Berndt Anthony J E, Tang Jonathan C Y, Ridyard Marc S, Lian Tianshun, Keatings Kathleen, Allan Douglas W
Department of Cellular and Physiological Sciences, University of British Columbia, Vancouver, British Columbia, Canada.
Department of Genetics, Harvard Medical School, Boston, Massachusetts, United States America.
PLoS Genet. 2015 Dec 29;11(12):e1005754. doi: 10.1371/journal.pgen.1005754. eCollection 2015 Dec.
Neuronal differentiation often requires target-derived signals from the cells they innervate. These signals typically activate neural subtype-specific genes, but the gene regulatory mechanisms remain largely unknown. Highly restricted expression of the FMRFa neuropeptide in Drosophila Tv4 neurons requires target-derived BMP signaling and a transcription factor code that includes Apterous. Using integrase transgenesis of enhancer reporters, we functionally dissected the Tv4-enhancer of FMRFa within its native cellular context. We identified two essential but discrete cis-elements, a BMP-response element (BMP-RE) that binds BMP-activated pMad, and a homeodomain-response element (HD-RE) that binds Apterous. These cis-elements have low activity and must be combined for Tv4-enhancer activity. Such combinatorial activity is often a mechanism for restricting expression to the intersection of cis-element spatiotemporal activities. However, concatemers of the HD-RE and BMP-RE cis-elements were found to independently generate the same spatiotemporal expression as the Tv4-enhancer. Thus, the Tv4-enhancer atypically combines two low-activity cis-elements that confer the same output from distinct inputs. The activation of target-dependent genes is assumed to 'wait' for target contact. We tested this directly, and unexpectedly found that premature BMP activity could not induce early FMRFa expression; also, we show that the BMP-insensitive HD-RE cis-element is activated at the time of target contact. This led us to uncover a role for the nuclear receptor, seven up (svp), as a repressor of FMRFa induction prior to target contact. Svp is normally downregulated immediately prior to target contact, and we found that maintaining Svp expression prevents cis-element activation, whereas reducing svp gene dosage prematurely activates cis-element activity. We conclude that the target-dependent FMRFa gene is repressed prior to target contact, and that target-derived BMP signaling directly activates FMRFa gene expression through an atypical gene regulatory mechanism.
神经元分化通常需要来自其支配细胞的靶源性信号。这些信号通常会激活神经亚型特异性基因,但其基因调控机制在很大程度上仍不清楚。果蝇Tv4神经元中FMRFa神经肽的高度受限表达需要靶源性BMP信号传导和包括Apterous在内的转录因子编码。利用增强子报告基因的整合酶转基因技术,我们在其天然细胞环境中对FMRFa的Tv4增强子进行了功能剖析。我们鉴定出两个必需但离散的顺式元件,一个结合BMP激活的pMad的BMP反应元件(BMP-RE),以及一个结合Apterous的同源结构域反应元件(HD-RE)。这些顺式元件活性较低,必须组合在一起才能产生Tv4增强子活性。这种组合活性通常是将表达限制在顺式元件时空活性交集处的一种机制。然而,发现HD-RE和BMP-RE顺式元件的串联体可独立产生与Tv4增强子相同的时空表达。因此,Tv4增强子非典型地组合了两个低活性顺式元件,它们从不同输入产生相同输出。靶依赖性基因的激活被认为是“等待”靶接触。我们直接对此进行了测试,意外地发现过早的BMP活性不能诱导早期FMRFa表达;此外,我们表明对BMP不敏感的HD-RE顺式元件在靶接触时被激活。这使我们发现了核受体seven up(svp)在靶接触前作为FMRFa诱导的抑制因子的作用。Svp通常在靶接触前立即下调,我们发现维持Svp表达可阻止顺式元件激活,而降低svp基因剂量则会过早激活顺式元件活性。我们得出结论,靶依赖性FMRFa基因在靶接触前受到抑制,并且靶源性BMP信号传导通过一种非典型的基因调控机制直接激活FMRFa基因表达。