The mode of action of Fruitless: Is it an easy matter to switch the sex?

Kosei Sato,Daisuke Yamamoto

doi:10.1111/gbb.12606

Abstract

The fruitless (fru) locus was originally defined by a male sterile mutation that promotes male‐to‐male courtship while suppressing male‐to‐female courtship in Drosophila melanogaster. The fru promoter‐1 pre‐RNA generates a set of BTB‐zinc finger family FruM proteins expressed exclusively in the male neurons, leading to the formation of sexual dimorphisms in neurons via male‐specific neuroblast proliferation, male‐specific neural survival, male‐specific neuritegenesis or male‐specific arbor patterning. Such a wide spectrum of phenotypic effects seems to result from chromatin modifications, in which FruBM recruits Bonus, Histone deacetylase 1 (HDAC1) and/or Heterochromatin protein 1a (HP1a) to ~130 target sites. One established FruBM transcriptional target is the axon guidance protein gene robo1. Multiple transcriptional regulator‐binding sites are nested around the FruBM‐binding site, and mediate sophisticated modulation of the repressor activity of FruBM. FruBM also binds to the Lola‐Q transcriptional repressor to protect it from proteasome‐dependent degradation in male but not female neurons as FruBM exists only in male neurons, leading to the formation of sexually dimorphic neural structures. These findings shed light on the multilayered network of transcription regulation orchestrated by the master regulator FruBM.

Highlights

The fruitless locus was originally defined by a male sterile mutation that promotes male-to-male courtship while suppressing male-to-female courtship in Drosophila melanogaster
The likely scenario is that a FruM-containing complex switches chromatin states, thereby silencing or activating a large set of genes that are required in neurons for taking on the female or male fate (Figure 2D)
Potential FruM downstream genes have impact on a select aspect of the sexual dimorphism in mAL neurons (Figure 2E): loss of three major cell death-inducing genes, grim, hid and reaper, affects primarily the sex difference in the number of mAL neurons[7]; the transcription factor Hunchback selectively acts to shape the sexually-dimorphic branching of the contralateral neurite[32]; robo[1] affects the sexdependent presence or absence of the ipsilateral neurite.[33] mAL neurons represent probably the most conspicuous example of neural sexual dimorphism, but many other fru-positive neurons are sexually dimorphic, as showed by the dedicated efforts to resolve the finer structures of individual neurons on the standardized brain

Summary

Introduction

The fruitless (fru) locus was originally defined by a male sterile mutation that promotes male-to-male courtship while suppressing male-to-female courtship in Drosophila melanogaster.

Results

Conclusion