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首页> 外文期刊>Nucleus >Cytoskeletal proteins regulate chromatin access of BR-C transcription factor and Rpd3-Sin3A histone deacetylase complex in Drosophila salivary glands
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Cytoskeletal proteins regulate chromatin access of BR-C transcription factor and Rpd3-Sin3A histone deacetylase complex in Drosophila salivary glands

机译：细胞骨架蛋白调节果蝇唾液腺中BR-C转录因子和Rpd3-Sin3A组蛋白脱乙酰酶复合物的染色质访问

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At the onset of Drosophila metamorphosis the steroid hormone ecdysone induces a process leading to a rapid &generation of the larval salivary glands (SGs). Ecdysone acts through the ecdysone receptor heterodimer, which activates primary response genes. In particular these genes include the Broad-Complex (BR-C) gene encoding a set of BTB/POZ-transcription factors, among which the Z1 isoform is critical for SG cell death. The timing of SG disappearance depends upon p127~(l(2)gl), a cytoskeletal tumor suppressor that interacts with nonmuscle myosin II heavy chain (nmMHC) encoded by the zipper (zip) gene. Reduced l(2)gl expression delays SG histolysis whereas overexpression accelerates this process without affecting larval and pupal development. However, the mechanism by which l(2)gl controls SG histolysis remains yet unknown. Here we analyze the regulation controlled by p127l~(2)gl and nmMHC in the cytoplasm on the association of BR-C Z1 with chromatin and remodeling factors, such as Rpd3, Sin3A and SMRTER. In wild-type SGs these factors bind to chromatin but in l(2)gl SGs they accumulate in the cytoplasm and the cortical nuclear zone (CNZ). Similar chromatin exclusion occurs in SGs of developmentally delayed zip~E(br)/+ larvae or can be achieved by high levels of nmMHC synthesis. The present data show that p127~(l(2)gl) and nmMHC regulate the access of BR-C Z1, Rpd3, Sin3A and SMRTER to chromatin. As the interaction between p127l~(l(2)gl) and nmMHC occurs in the cytoplasm, we propose that these nuclear factors are processed by p127~(l(2)gl) and then released from p127~(l(2)gl) by nmMHC to allow their binding to chromatin. This process may constitute a novel mechanism of gene regulation, which in the absence of p127~l(2)gl), or excessive amounts of nmMHC, could lead to a fixed configuration in the pattern of gene expression that prevents further progression of SG differentiation and programmed cell death (PCD). Such a transcriptional block could play a critical role in the neoplastic transformation of l(2)gl tissues.
机译：在果蝇变态开始时，类固醇激素蜕皮激素会诱导导致幼虫唾液腺（SGs）快速繁殖的过程。蜕皮激素通过蜕皮激素受体异二聚体起作用，后者激活主要反应基因。特别是这些基因包括编码一组BTB / POZ转录因子的Broad-Complex（BR-C）基因，其中Z1亚型对SG细胞死亡至关重要。 SG消失的时机取决于p127〜（l（2）gl），p127〜（1（2）gl）是一种细胞骨架肿瘤抑制因子，与拉链（zip）基因编码的非肌肉肌球蛋白II重链（nmMHC）相互作用。降低的l（2）gl表达可延迟SG组织溶解，而过表达可加速该过程，而不会影响幼虫和p的发育。然而，l（2）gl控制SG组织溶解的机制仍然未知。在这里，我们分析了p1271〜（2）gl和nmMHC在细胞质中对BR-C Z1与染色质和Rpd3，Sin3A和SMRTER等重塑因子的关联的调控。在野生型SG中，这些因子与染色质结合，但在1（2）gl SG中，它们在细胞质和皮质核区（CNZ）中积累。类似的染色质排斥发生在发育迟缓的zip_E（br）/ +幼虫的SG中，或者可以通过高水平的nmMHC合成来实现。目前的数据表明p127〜（l（2）gl）和nmMHC调节BR-C Z1，Rpd3，Sin3A和SMRTER对染色质的访问。由于p127l〜（l（2）gl）与nmMHC之间的相互作用发生在细胞质中，我们建议这些核因子由p127〜（l（2）gl）处理，然后从p127〜（l（2）gl中释放出来通过nmMHC使它们与染色质结合。该过程可能构成基因调节的新机制，在缺乏p127〜l（2）gl）或过量的nmMHC的情况下，可能会导致基因表达模式的固定配置，从而阻止SG分化的进一步发展和程序性细胞死亡（PCD）。这种转录阻滞可能在l（2）gl组织的肿瘤转化中起关键作用。

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