Project description:This study is to analyze the transcriptomic profiles of Rosa26-CreERT2;QkLoxP/LoxP (Qk-Rosa26-iCKO) mice and littermate controls to determine the differentially expressed genes after Qk deletion.
Project description:This study is to analyze the transcriptomic profiles of Plp-CreERT2;QkLoxP/LoxP (Qk-Plp-iCKO) mice and littermate controls to determine the differentially expressed genes after Qk deletion.
Project description:This study is to analyze the transcriptomic profiles of 6 weeks 0.2% cuprizone treated Cx3cr1-CreER;QKLoxP/LoxP (Qk-KO) and Cx3cr1-CreER;QK LoxP/+ (WT) mice
Project description:This study is to analyze the transcriptomic profiles of Plp-CreERT2;QKLoxP/LoxP (Qk-KO) and Plp-CreERT2;QKLoxP/+ (WT) mice and WT and Qk-KO oligodendrocytes to determine the differentially expressed genes.
Project description:During mammalian brain development, neural stem cells (NSCs) initially produce only neurons and subsequently shift to glial production, while it is still unknown what regulates this drastic fate change. Here we discovered RNA-binding protein (RBP) of quaking (Qk) is selectively expressed in NSCs and is essential for switching from neurogenesis to gliogenesis. Using CNS-specific KO mice for Qk, we found that gliogenesis, but not neurogenesis, was specifically disrupted in Qk-/- brains. In glial differentiating condition, Qk-/- NSCs failed to enter gliogenesis but caused ectopic neurogenic gene expression. Pathway analysis of Qk-/- NSCs identified endocytosis as the regulatory functional cluster of Qk which has been shown to facilitate extra-cellular signaling receptors replacement and promote NSC differentiation. Mechanistically, Qk regulates endocytosis pathway genes through stabilizing their mRNAs via Qk binding sequences in 3’UTR. These results uncovered the cell fate determination mechanism of NSCs through mRNA regulation.
Project description:During mammalian brain development, neural stem cells (NSCs) initially produce only neurons and subsequently shift to glial production, while it is still unknown what regulates this drastic fate change. Here we discovered RNA-binding protein (RBP) of quaking (Qk) is selectively expressed in NSCs and is essential for switching from neurogenesis to gliogenesis. Using CNS-specific KO mice for Qk, we found that gliogenesis, but not neurogenesis, was specifically disrupted in Qk-/- brains. In glial differentiating condition, Qk-/- NSCs failed to enter gliogenesis but caused ectopic neurogenic gene expression. Pathway analysis of Qk-/- NSCs identified endocytosis as the regulatory functional cluster of Qk which has been shown to facilitate extra-cellular signaling receptors replacement and promote NSC differentiation. Mechanistically, Qk regulates endocytosis pathway genes through stabilizing their mRNAs via Qk binding sequences in 3’UTR. These results uncovered the cell fate determination mechanism of NSCs through mRNA regulation.
Project description:Identify potential miR-20a regulated mRNAs and linked pathways in the setting of QK knockdown by comparing the transcriptional profiles of shQK-transduced human U87 cells together with miR-20a or a scrambled miRNA control (miR-NT)
Project description:Identify potential miR-20a regulated mRNAs and linked pathways in the setting of QK knockdown by comparing the transcriptional profiles of shQK-transduced human Hs683 cells together with miR-20a or a scrambled miRNA control (miR-NT)