Comparative genomics of transcriptional control in the human malaria parasite Plasmodium falciparum
Comparative genomics of transcriptional control in the human malaria parasite Plasmodium falciparum
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DOI：
10.1101/gr.2218604
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发表时间：
2004-08-01
期刊：
影响因子：
7
通讯作者：
Ouzounis, CA
中科院分区：
文献类型：
--
作者：
Coulson, RMR;Hall, N;Ouzounis, CA
恶性疟原虫（Plasmodium falciparum）是最致命的人类疟疾形式，其生命周期需要在哺乳动物宿主和昆虫媒介中表达特定的蛋白质才能存活。为了确定在其生命周期中控制基因表达的过程的组成部分，用一组转录相关蛋白（TAPS）对疟疾基因组以及7个冠真核生物群基因组进行了查询。通过序列相似性聚类，结合隐马尔可夫模型搜索，共鉴定出156个恶性疟原虫的TAPS。这代表了通常在自由生活的真核生物基因组中发现的tap数量的三分之一。此外，恶性疟原虫基因组似乎包含少量序列，这些序列在自由生活的真核生物王国中高度保守且丰富，有助于基因特异性转录调控。然而，与其他真核生物基因组相比，ccch型锌指（在调节mRNA衰变和翻译率的蛋白质中常见）在恶性疟原虫基因组中最为丰富。这一观察结果，加上疟疾转录调节因子的缺乏，表明疟原虫蛋白水平主要由转录后机制决定。
The life cycle of the parasite Plasmodium falciparum, responsible for the most deadly form of human malaria, requires specialized protein expression for survival in the mammalian host and insect vector. To identify components of processes controlling gene expression during its life cycle, the malarial genome-along with seven crown eukaryote group genomes-was queried with a reference set of transcription-associated proteins (TAPS). Following clustering on the basis of sequence similarity of the TAPS with their homologs, and together with hidden Markov model profile searches, 156 P. falciparum TAPS were identified. This represents about a third of the number of TAPS usually found in the genome of a free-living eukaryote. Furthermore, the P. falciparum genome appears to contain a low number of sequences, which are highly conserved and abundant within the kingdoms of free-living eukaryotes, that contribute to gene-specific transcriptional regulation. However, in comparison with these other eukaryotic genomes, the CCCH-type zinc finger (common in proteins modulating mRNA decay and translation rates) was found to be the most abundant in the P. falciparum genome. This observation, together with the paucity of malarial transcriptional regulators identified, suggests Plasmodium protein levels are primarily determined by posttranscriptional mechanisms.