Lifespan and protein synthesis in several Bombyx mori mutants with genetic abnormalities in amino acid and protein metabolism

Abstract

Three kinds of “white eggs” and red-blooded Bombyx mutants (w 1, w 2, w 3 and rb) which lack enzymes in tryptophan metabolism showed almost no difference in their lifespans from that of normal stock. However, other Bombyx mutants, such as Nd, Nd-s and DES-Nd, unable to synthesize fibroin, had shorter lifespans than normal. Among these fibroin-deficient mutants, only the lifespan of DES-Nd was similar to the normal. However, further analysis of the amino acid composition in the cocoon of the mutant showed that its lifespan was also dependent on its ability to synthesize fibroin-like protein. It is very likely that, different from abnormalities in amino acid metabolism, a genetic abnormality in protein metabolism affects the maintenance of adult life in silkmoths and this results in the short lifespan. Generally speaking, an abnormality in amino acid metabolism seems to have no influence on silkmoth lifespan. However, an abnormality in protein metabolism results in shortening lifespan. The greater the abnormality in protein metabolism possessed by a silkmoth, the shorter the lifespan.