TY - JOUR
T1 - Fruitless recruits two antagonistic chromatin factors to establish single-neuron sexual dimorphism
AU - Ito, Hiroki
AU - Sato, Kosei
AU - Koganezawa, Masayuki
AU - Ote, Manabu
AU - Matsumoto, Ken
AU - Hama, Chihiro
AU - Yamamoto, Daisuke
N1 - Funding Information:
We thank the Bloomington Stock Center, Kyoto Genetic Resource Center and Vienna Drosophila RNAi Center for numerous stocks, the Developmental Studies Hybridoma Bank for antibodies, B. Baker, H.J. Bellen, L.A. Pile, R. Mottus, J.C. Eissenberg, K. Kimura, J. Levine, J. Bernués, J. Müller, and M. Buszczak for the cDNAs, antibodies, and flies, Y. Ishikawa for help in statistics, and H. Sato and K. Sawaguchi for secretarial assistance. This work was supported in part by Grants-in-Aid for Scientific Research (24113502, 23220007, 1802012) from the Japanese Government Ministry of Education, Culture, Sports, Science and Technology (MEXT) to D.Y., a grant from the Strategic Japanese-French Cooperative Program from the Japan Science and Technology Agency to D.Y., a grant from the Tohoku Neuroscience Global COE program to D.Y., and the Life Science Grant from Takeda Science Foundation to D.Y.
PY - 2012/6/8
Y1 - 2012/6/8
N2 - 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.
AB - 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.
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U2 - 10.1016/j.cell.2012.04.025
DO - 10.1016/j.cell.2012.04.025
M3 - Article
C2 - 22682252
AN - SCOPUS:84861980277
VL - 149
SP - 1327
EP - 1338
JO - Cell
JF - Cell
SN - 0092-8674
IS - 6
ER -