Osteoporosis is a disease of low bone mineral density (BMD) and altered bone architecture leading to an increased risk of fracture. Worldwide, osteoporosis affects millions of people and causes an enormous and increasing healthcare burden. Reduced BMD is the major risk factor for fracture and is a highly heritable trait. Genome wide association studies (GWAS) have identifed the 9q34.11 locus containing Far Upstream Binding Protein 3 (FUBP3) as associated with BMD, fracture and height. FUBP3 is a DNA and RNA binding protein and transcriptional regulator of c-myc, but has no previously confrmed role in the skeleton. I hypothesised that FUBP3 is the causative gene underlying the association with BMD, fracture and height at the 9q34.11 locus and that FUBP3 is needed for normal bone development and maintenance. To test this hypothesis, I used bioinformatic tools to interrogate the 9q34.11 locus and prioritise FUBP3 for further study and studied the skeletal phenotype of an FUBP3 deficient mouse. Skeletal assessment included analysis of growth, bone mineral content and bone structure, strength, and cellular parameters. Analysis of the 9q34.11 locus confirmed that FUBP3 was the most likely causal gene underlying the association with BMD and was expressed in bone. Compared to wild type mice, FUBP3 defcient mice were short and demonstrated reduced bone mineral content, altered trabecular bone parameters and reduced strength, suggesting an important role of FUBP3 in both development and adult bone maintenance. Finally, I investigated the cellular phenotype underlying the skeletal changes seen with FUBP3 loss. These did not demonstrate a deficit in osteoblastic bone formation or osteoclastic bone resorption with FUBP3 deficiency. Nevertheless, the data presented in this thesis provide the first demonstration of a functional role of FUBP3 in the skeleton and confirm FUBP3 as the most likely causal gene at the 9q34.11 BMD, height and fracture GWAS locus.