A neural mechanism coordinates pupariation behavior and tanning in the tsetse larva. At parturition, the mature larva has already received sufficient ecdysteroid to commit the epidermal cells to metamorphosis but, before sclerotization and tanning of the cuticle can begin, the larva must first select a pupariation site and then proceed through a stereotypic sequence of pupariation behavior that culminates in the formation of a smooth, ovoid puparium. Both pupariation behavior and tanning are inhibited by the central nervous system (CNS) during the wandering phase. This central inhibition is maintained by sensory input originating in the extreme posterior region of the body. At the transition from wandering to pupariation, the posterior signal that induces inhibition of pupariation behavior is removed and the larva begins the contractions associated with pupariation, but the CNS inhibition of tanning persists. At this point, separation of the body into two halves by ligation or nerve transection prevents tanning of the anterior half (containing the CNS), whereas the denervated integument of the posterior half tans completely. Transection of nerves to the midline of the body produces larvae with a tanning pattern that ends abruptly along a sagittal plane, implying that the central control of this process is uncoupled between the left and right regions of the CNS. A few minutes later, when the final shape of the puparium is completed, the CNS inhibition is lifted and the tanning process begins. At this time, separation of the body into two halves by ligation or nerve transection has no inhibitory effects on either part. Exogenous ecdysteroids fail to release the CNS inhibition, and hemolymph containing the pupariation factors from Sarcophaga bullata have no accelerating effects on tsetse pupariation. These results imply that regulation of metamorphosis in the insect integument is not the exclusive domain of blood-borne hormones.

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