The formation of the unsegmented terminal regions of the Drosophila larva, acron and telson requires the function of at least five maternal genes (terminal genes class1). In their absence, the telson and acron are not formed. One of them, torso (tor)2, has gain-of-function alleles which have an opposite phenotype to the lack-of-function (tor-) alleles: the segmented regions of the larval body, thorax and abdomen, are missing, whereas the acron is not affected and the telson is enlarged. In strong gain-of-function mutants, the pair-rule gene fushi tarazu3 (ftz) is not expressed, demonstrating the suppression of the segmentation process in an early stage of development. The tor gain-of-function effect is neutralized, and segmentation is restored in double mutants with the zygotic gene tailless4,5 (tll), which has a phenotype similar (but not identical) to that of tor-. This suggests that tor acts through tll, and that in the gain-of-function alleles of tor, the tll gene product is ectopically expressed at middle positions of the embryo, where it inhibits the expression of segmentation genes like ftz.
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