Firefly “femmes fatales” acquire defensive steroids (lucibufagins) from their firefly prey

Female fireflies of the genus Photuris, the so-called firefly “femmes fatales,” prey on male fireflies of the genus Photinus. The females are able to entrap the males by faking the flash signal characteristics of the Photinus female. We found that by feeding on Photinus males, Photuris females gain more than nutrients. They also acquire defensive steroidal pyrones called lucibufagins, which are contained in Photinus but which Photuris fireflies are unable to produce on their own. Photuris females that eat Photinus males or lucibufagin are rejected by Phidippus jumping spiders. Lucibufagin itself proved to be a deterrent to such spiders. Field-collected Photuris females contain lucibufagin in varying amounts. The more lucibufagin they contain the more unacceptable they are to Phidippus.

A Tropomyosin-2 Mutation Suppresses a Troponin I Myopathy in Drosophila

A suppressor mutation, D53, of the held-up2 allele of the Drosophila melanogaster Troponin I (wupA) gene is described. D53, a missense mutation, S185F, of the tropomyosin-2, Tm2, gene fully suppresses all the phenotypic effects of held-up2, including the destructive hypercontraction of the indirect flight muscles (IFMs), a lack of jumping, the progressive myopathy of the walking muscles, and reductions in larval crawling and feeding behavior. The suppressor restores normal function of the IFMs, but flight ability decreases with age and correlates with an unusual, progressive structural collapse of the myofibrillar lattice starting at the center. The S185F substitution in Tm2 is close to a troponin T binding site on tropomyosin. Models to explain suppression by D53, derived from current knowledge of the vertebrate troponin-tropomyosin complex structure and functions, are discussed. The effects of S185F are compared with those of two mutations in residues 175 and 180 of human α-tropomyosin 1 which cause familial hypertrophic cardiomyopathy (HCM).