Project description:To study the effect of GLI3 knockout on early brain organoid development, we collected single-cell multiome data from 18 day old brain organoids
Project description:To study developmental trajectories in brain organoids, we conducted scRNA-seq and scATAC-seq in parallel on a dense timecourse of early development.
Project description:To study developmental trajectories in brain organoids, we conducted scRNA-seq and scATAC-seq in parallel on a dense timecourse of early development.
Project description:Purpose: This study seeks to determine whether GLI3 is required to recruit the SMARCC1 complex to GLI enhancers in the limb. Methods: To determine if Gli3 is required to recruit SMARCC1 to its anhancers, we performed differential chromatin binding to compare SMARCC1 binding in control and Gli3 mutants. We performed Cut&Run for SMARCC1 binding on individually genotyped E11.5 (40-43s) anterior forelimb pairs from control (Gli3+/+; 3 replicates) and Gli3 mutant (Gli3-/-; 4 replicates) embryos. Results: We found that there is no major difference in SMARCC1 binding in Gli3-mutants compared to controls.
Project description:To investigate how SHH treatment influences patterning of early brain organoids, we performed multiome sequencing of brain organoids during early development
Project description:We used Affymetrix microarrays to understand the genome wide differences in Wildtype and Gli3 mutant (Gli3+/- and Gli3-/-) (n=2) embryonic day 18.5 DP CD69-, DP CD69+ and SP4 thymocytes.
Project description:Satellite stem cells are required for the growth, maintenance, and regeneration of skeletal muscle. Quiescent satellite stem cells possess a primary cilium, a structure that regulates the processing of the GLI-family of transcription factors. We find that GLI3, specifically, plays a critical role in satellite cell activation. Strikingly, primary cilia-mediated processing of GLI3, independent of canonical Hedgehog signaling, is required to maintain satellite cells in a G0 dormant state, as satellite cells lacking GLI3 enter GAlert in absence of injury. Furthermore, GLI3 depletion or inhibition of its processing stimulates symmetrical division in satellite cells and expansion of the stem cell pool. As a result, satellite cells lacking GLI3 display rapid cell-cycle entry, increased proliferation and augmented self-renewal, and markedly enhanced long-term regenerative capacity. Therefore, our results reveal an essential role for primary cilia processing of GLI3 in regulating muscle stem cell activation.