12.00-12.15 Elisa Galliano, King’s College London, UK & Harvard University, USA
“Embryonic and postnatal neurogenesis produce functionally distinct subclasses of dopaminergic neuron”

Most neurogenesis in the mammalian brain is completed embryonically, but in certain areas the production of neurons continues throughout postnatal life. The properties of mature postnatally-generated neurons often match those of their embryonically-produced counterparts. However, we show that in the olfactory bulb, embryonic and postnatal neurogenesis produce functionally distinct subpopulations of dopaminergic neurons, placing important constraints on the functional roles of adult-born neurons.


 

12.15-12.30 Tom Watson, The Francis Crick Institute, London, UK
“The Gene Regulatory Network Underlying the Neural-to-Glial Fate Transition in the Developing Spinal Cord”

Neurons and glia are generated sequentially in the central nervous system. In vivo, this process is under tight spatial and temporal control. Although several factors have been defined, the underlying gene regulatory network mediating the transition remains unclear. Using single-cell transcriptomics, we define the transcriptional changes that accompany the transition and identify novel candidate genes involved. With CRISPR-Cas9 and lentiviral technologies, we test these candidates and reveal a novel player in the activation of the glial lineage.



12.30-12.45 Barbara Vacca, University College London, UK
“The tight junction protein MarvelD3 regulates eye development and neural crest induction in Xenopus laevis”

Epithelial integrity is maintained via tight junctions (TJ); however, TJ role in vivo remains unclear. We established the function of MarvelD3 (MD3), a new TJ protein, as regulator of eye morphogenesis by balancing cell proliferation and survival and of neural plate border positioning where the NC arises during Xenopus laevis development. MD3-induced attenuation of JNK activity is required for NC induction while JNK activation ensures eye morphogenesis. Thus, MD3 signalling is conserved as a switch to regulate the levels of JNK guiding crucial cellular and developmental processes.

 

<– Back to programme