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核心启动子因子 TRF2 介导 Fruitless 作用以雄性化果蝇的神经行为特征。

The core-promoter factor TRF2 mediates a Fruitless action to masculinize neurobehavioral traits in Drosophila.

机构信息

Tohoku University Graduate School of Life Sciences, Sendai, 9808577, Japan.

出版信息

Nat Commun. 2017 Nov 14;8(1):1480. doi: 10.1038/s41467-017-01623-z.

DOI:10.1038/s41467-017-01623-z
PMID:29133872
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5684138/
Abstract

In fruit flies, the male-specific fruitless (fru) gene product FruBM plays a central role in establishing the neural circuitry for male courtship behavior by orchestrating the transcription of genes required for the male-type specification of individual neurons. We herein identify the core promoter recognition factor gene Trf2 as a dominant modifier of fru actions. Trf2 knockdown in the sexually dimorphic mAL neurons leads to the loss of a male-specific neurite and a reduction in male courtship vigor. TRF2 forms a repressor complex with FruBM, strongly enhancing the repressor activity of FruBM at the promoter region of the robo1 gene, whose function is required for inhibiting the male-specific neurite formation. In females that lack FruBM, TRF2 stimulates robo1 transcription. Our results suggest that TRF2 switches its own role from an activator to a repressor of transcription upon binding to FruBM, thereby enabling the ipsilateral neurite formation only in males.

摘要

在果蝇中,雄性特异性 fru 基因产物 FruBM 通过协调个体神经元雄性类型特化所需基因的转录,在建立雄性求偶行为的神经回路中发挥核心作用。我们在此确定核心启动子识别因子基因 Trf2 是 fru 作用的主要修饰因子。在性二态 mAL 神经元中敲低 Trf2 会导致雄性特异性神经突的丢失和雄性求偶活力的降低。TRF2 与 FruBM 形成一个抑制复合物,在 robo1 基因的启动子区域强烈增强 FruBM 的抑制活性,robo1 基因的功能是抑制雄性特异性神经突的形成。在缺乏 FruBM 的雌性果蝇中,TRF2 刺激 robo1 转录。我们的结果表明,TRF2 在与 FruBM 结合后,将其自身的转录作用从激活剂转换为抑制剂,从而仅在雄性中允许同侧神经突形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bd/5684138/b98f454343cb/41467_2017_1623_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bd/5684138/984ec9266043/41467_2017_1623_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bd/5684138/1a77e8af7f37/41467_2017_1623_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bd/5684138/f1aa459b5630/41467_2017_1623_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bd/5684138/a561d3bb1389/41467_2017_1623_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bd/5684138/b98f454343cb/41467_2017_1623_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bd/5684138/984ec9266043/41467_2017_1623_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bd/5684138/1a77e8af7f37/41467_2017_1623_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bd/5684138/f1aa459b5630/41467_2017_1623_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bd/5684138/a561d3bb1389/41467_2017_1623_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bd/5684138/b98f454343cb/41467_2017_1623_Fig5_HTML.jpg

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