Department of Anatomy, Histology and Embryology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Department of Laboratory Animal Science, Fudan University, Shanghai, China.
Brain Pathol. 2023 Sep;33(5):e13186. doi: 10.1111/bpa.13186. Epub 2023 Jul 3.
Krüppel-like Factor 7 (KLF7) is a zinc finger transcription factor that has a critical role in cellular differentiation, tumorigenesis, and regeneration. Mutations in Klf7 are associated with autism spectrum disorder, which is characterized by neurodevelopmental delay and intellectual disability. Here we show that KLF7 regulates neurogenesis and neuronal migration during mouse cortical development. Conditional depletion of KLF7 in neural progenitor cells resulted in agenesis of the corpus callosum, defects in neurogenesis, and impaired neuronal migration in the neocortex. Transcriptomic profiling analysis indicated that KLF7 regulates a cohort of genes involved in neuronal differentiation and migration, including p21 and Rac3. These findings provide insights into our understanding of the potential mechanisms underlying neurological defects associated with Klf7 mutations.
Krüppel 样因子 7（KLF7）是一种锌指转录因子，在细胞分化、肿瘤发生和再生中具有关键作用。Klf7 突变与自闭症谱系障碍有关，自闭症谱系障碍的特征是神经发育迟缓和智力残疾。在这里，我们表明 KLF7 在小鼠大脑皮层发育过程中调节神经发生和神经元迁移。神经祖细胞中 KLF7 的条件性缺失导致胼胝体发育不全、神经发生缺陷和新皮层中神经元迁移受损。转录组谱分析表明，KLF7 调节一组参与神经元分化和迁移的基因，包括 p21 和 Rac3。这些发现为我们理解与 Klf7 突变相关的神经缺陷的潜在机制提供了线索。
