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Grb10-Interacting GYF Protein 2 (GIGYF2) was initially identified through its interaction with Grb10, an adapter protein that binds activated IGF-I and insulin receptors. The  GIGYF2  gene maps to human chromosome 2q37 within a region linked to familial Parkinson's disease (PARK11 locus), and association of  GIGYF2  mutations with Parkinson's disease has been described in some but not other recent publications. This study investigated the consequences of  Gigyf2  gene disruption in mice.  Gigyf2  null mice undergo apparently normal embryonic development, but fail to feed and die within the first 2 post-natal days. Heterozygous  Gigyf2  +/−  mice survive to adulthood with no evident metabolic or growth defects. At 12–15 months of age, the  Gigyf2  +/−  mice begin to exhibit motor dysfunction manifested as decreased balance time on a rotating horizontal rod. This is associated with histopathological evidence of neurodegeneration and rare intracytoplasmic Lewy body-like inclusions in spinal anterior horn motor neurons. There are α-synuclein positive neuritic plaques in the brainstem and cerebellum, but no abnormalities in the substantia nigra. Primary cultured embryo fibroblasts from  Gigyf2  null mice exhibit decreased IGF-I-stimulated IGF-I receptor tyrosine phosphorylation and augmented ERK1/2 phosphorylation. These data provide further evidence for an important role of GIGYF2 in age-related neurodegeneration and IGF pathway signaling.

GIGYF2 gene disruption in mice results in neurodegeneration and altered insulin-like growth factor signaling