Lecture
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04 Mar 2024 (2h 00m)
Federico Cremisi - Course (teaching activity) - Face to face
Lesson 2. The nature of the radial glial progenitor cell. Lateral inhibition in flyes and vertebrates. Neurogenic and proneural genes. The role of Notch signaling in vertebrate neurogenesis.
11 Mar 2024 (2h 00m)
Federico Cremisi - Course (teaching activity) - Face to face
Lesson 3. The adult neuronal stem cell niche. B, C and A type cells. The role of VCam1, Notch, BMP and Shh in the stem cell niche maintenance. Extrinsic signals from blood and cerebrospinal fluid regulating the niche.
20 Mar 2024 (2h 00m)
Federico Cremisi - Course (teaching activity) - Face to face
Lesson 4. Studies on the mechanisms of action of the SHH signaling in maintaining the SVZ neural stem cell niche. Transgenic approaches to identify NSC cell progeny and analyze its composition in longitudinal studies. SHH signaling promotes the maintainance and increases the number of quiescent NSCs, while depleting the activated NSCs. SHH signaling affects NSCs by shorthening the G1 cell cycle phase.
08 Apr 2024 (2h 00m)
Federico Cremisi - Course (teaching activity) - Face to face
Lesson 5. SHH and the adult hippocampal niche. Long-lived NSCs dramatically expand in the first postnatal week before entering the quiescent state over several days. Sufu deletion impairs the ability of long-lived NSCs to expand in the first postnatal week, which results in the premature entry of NSCs into the quiescent state. This defect is a result of decreased Shh signaling activity as a result of Sufu deletion in NSCs. Highly activated mossy cells increase NSC proliferation. Seizure-induced neurogenesis is attenuated by selective deletion of Shh in mossy cells. Shh from mossy cells is needed to preserve the NSC pool after seizure-induced neurogenelsis. Deletion of Shh results in premature depletion of the NSC pool after seizures.
15 Apr 2024 (2h 00m)
Federico Cremisi - Course (teaching activity) - Face to face
Lesson 6. Other adult stem cells: intestinal, hematopoietic, mesenchimal cells (from Developmental Biology, Gilbert, 9th edition, pgs 158-167).
22 Apr 2024 (2h 00m)
Federico Cremisi - Course (teaching activity) - Face to face
Lesson 7. The Human Model System to Study Development and Disease::starting from mouse embryonic stem cells and proceeding through human cell reprogramming to pluripotency..Gilbert, Developmental Biology, 166--177. Selected papers: Qi-Long Ying et al. Nature 2008.; Warmflash et al., Nature 2014; Ghimire et al., Scientific Report 2017.
23 Apr 2024 (2h 00m)
Federico Cremisi - Course (teaching activity) - Face to face
Lesson 8. The molecular nature of pluripotent stem cells. Pervasive transcription, relaxed chromatin and enhanced RNA interference of chromatin remodellers are peculiar traits of embryonic stem cells Selected papers: Takahashi et al., Cell 2006; Efroni et al., Cell Stem Cell 2008; Huangfu et al., Nature Biotechnology 2008; Pandolfini et al., Genome Biology 2014.
06 May 2024 (2h 00m)
Federico Cremisi - Course (teaching activity) - Face to face
Lesson 10. Patterning different cell identities of neurons in vitro: examples from the literature. Highly efficient neural conversion of human ES and iPS cells by dual inhibition of SMAD signaling. An intrinsic mechanism of corticogenesis from embryonic stem cells. Activin/Nodal signaling supports retinal rogenitor specification in a narrow time window during pluripotent stem cell neuralization. A eutherian-specific microRNA controls the translation of Satb2 in a model of cortical differentiation.
30 May 2024 (2h 00m)
Federico Cremisi - Course (teaching activity) - Face to face
Lesson 9. The role of Sox2 transcription factor in the control of pluripotency and neural specification. The binding of Sox2 to different classes of gene promoters and enhancers. The interaction of Sox2 with POU factors. The identification of BRN2 motifs of binding in promoters and enhancers bound by Sox2 in neural progenitor cells. Sox2 binds to different enhancers when interacting with Oct4 or BRN2, orchestration the progression from pluripotency to neural identity in the early steps of embryonic development.
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