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蜕皮激素信号传导调节具有雄性特异性神经突的神经元的特化。

Ecdysone signaling regulates specification of neurons with a male-specific neurite in .

作者信息

Zhang Binglong, Sato Kosei, Yamamoto Daisuke

机构信息

Division of Neurogenetics, Tohoku University Graduate School of Life Sciences, Sendai, 980-8577, Japan.

Division of Neurogenetics, Tohoku University Graduate School of Life Sciences, Sendai, 980-8577, Japan

出版信息

Biol Open. 2018 Feb 20;7(2):bio029744. doi: 10.1242/bio.029744.

Abstract

Some mAL neurons in the male brain form the ipsilateral neurite (ILN[+]) in a manner dependent on FruBM, a male-specific transcription factor. FruBM represses transcription, allowing the ILN to form. We found that the proportion of ILN[+]-mALs in all observed single cell clones dropped from ∼90% to ∼30% by changing the heat-shock timing for clone induction from 4-5 days after egg laying (AEL) to 6-7 days AEL, suggesting that the ILN[+]-mALs are produced predominantly by young neuroblasts. Upon EcR-A knockdown, ILN[+]-mALs were produced at a high rate (∼60%), even when heat shocked at 6-7 days AEL, yet EcR-B1 knockdown reduced the proportion of ILN[+]-mALs to ∼30%. Immunoprecipitation assays in S2 cells demonstrated that EcR-A and EcR-B1 form a complex with FruBM. reporter transcription was repressed by FruBM and ecdysone counteracted FruBM. We suggest that ecdysone signaling modulates the FruBM action to produce an appropriate number of male-type neurons.

摘要

雄性大脑中的一些雄性特异的mAL神经元以一种依赖于雄性特异性转录因子FruBM的方式形成同侧神经突(ILN[+])。FruBM抑制转录,从而使ILN得以形成。我们发现,通过将克隆诱导的热休克时间从产卵后4 - 5天(AEL)改为6 - 7天AEL,所有观察到的单细胞克隆中ILN[+]-mALs的比例从约90%降至约30%,这表明ILN[+]-mALs主要由年轻的神经母细胞产生。在敲低EcR-A后,即使在6 - 7天AEL进行热休克,ILN[+]-mALs仍以高比例(约60%)产生,然而敲低EcR-B1会使ILN[+]-mALs的比例降至约30%。在S2细胞中的免疫沉淀试验表明,EcR-A和EcR-B1与FruBM形成复合物。报告基因转录受到FruBM的抑制,而蜕皮激素可抵消FruBM的作用。我们认为蜕皮激素信号传导调节FruBM的作用,以产生适当数量的雄性型神经元。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0d4/5861360/b5f043a96970/biolopen-7-029744-g1.jpg

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