Abstract
Sexual dimorphism of the brain has been well characterized anatomically in Drosophila melanogaster at the single neuron level, yet little is known about the molecular mechanism whereby cellular sex differences are generated except that the neural sex determination gene fruitless (fru) plays a key role. The fru-expressing mAL interneuron cluster is sexually dimorphic in three aspects: the number of cells composing the cluster is 5 in females and 30 in males; the ipsilateral neurite is absent in females and present in males; the contralateral neurite forms Y-shaped branches in the subesophageal ganglion in females while it ends with a simple horsetail-like structure in males. By screens in the compound eye for modifiers of roughness induced by fru+ overexpression, we identified a loss-of-function allele of hunchback (hb) to be a suppressor of this phenotype. Hb was expressed in most of the fru-expressing neurons in the pupal and adult stages. Knocking down hb in mAL MARCM (Mosaic Analysis with a Repressible Cell Marker) clones in the male brain resulted in partial demasculinization of the branching pattern of the contralateral neurites without affecting the cell number and the ipsilateral neurite formation. The present results suggest that Hb is essential for male-typical shaping of the contralateral neurites by Fru.
In this issue
