INVESTIGADORES
CARCAGNO Abel Luis
congresos y reuniones científicas
Título:
Ascl1 controla la especificación neuronal tardía de las neuronas del canal central de la medula espinal
Autor/es:
DANIELA DI BELLA; ABEL CARCAGNO; GUILLERMO LANUZA
Lugar:
Chascomús
Reunión:
Taller; III Taller de Biología Celular y del Desarrollo 2016; 2016
Resumen:
The production of a functional nervous system consists of an integrated series of steps that depends on the generation of diverse neuronal and glial cell types at their correct positions and appropriate number. During development, the acquisition of specific neural identities is initiated by inductive signals and dedicated transcriptional networks acting in progenitors and newborn neurons. We have recently identified that spinal cord cerebrospinal fluid-contacting neurons (CSF-cN) are born at stages when progenitors are massively committed to glial and ependymal fates. How these late neurogenic events are controlled remains unknown. Expression analysis and genetic lineage tracings in the mouse show that the bHLH-containing transcription factor Ascl1 is expressed in progenitors that produce CSF-cN. Mice carrying null or hypomorphic Ascl1 alleles fail to generate CSF-cNs. These experiments also indicate that Ascl1 controls the initial steps of the conversion of late ventral spinal progenitors into CSF-cN. Finally, genetic labeling of prospective CSF-cN progenitors in the Ascl1 mutant background shows that late progenitors that fail to acquire neuronal CSF-cN identity become cells that possess the morphology, marker expression and electrophysiological signature of ependymocytes. In summary, our results demonstrate that Ascl1 is expressed in the ventral progenitors that give rise to CSF-cN and that Ascl1 provides neuronal potential to late ventral progenitors in the amniote spinal cord.