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:In order to study the importance of HSFA1 in thermotolerance in Arabidopsis, we generated the HSFA1a, b, d and e quadruple mutant (QK). QK is very sensitive to heat. Therefore, we used microarray to study how many genes regulated by HSFA1 after heat shock. Seven-day-old seedlings of Col-0, Ws and QK grown at 22oC on 0.5x MS plates containing 1% sucrose were incubated for 1 h at 37 °C. Subsequently, samples were collected for RNA extraction. The experiment was repeated, and two biological replicates were processed for analysis.
Project description:In order to study the importance of HSFA1 in thermotolerance in Arabidopsis, we generated the HSFA1a, b, d and e quadruple mutant (QK). QK is very sensitive to heat. Therefore, we used microarray to study how many genes regulated by HSFA1 after heat shock.