Practice question

Ethanol exposure disrupts maintenance of neural crest stemness by increasing intracellular free radicals and altering histone acetylation, prompting premature exit from multipotent state. Normal neural crest cells undergo extensive migration before differentiating into craniofacial cartilage, peripheral ganglia and melanocytes, requiring precise timing control by Wnt and BMP signals. Early differentiation depletes migratory pool, causing insufficient colonization of facial prominences and pharyngeal arches. Markers of differentiation such as neurofilament and melanin appear early in vitro after ethanol treatment, while progenitor markers p75 and Sox10 decline, illustrating accelerated maturation detrimental to craniofacial morphogenesis and leading to dysmorphology.