyslexia. We would like to thank all the parents and children who took part in the study and would extend a call to new volunteers to take part in this important research."
The researchers want to hear from more families with at least one child who has dyslexia.
Professor O'Donovan said: "The finding vindicates our optimism that a disorder as apparently complicated as impaired reading ability can be amenable to molecular genetic dissection." However, he added: "Much more remains to be done before the finding is translated into therapy. To tackle the genetic origins of disorders like dyslexia, both quality of assessment and sample size are crucial. We have the tools to take care of the latter, but we are entirely dependent on the altruism of the public in offering their time and DNA".
cardiff.ac/
These important sensors aren't confined to the kidneys, however. "Sensory cilia are universal devices which can sense very divergent stimuli “ such as motion in the kidney, photons in the photoreceptors in the eye, hormones, or scent in the olfactory epithelium," Hildebrandt says. "Whenever Nature needs a device to sense a signal from outside the cell, it seems to be using a cilium.
"Dr. Otto found that the gene product of the NPHP5 gene, which we call nephrocystin-5, directly interacts with calmodulin, which is known to be an important signaling protein in photoreceptors," Hildebrandt adds. "Our collaborators at U-M's Kellogg Eye Center found that nephrocystin-5 is part of a protein complex together with another protein called RGPR. If mutated, the gene for RGPR is a frequent cause of retinitis pigmentosa.
"What was also very striking was that nephrocystin-5, together with calmodulin and RGPR, is expressed in the cilia of kidney epithelial cells, and also in the connecting cilia of photoreceptors," Hildebrandt explains. "In other words, defects in cilia tie together the disease phenotypes of the kidney and the eyes."
Work by other researchers suggests additional connections. "In a disease called Bardet-Biedl Syndrome, patients have a combination of nephronophthisis with retinitis pigmentosa, but also diabetes mellitus, obesity, infertility and mental retardation," says Hildebrandt. "Scientists studying this disease have shown that the genes involved are all expressed in cilia."
There is even evidence that defective ciliated neurons may be involved in Alzheimer's disease, according to Hildebrandt. "Cilia have a scaffold of tubulin, where motor proteins move up and down, carrying cargo. It seems that the proteins involved in nephronophthisis are cargo. Similarly, some of the proteins involved in Alzheimer's also appear to be cargo on cilia."
med.umich