In this mutation, an inversion on the X chromosome placed the white gene next to pericentric heterochromatin, or a sequence of repeats that becomes heterochromatic.
[3] Normally, the white gene is expressed in every cell of the adult Drosophila eye resulting in a red-eye phenotype.
[5] Typically, the barrier DNA sequences prevent the heterochromatic region from spreading into the euchromatin but they are no longer present in the flies that inherit certain chromosomal rearrangements.
[7] The effect is the variegation in a particular phenotype i.e., the appearance of irregular patches of different colour(s), due to the expression of the original wild-type gene in some cells of the tissue but not in others,[8] as seen in the eye of mutated Drosophila melanogaster.
[5] In other words, the heterochromatin spreads and causes gene silencing by packaging the normally euchromatic region.
Which mechanism dominates to influence the phenotype depends upon the type of heterochromatin and the intricacy of the rearrangement.
Chromosome structure in the vicinity of the breakpoint appears to be an important determinant of the gene inactivation process.
When an autosomal region carrying a fur color gene is inserted onto the X chromosome, variable silencing of the allele is seen.
Variegation is, however, observed only in the female having this insertion along with a homozygous mutation in the original coat color gene.