Yiling Li 李怡灵
@fionalyl.bsky.social
PhD at Magdalena Goetz Lab in Munich. Brain lover. Foodie.
6/ These findings establish TGIF2 as a major regulator of NSC fate, integrating transcriptional repression with lineage priming to fine-tune neurogenesis.
Looking forward to discussions and feedback! 🔬💡
Looking forward to discussions and feedback! 🔬💡
February 17, 2025 at 12:08 PM
6/ These findings establish TGIF2 as a major regulator of NSC fate, integrating transcriptional repression with lineage priming to fine-tune neurogenesis.
Looking forward to discussions and feedback! 🔬💡
Looking forward to discussions and feedback! 🔬💡
5/ Importantly, TGIF2 is not just a repressor of differentiation—it plays an active role in neurogenic priming. By keeping neurogenic priming genes at low levels to keep NSCs poised but undifferentiated, ensuring proper lineage priming.
February 17, 2025 at 12:08 PM
5/ Importantly, TGIF2 is not just a repressor of differentiation—it plays an active role in neurogenic priming. By keeping neurogenic priming genes at low levels to keep NSCs poised but undifferentiated, ensuring proper lineage priming.
4/ Overexpressing TGIF2 increased NSCs in vitro and in vivo, delaying differentiation. scRNA-seq, Cut&Run, and interactome analyses revealed that TGIF2 recruits the SIN3A/HDAC repressor complex to suppress key neuronal differentiation and maturation genes.
February 17, 2025 at 12:08 PM
4/ Overexpressing TGIF2 increased NSCs in vitro and in vivo, delaying differentiation. scRNA-seq, Cut&Run, and interactome analyses revealed that TGIF2 recruits the SIN3A/HDAC repressor complex to suppress key neuronal differentiation and maturation genes.
3/ TGIF2 stood out—it was the only TF whose expression and motif enrichment correlated with “neurogenesis”, independent of brain region and time.
February 17, 2025 at 12:08 PM
3/ TGIF2 stood out—it was the only TF whose expression and motif enrichment correlated with “neurogenesis”, independent of brain region and time.
2/ We profiled NSCs from the mouse embryonic cortex and lateral ganglionic eminence (LGE) at the peak of neurogenesis and at birth (when cortex transitions to gliogenesis but LGE continues neurogenesis) using RNA-seq and ATAC-seq to identify key regulators.
February 17, 2025 at 12:08 PM
2/ We profiled NSCs from the mouse embryonic cortex and lateral ganglionic eminence (LGE) at the peak of neurogenesis and at birth (when cortex transitions to gliogenesis but LGE continues neurogenesis) using RNA-seq and ATAC-seq to identify key regulators.
1/ NSCs express neurogenic genes at low levels, but how do they prevent premature differentiation while staying poised for neurogenesis? How is the balance between self-renewal and differentiation regulated?
February 17, 2025 at 12:08 PM
1/ NSCs express neurogenic genes at low levels, but how do they prevent premature differentiation while staying poised for neurogenesis? How is the balance between self-renewal and differentiation regulated?
4/ Overexpressing TGIF2 increased NSCs in vitro and in vivo, delaying differentiation. scRNA-seq, Cut&Run, and interactome analyses revealed that TGIF2 recruits the SIN3A/HDAC repressor complex to suppress key neuronal differentiation and maturation genes.
February 17, 2025 at 9:26 AM
4/ Overexpressing TGIF2 increased NSCs in vitro and in vivo, delaying differentiation. scRNA-seq, Cut&Run, and interactome analyses revealed that TGIF2 recruits the SIN3A/HDAC repressor complex to suppress key neuronal differentiation and maturation genes.
3/ TGIF2 stood out—it was the only TF whose expression and motif enrichment correlated with “neurogenesis”, independent of brain region and time.
February 17, 2025 at 9:26 AM
3/ TGIF2 stood out—it was the only TF whose expression and motif enrichment correlated with “neurogenesis”, independent of brain region and time.
2/ We profiled NSCs from the mouse embryonic cortex and lateral ganglionic eminence (where neurogenesis continues) at the peak and the transition to gliogenesis using RNA-seq and ATAC-seq to identify key regulators.
February 17, 2025 at 9:26 AM
2/ We profiled NSCs from the mouse embryonic cortex and lateral ganglionic eminence (where neurogenesis continues) at the peak and the transition to gliogenesis using RNA-seq and ATAC-seq to identify key regulators.
1/ NSCs express neurogenic genes at low levels, but how do they prevent premature differentiation while staying poised for neurogenesis? How is the balance between self-renewal and differentiation regulated?
February 17, 2025 at 9:26 AM
1/ NSCs express neurogenic genes at low levels, but how do they prevent premature differentiation while staying poised for neurogenesis? How is the balance between self-renewal and differentiation regulated?