Fragile X mental retardation protein (FMRP) interacting proteins exhibit different expression patterns during development.

摘要: Fragile X syndrome is caused by the lack of expression fragile mental retardation protein (FMRP), an RNA-binding involved in mRNA transport and translation. FMRP a component ribonucleoprotein complexes it can interact with range proteins either directly or indirectly, as demonstrated two-hybrid selection co-immunoprecipitation, respectively. Most FMRP-interacting are such FXR1P, FXR2P 82-FIP. Interestingly, also cytoplasmic CYFIP1 CYFIP2, which do not bind RNA link to RhoGTPase pathway. The interaction these different may modulate functions influencing its affinity affecting ability cytoskeleton remodeling through Rho/Rac GTPases. To better define relationship interacting during brain development, we have analyzed pattern cortex, striatum, hippocampus cerebellum at ages wild type (WT) mice. were strongly expressed first week gradually decreased thereafter, more rapidly than cortex. FXR1P was early showed reduction later stages development similar developmental two regions. all peaked third post-natal week. In contrast, CYFIP2 82-FIP (only forebrain regions) moderately P3 increased after P7. general, each regions examined, except for 82-FIP, exhibited strong low levels cerebellum. Our data indicate that distinct patterns suggest be preferentially associated certain late periods. particular, differently modulated development.