Two independent research groups, led by Drs. Haruhiko Siomi (Institute for Genome Research, University of Tokushima, Japan) and Gregory Hannon (Cold Spring Harbor Laboratory, USA) have discovered that the Drosophila version of the human fragile X mental retardation protein associates with components of the RNAi pathway, suggesting that the molecular mechanism underlying fragile X syndrome may involve an RNAi-related process.
"It has been our feeling since we became involved in the field several years ago that only through an understanding of the mechanism of RNAi would we be able to understand the biological implications of this process," states Dr. Hannon.
Fragile X syndrome is the most common form of hereditary mental retardation, affecting 1 in 4000 males and 1 in 8000 females. Fragile X syndrome is the result of a genetic mutation at one end of the fragile X mental retardation 1 gene (FMR1) that causes the abnormal inactivation of the gene. It is known that the protein encoded by FMR1 -- the so-called fragile X mental retardation protein (FMRP) -- binds to RNA and is thought to regulate the expression of specific genes during neural development, but the mode of FMRP action in cells is yet to be defined.
Heather Cosel | EurekAlert!
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