The dominant temperature‐sensitive mutation L(3)3 DTS ( DTS‐3 ) in Drosophila melanogaster causes lethality of heterozygotes during the third larval instar at the restrictive temperature (29°C). Temperature‐shift experiments revealed two distinct temperature‐sensitive periods, with lethal phases during the third larval instar (which may persist for 4 weeks) and during the late pupal stage. At 29°C mutant imaginal discs are unable to evert in situ, but did evert normally if cultured in the presence of exogenous ecdysterone or when implanted into wild‐type larval hosts. The only morphologically abnormal tissue present in the lethal larvae is the ring gland, the prothoracic gland being greatly hypertrophied in third instar DTS‐3 larvae. Injection of a single wild‐type ring gland rescued these mutant larvae, indicating that the mutant gland is functionally, as well as morphologically, abnormal. Finally, the mutant larvae were shown to have less than 10% of the wild‐type ecdysteroid levels. These results are all consistent with a proposed lesion in ecdysteroid hormone production in DTS‐3 larvae. A comparison with the phenotypes of other “ecdysone‐less” mutants is presented.
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Holden et al. (1985) studied this question.
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