Polycomb-dependent Ultrabithorax Hox gene silencing induced by high Ultrabithorax levels in Drosophila
Polycomb-dependent Ultrabithorax Hox gene silencing induced by high Ultrabithorax levels in Drosophila
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DOI：
10.1242/dev.025809
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发表时间：
2008-10-01
期刊：
影响因子：
4.6
通讯作者：
Sanchez-Herrero, Ernesto
中科院分区：
文献类型：
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作者：
Garaulet, Daniel L.;Foronda, David;Sanchez-Herrero, Ernesto
果蝇的超双胸(UBx)基因规定了第三个胸段和第一个腹段。UBX的表达受多种机制的控制，包括其自身产物的负调控。我们在这里表明，如果Ubx的表达水平不适当地升高，凌驾于自动调节控制之上，就建立了对Ubx的永久抑制。这种持续的抑制独立于外源Ubx的存在，并导致矛盾的结果，即Ubx过量会导致Ubx丢失的表型。永久抑制的机制取决于多梳基因。当Ubx水平高度升高时，缺乏内源性Ubx转录可能激活位于Ubx主要内含子的多梳反应元件上的多梳复合体。这反过来又会永久抑制Ubx转录。同样的结果也适用于基因累加，这表明当表达水平短暂升高时，这种永久抑制的机制可能是具有负自动调节的基因的一般机制。
The Ultrabithorax (Ubx) gene of Drosophila specifies the third thoracic and first abdominal segments. Ubx expression is controlled by several mechanisms, including negative regulation by its own product. We show here that if Ubx expression levels are inappropriately elevated, overriding the auto-regulatory control, a permanent repression of Ubx is established. This continuous repression becomes independent of the presence of exogenous Ubx and leads to the paradoxical result that an excess of Ubx results in a phenotype of Ubx loss. The mechanism of permanent repression depends on Polycomb-group genes. Absence of endogenous Ubx transcription when Ubx levels are highly elevated probably activates Polycomb complexes on a Polycomb response element located in the Ubx major intron. This, in turn, brings about permanent repression of Ubx transcription. Similar results are obtained with the gene engrailed, showing that this mechanism of permanent repression may be a general one for genes with negative auto-regulation when levels of expression are transitorily elevated.