Evolution of dyskinetoplastic trypanosomes: how, and how often?
Evolution of dyskinetoplastic trypanosomes: how, and how often?
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运动障碍锥虫的进化：如何进化以及多久进化一次？
DOI：
10.1016/j.pt.2010.08.001
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发表时间：
2010
影响因子：
9.6
通讯作者：
Schnaufer,Achim
中科院分区：
文献类型：
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作者：
Schnaufer,Achim
传播T. Equiperdumand T.哺乳动物之间的伊文思病是机械发生的：前者是通过性传播，后者主要是通过叮咬苍蝇[4]。这使得它们的广泛的地理分布，而T。依赖采采蝇媒介的周期性发展的布氏锥虫仅限于撒哈拉以南非洲。t.布鲁氏菌kDNA由40 - 50个大环（相当于其他生物体中的mtDNA）和数千个异质性小环组成，这些小环编码编辑大环编码的mRNA所需的指导RNA（gRNA）[10]。不同的小环类编码不同的gRNA集合，并且T.布鲁氏菌kDNA估计含有300 - 400个类[1]。所有T。equiperdum和T.伊氏菌株显示出一定程度的kDNA损失，范围从具有完整大环但小环均质化的完整网络（见表）到完全kDNA损失[1，3]。最初，运动发育障碍和运动不能这两个术语描述的是完全缺乏kDNA结构的细胞。然而，即使在一些T.马毒菌株预期会导致完全编辑的mRNA完全丢失，cox 2和MURF2除外[3]。因此，最近的出版物，包括这一个，是指所有T。equiperdum和T. evansi菌株作为运动发育不良，而保留术语运动发育不全的菌株完全缺乏可检测的kDNA [1，3，12]。线粒体基因表达是T.布氏杆菌[1]，并且在运动发育障碍形式中对其损失的补偿被认为涉及线粒体ATP酶复合物的核编码γ亚基中的突变（见表）[3，13]，这一假设有待实验证实。
Transmission of T. equiperdumand T. evansi between mammals occurs mechanically: venereally in case of the former and mostly via biting flies in case of the latter [4]. This permits their wide geographical distribution, while T. brucei, dependent on cyclical development in the tsetse vector, is restricted to sub-Saharan Africa. T. brucei kDNA consists of 40–50 maxicircles, the equivalent of mtDNA in other organisms, and thousands of heterogeneous minicircles, which encode the guide RNAs (gRNAs) required for editing of maxicircle-encoded mRNAs [10]. Different minicircle classes encode different gRNA sets, and T. brucei kDNA contains an estimated 300–400 classes [1]. All T. equiperdum and T. evansi strains show some degree of kDNA loss, ranging from intact networks with complete maxicircles, but minicircle homogenization (see table), to complete kDNA loss [1, 3]. Originally, the terms dyskinetoplastic and akinetoplastic described cells completely lacking a kDNA structure. However, the minicircle homogenization in even the mild forms of kDNA loss in some T. equiperdum strains is expected to result in complete loss of fully edited mRNAs, except cox2 and MURF2 [3]. Therefore, most recent publications, including this one, refer to all T. equiperdum and T. evansi strains as dyskinetoplastic while reserving the term akinetoplastic for strains completely lacking detectable kDNA [1, 3, 12]. Mitochondrial gene expression is essential in T. brucei [1], and the compensation for its loss in dyskinetoplastic forms was suggested to involve mutations in the nuclearly encoded γ subunit of the mitochondrial ATPase complex (see table)[3, 13], a hypothesis that awaits experimental confirmation.