Common-variant associations with fragile X syndrome View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2019-03

AUTHORS

James J. Crowley, Jin Szatkiewicz, Anna K. Kähler, Paola Giusti-Rodriguez, NaEshia Ancalade, Jessica K. Booker, Jennifer L. Carr, Greg E. Crawford, Molly Losh, Craig A. Stockmeier, Annette K. Taylor, Joseph Piven, Patrick F. Sullivan

ABSTRACT

Fragile X syndrome is rare but a prominent cause of intellectual disability. It is usually caused by a de novo mutation that occurs on multiple haplotypes and thus would not be expected to be detectible using genome-wide association (GWA). We conducted GWA in 89 male FXS cases and 266 male controls, and detected multiple genome-wide significant signals near FMR1 (odds ratio = 8.10, P = 2.5 × 10-10). These findings withstood robust attempts at falsification. Fine-mapping yielded a minimum P = 1.13 × 10-14, but did not narrow the interval. Comprehensive functional genomic integration did not provide a mechanistic hypothesis. Controls carrying a risk haplotype had significantly longer FMR1 CGG repeats than controls with the protective haplotype (P = 4.75 × 10-5), which may predispose toward increases in CGG number to the premutation range over many generations. This is a salutary reminder of the complexity of even "simple" monogenetic disorders. More... »

PAGES

338-344

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41380-018-0290-3

DOI

http://dx.doi.org/10.1038/s41380-018-0290-3

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1110452980

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30531935


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