Cooperation of Sall4 and Sox8 transcription factors in the regulation of the chicken Sox3 gene during otic placode development
Cooperation of Sall4 and Sox8 transcription factors in the regulation of the chicken Sox3 gene during otic placode development
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Sall4 和 Sox8 转录因子在耳基板发育过程中鸡 Sox3 基因调控中的合作
DOI：
10.1111/dgd.12427
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Uchikawa Masanori
中科院分区：
文献类型：
--
作者：
Okamoto Yu;Nishimura Naoko;Matsuda Kazunari;Ranawakage Deshani C.;Kamachi Yusuke;Kondoh Hisato;Uchikawa Masanori
为了阐明基因位点特异性的转录调控机制，我们研究了鸡的ox3下游增强子Otic1，该增强子的活性局限于并分布于整个基因位点。181 bp的Otic1增强子序列被分解为68 bp的最小激活序列，该最小激活序列在耳位和头神经嵴表现出二聚体增强子活性，并进一步被还原为25 bp的Otic1核心序列，该核心序列在相同区域也表现出八聚体增强子活性。Otic1核心八聚体被Sall4和SoxE转录因子（tf） Sox8或Sox9联合激活。通过ChIP‐qPCR分析证实了胚胎组织中Sall4、Sox8和Sox9与Otic1序列的结合。Otic1的核心-毗邻3 ‘侧序列增强了其增强子活性，而在68 - bp序列的直接3 ’端包含CAGGTG序列抑制了其在Otic1位点外的增强子活性。CAGGTG序列可能是tf抑制因子δEF1 （Zeb1）、Sip1 （Zeb2）和Snail2的结合位点，这些抑制因子均在头神经嵴表达，而不在脑区表达。因此，Sall4 - Sox8依赖性激活和CAGGTG序列依赖性抑制的结合决定了位点的发育。尽管Otic1序列在哺乳动物或鱼类中并不保守，但其激活机制是保守的，因为Otic1在小鼠胚胎干细胞和瞬时转基因斑马鱼胚胎发育的耳基板组织中也被激活。
To elucidate the transcriptional regulation that underlies specification of the otic placode, we investigated theSox3downstream enhancer Otic1 of the chicken, the activity of which is restricted to and distributed across the entire otic placode. The 181‐bp Otic1 enhancer sequence was dissected into a 68‐bp minimal activating sequence, which exhibited dimer enhancer activity in the otic placode and cephalic neural crest, and this was further reduced to a 25‐bp Otic1 core sequence, which also showed octamer enhancer activity in the same regions. The Otic1 core octamer was activated by the combined action of Sall4 and the SoxE transcription factors (TFs) Sox8 or Sox9. Binding of Sall4, Sox8 and Sox9 to the Otic1 sequence in embryonic tissues was confirmed by ChIP‐qPCR analysis. The core‐adjoining 3′ side sequences of Otic1 augmented its enhancer activity, while inclusion of the CAGGTG sequence in the immediate 3′ end of the 68‐bp sequence repressed its enhancer activity outside the otic placode. The CAGGTG sequence likely serves as the binding sites of the repressor TFs δEF1 (Zeb1), Sip1 (Zeb2), and Snail2, all of which are expressed in the cephalic neural crest but not in the otic placode. Therefore, the combination of Sall4‐Sox8‐dependent activation and CAGGTG sequence‐dependent repression determines otic placode development. Although the Otic1 sequence is not conserved in mammals or fishes, the activation mechanism is, as Otic1 was also activated in otic placode tissues developed from mouse embryonic stem cells and transient transgenic zebrafish embryos.
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影响因子：
2.7
作者：
Sato, Yuki;Kasai, Toshiharu;Takahashi, Yoshiko
通讯作者：
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影响因子：
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作者：
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DOI：
--
发表时间：
2009
期刊：
影响因子：
--
作者：
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通讯作者：
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影响因子：
2.7
作者：
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通讯作者：
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影响因子：
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作者：
Y. Kamachi;Hisato Kondoh
通讯作者：
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