Findings revealed Dyslexia-linked Genes, DCDC2 Control Cilia of Cells

Scientists at Karolinska Institutet in Sweden discovered that a gene linked to dyslexia has a surprising biological function namely it controls cilia, the antenna-like projections that cells use to communicate. The study led by Professor Eero Castrén of Helsinki University and Professor Eero Castrén of Helsinki University presented the scientists with a possible new neurobiological mechanism for dyslexia.

The new findings presented in the scientific journal PLoS ONE showed that DCDC2 governs the length of the cilia and activates two different signal systems in the cell, depending on the degree of gene activity. When the human variant of the gene was transferred to nerve cells in the roundworm C. elegans, it gave rise to unusual neural projections exclusively in ciliated cells.

Dyslexia is largely hereditary and linked to a number of genes whose functions of which are, however, arelargely unknown. This present study from Karolinska Institutet and Helsinki University revealed that one of these genes linked to dyslexia, DCDC2, is involved in regulating the signalling of cilia in brain neurons.

Cilia are hair-like structures that project from the surface of most cells. Recent research revealed that the cells use cilia to communicate and that they play a crucial part in the development of the body's organs.

The results of this study and that of a previous research in mice show that DCDC2 and two other dyslexia genes are involved in cell migration, a process by which nerve cells are moved to their correct location in the brain during embryonic development. The cilia are important parts of the machinery that controls cell migration.

Ciliary dysfunction in different organs has been associated with a wide range of disorders from rare genetic diseases such as polycystic kidney disease and Kartagener's syndrome, to diabetes, obesity and schizophrenia.