![]() ![]() ![]() We increased mapping resolution further by the incorporation of sequence information. In this study, we used genetic mapping data from heterogeneous stock (HS) mice to identify loci associated with neurogenesis ( 11). We hypothesized that one way to identify genes that influence learning is to identify those that contribute to heritable variation in neurogenesis ( 10). Collectively, our study reveals the functions for FST in adult neurogenesis and learning behaviors. Long-term overexpression of hippocampal Fst in C57BL/6 wild-type mice alleviates age-related decline in cognition, neurogenesis, and LTP. By utilizing RNA sequencing and chromatin immunoprecipitation, we identified Asic4 as a target gene regulated by FST and show that Asic4 plays a critical role in learning deficits caused by Fst deletion. In contrast, hippocampal overexpression of Fst in KO mice reversed these impairments. Fst KO mice exhibit deficits in spatial learning, working memory, and long-term potentiation (LTP). We confirmed that brain-specific Fst knockout (KO) mice exhibited decreased hippocampal neurogenesis and demonstrated that FST is critical for learning. ![]() Here, using high-resolution genetic mapping of adult neurogenesis, combined with sequencing information, we identify follistatin ( Fst) and demonstrate its involvement in learning and adult neurogenesis. Mounting evidence has suggested that adult hippocampal neurogenesis is involved although a causal relationship has not been well defined. The biological mechanisms underpinning learning are unclear. ![]()
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