Mutation analysis of Drosophila dikar/CG32394, homologue of the chromatin-remodelling gene CECR2.
Mutation analysis of Drosophila dikar/CG32394, homologue of the chromatin-remodelling gene CECR2.
复制标题
果蝇 dikar/CG32394（染色质重塑基因 CECR2 的同源物）的突变分析。
DOI：
10.1139/g07-050
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发表时间：
2007
期刊：
影响因子：
3.1
通讯作者：
McDermid,HeatherE
中科院分区：
文献类型：
--
作者：
Keuling,Angela;Yang,Fang;Hanna,Scott;Wang,Huaien;Tully,Tim;Burnham,Amanda;Locke,John;McDermid,HeatherE
哺乳动物CECR 2蛋白含有高度保守的布罗莫结构域，并与ISWI同源物SNF 2L形成染色质重塑复合物。小鼠CECR 2同源物突变导致神经管缺陷。在这里，我们描述了果蝇同源的CECR 2的特性。dikar和CG 32394最初被注释为2个基因，现在似乎编码与CECR 2同源的longdikar/CG 32394转录物和缺失溴结构域的截短转录物。这种截短的转录物可能对双翅目是特异性的，因为它是从几种其他双翅目物种的基因组序列预测的，但它在蜜蜂中没有预测到，意大利蜜蜂，它在哺乳动物中没有发现。产生了5种不同的P元件介导的果蝇adikar基因5′端缺失。所有突变体均为同源活的，并且进一步检查的3个突变体显示出dikar/CG 32394的持续转录，尽管是异常的。在以前的研究中，adikarinsertion突变与长期记忆缺陷有关。然而，这里测试的2个缺失突变体显示正常的长期记忆，这表明与dikar P元件插入相关的记忆缺陷不是由于dikar的破坏。Iswianddikarmutations之间没有遗传相互作用。因此，这项研究表明，缺乏一个可见的表型indikar突变体是由于补偿的第二个基因，可能acf 1。
The mammalian CECR2 protein contains a highly conserved bromodomain and forms a chromatin-remodelling complex with the ISWI homologue SNF2L. Mutation of the mouseCECR2homologue results in a neural tube defect. Here we describe the characterization of the Drosophila melanogaster homologue ofCECR2. Originally annotated as 2 genes,dikarand CG32394 now appear to encode both a longdikar/CG32394 transcript homologous toCECR2and a truncated transcript missing the bromodomain. This truncated transcript may be specific to Diptera, as it is predicted from the genomic sequences of several other dipteran species but it is not predicted in the honey bee, Apis mellifera, and it is not found in mammals. Five different P element–mediated 5′ deletions of theDrosophiladikargene were generated. All mutants were homozygous-viable and the 3 mutants examined further displayed continued, albeit aberrant, transcription ofdikar/CG32394. In a previous study, adikarinsertion mutation was associated with long-term memory deficits. However, the 2 deletion mutants tested here showed normal long-term memory, suggesting that the memory deficit associated with thedikarP element insertion is not due to disruption ofdikar. No genetic interaction was seen betweenIswianddikarmutations. This study therefore suggests that the lack of a visible phenotype indikarmutants is due to compensation by a second gene, possiblyacf1.