Abstract
The albino gene (al) is a simple recessive gene. Embryos homozygous for al develop normally to young larvae which are able to hatch out by chewing up the egg chorion and grow normally during the 1st instar. Their lethality appears immediately after the 1st molting.
The phenotype of lethal albino larvae resembles that of lethal lemon larvae. Neither can chew up mulberry leaves owing to insufficient sclerotization of the hypodermal cuticle.
Abnormal pteridine metabolism was found in the lethal albino larvae. It is assumed that a step of sepiapterin formation is blocked in their main pteridine metabolic activities.
It was found that al/al larval extracts have a lower activity of phenol oxidase than. +al/+al larval extracts.
It was suggested that al/al larval extracts have also a lower activity of phenylalaine hydroxylation than +al/+al larval extracts.
It seems that in the lethal albino larvae abnormal pteridine metabolism has some close relation to a defective phenylalanine metabolism.
Maternal effects of +al gene may explain why young al/al larvae do not show their lethal phenotype inside the eggs.
