Division of Neurogenetics, Tohoku University Graduate School of Life Sciences, Sendai, Japan.
Cell. 2012 Jun 8;149(6):1327-38. doi: 10.1016/j.cell.2012.04.025.
The Drosophila fruitless (fru) gene encodes a set of putative transcription factors that promote male sexual behavior by controlling the development of sexually dimorphic neuronal circuitry. However, the mechanism whereby fru establishes the sexual fate of neurons remains enigmatic. Here, we show that Fru forms a complex with the transcriptional cofactor Bonus (Bon), which, in turn, recruits either of two chromatin regulators, Histone deacetylase 1 (HDAC1), which masculinizes individual sexually dimorphic neurons, or Heterochromatin protein 1a (HP1a), which demasculinizes them. Manipulations of HDAC1 or HP1a expression change the proportion of male-typical neurons and female-typical neurons rather than producing neurons with intersexual characteristics, indicating that on a single neuron level, this sexual switch operates in an all-or-none manner.
果蝇 fru 基因编码了一组假定的转录因子，通过控制性二型神经元回路的发育来促进雄性性行为。然而，fru 确定神经元的性命运的机制仍然是个谜。在这里，我们表明 Fru 与转录共激活因子 Bonus（Bon）形成复合物，而 Bon 反过来又招募两种染色质调节剂之一，即组蛋白去乙酰化酶 1（HDAC1），其使个别性二型神经元雄性化，或异染色质蛋白 1a（HP1a），使其去雄性化。HDAC1 或 HP1a 表达的操纵改变了典型雄性神经元和典型雌性神经元的比例，而不是产生具有两性特征的神经元，这表明在单个神经元水平上，这种性转换以全或无的方式运作。
