LIFR beta plays a major role in neuronal identity determination and glial differentiation in the mouse facial nucleus.

Summary

In the hindbrain, generation of the facial nucleus involves complex developmental processes that will lead to the formation of a structure composed of motor neurons, astrocytes and oligodendrocytes. The implication of LIF-related cytokines in the development of this nucleus came to light with the analysis of mice mutant for the receptor of these cytokines, LIFR beta, which exhibit a massive loss of facial branchiomotor (fbm) neurons at birth and a severe decrease in GFAP expression, a marker of astrocytes. To uncover the cellular mechanisms regulated by LIFR beta during facial nucleus development, we first analyzed its expression pattern in the hindbrain. lifr beta is first expressed at E11.5 in the hindbrain neuroepithelium. The receptor is absent during the migration of fbm post-mitotic neurons but is strongly expressed when fbm neurons have reached rhombomere 6 at E12.5, and its expression is maintained until E18.5. From the analysis of lifr beta mutant embryos, we established that LIFR beta is necessary for fbm neurons’ identity determination. We also show that LIFR beta is implicated in astrocyte and oligodendrocyte differentiation, specifically within the facial nucleus.