초파리의 vermilion locus에서 합성되는 tryptophan oxygenase는 억제 유전자 su(s)에 의하여 그 활성이 조절된다. 즉, $su(s)^+$의 산물은 in vitro에서 돌연변이형의 tryptophan oxygenase 활성을 특이하게 억제한다. In vivo에서도 $su(s)^+$ 유전자의 copy수가 증가하면 tryptophan oxygenase에 의하여 합성되는 갈색의 xanthommatin 색소체 양이 감소한다. 이 사실은 $su(s)^+$에 의하여 target 효소의 돌연변이형만이 불활성화 되며, su(s)에서의 돌연변이 결과 이 저해물질이 사라짐으로 유전적 억제현상이 야기됨을 시사해 준다.
The suppressor gene, $su(s)^2$, in Drosophila melanogaster restores the production of brown eye pigment in the vermilion mutant by partially restoring tryptophan oxygenase activity. Our data indicate that the product of the $su(s)^+$ allele inhibits the activity of the mutant tryptophan oxygenase but not that of the wild type enzyme. An epigenetic reactivation of brown eye pigment formation was shown to be reduced by increasing the number of $su(s)^+$ copies in vivo. These data support a previously proposed mechanism for suppression by $su(s)^+$ which postulates that the enzyme produced by a mutant form of a suppressible gene (vermilion in this case) is inhibited or inactivated by the product of the $su(s)^+$ allele. When the $su(s)^+$ allele replaces $su(s)^+$ the inhibitory product is either absent or ineffective and the tryptophan oxygenase activity reappears.
