Final answer:
UBE3A is not made from paternal DNA in neurons due to genomic imprinting, where only the maternal allele is expressed in the brain, leading to disorders like Angelman syndrome if the maternal allele is affected. This epigenetic mechanism may influence neurodevelopment and be relevant in conditions such as autism.
Step-by-step explanation:
The reason no UBE3A is made from the paternal DNA in neurons is due to a genetic phenomenon known as genomic imprinting. In this case, the UBE3A gene is imprinted in such a way that it is only actively expressed from the maternal allele in certain tissues, including neurons of the central nervous system. The paternal UBE3A allele is silenced by epigenetic mechanisms, so if the maternal allele is lost or mutated, it leads to disorders such as Angelman syndrome, which can include symptoms like intellectual disability, seizures, and problems with movement and balance.
In the context of neurodevelopmental disorders such as autism, variations in the expression of genes like UBE3A could contribute to differences in neuronal growth and synaptic formation. As with the in vitro findings from stem cells derived from fathers and sons, where neurons from the sons demonstrated accelerated growth with more synapses, if this pattern of growth occurs in vivo, it might affect information processing and integration in the brain.