Regulation of the transposable element mariner
Regulation of the transposable element mariner
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DOI：
10.1023/a:1018333629222
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发表时间：
1997-01-01
期刊：
影响因子：
1.5
通讯作者：
Lozovskaya, ER
中科院分区：
文献类型：
--
作者：
Hartl, DL;Lohe, AR;Lozovskaya, ER
mariner/Tc1转座因子超家族广泛存在于动物基因组中，在昆虫中尤为普遍。它们的广泛分布是因为它们能够通过水平传播在宿主之间传播，也因为它们能够通过多个物种形成事件在基因组中持续存在。虽然我们对转位和切除的分子机制了解甚多，但对基因组内控制转位的机制了解甚少。鉴于人们对这些元素作为害虫种系转化和人类疾病媒介的极大兴趣，mariner/Tc1调控问题至关重要。几个潜在的重要调控机制已经确定在研究基因工程水手元素。一种机制是过度生产抑制，其中过度的野生型转座酶降低了目标元件的切除率。第二种机制是由某些突变的转座酶蛋白介导的，它可以拮抗野生型转座酶的活性。后一个过程可能有助于解释为什么自然界中绝大多数mle通过多次突变和最终的随机损失而经历“垂直失活”。另一种潜在的调节机制可能是由转座酶滴定的缺陷元件引起的，这些缺陷元件保留了它们的DNA结合位点和转座能力。也有证据表明，一些mariner/Tc1基因可以在一种混合型发育不良中被调动。
The mariner/Tc1 superfamily of transposable elements is widely distributed in animal genomes and is especially prevalent in insects. Their wide distribution results from their ability to be disseminated among hosts by horizontal transmission and also by their ability to persist in genomes through multiple speciation events. Although a great deal is known about the molecular mechanisms of transposition and excision, very little is known about the mechanisms by which transposition is controlled within genomes. The issue of mariner/Tc1 regulation is critical in view of the great interest in these elements as vectors for germline transformation of insect pests and vectors of human disease. Several potentially important regulatory mechanisms have been identified in studies of genetically engineered mariner elements. One mechanism is overproduction inhibition, in which excessive wild-type transposase reduces the rate of excision of a target element. A second mechanism is mediated by certain mutant transposase proteins, which antagonize the activity of the wild-type transposase. The latter process may help explain why the vast majority of MLEs in nature undergo 'vertical inactivation' by multiple mutations and, eventually, stochastic loss. Another potential mechanism of regulation may result from transposase titration by defective elements that retain their DNA binding sites and ability to transpose. There is also evidence that some mariner/Tc1 elements can be mobilized in a type of hybrid dysgenesis.