Autosomal random stochastic inactivation was initially described for a group of immune and nervous system gene families (see Chess, 2012 for review) including immunoglobulins, interleukin receptors, odorant receptors, and neural protocadherin genes. More recent genomic studies have revealed that random mono-allelic expression is widespread and involves a much larger number of autosomal genes (5–20% in mammalian cells) (Gimelbrant et al., 2007, Serre et al., 2008). Mitotically stable, random mono-allelic expression has been demonstrated in clonal lymphoblastoid cell lines (Gimelbrant et al., 2007, Serre et al., 2008), in clonal groups of cells in placental tissue (Gimelbrant et al., 2007), in iPSCs and iPSC-derived neural cultures (Lin et al., 2012), and in human clonal neural stem cells derived from fetal brain and spinal cord (Jeffries et al., 2012). This process typically does not result in exclusively mono-allelic expression but rather clonal lines expressing either one or both alleles at loci showing random clonal allelic bias potential (Gimelbrant et al., 2007, Jeffries et al., 2012). Functional outcomes of allelic bias in the expression of cell surface proteins include the potential for increasing the cellular diversity of immune and neural cells.
