Hartl D L, Lohe A R, Lozovskaya E R
Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, Massachusetts 02138, USA.
Annu Rev Genet. 1997;31:337-58. doi: 10.1146/annurev.genet.31.1.337.
The mariner/Tc1 superfamily of transposable elements is one of the most diverse and widespread Class II transposable elements. Within the larger assemblage, the mariner-like elements (MLEs) and the Tc1-like elements (TLEs) are distinct families differing characteristically in the composition of the "D,D(35)E" cation-binding domain. Based on levels of sequence similarity, the elements in each family can be subdivided further into several smaller subfamilies. MLEs and TLEs both have an extraordinarily wide host range. They are abundant in insect genomes and other invertebrates and are found even in some vertebrate species including, in the case of mariner, humans, in which one element on chromosome 17p has been implicated as a hotspot of recombination. In spite of the extraordinary evolutionary success of the elements, virtually nothing is known about their mode of regulation within genomes. There is abundant evidence that the elements are disseminated to naive host genomes by horizontal transmission, and there is a substantial base of evidence for inference about the subsequent population dynamics. Studies of engineered mariner elements and induced mutations in the transposase have identified two mechanisms that may be operative in mariner regulation. One mechanism is overproduction inhibition, in which excessive wild-type transposase reduces the rate of excision of a target element. A second mechanism is dominant-negative complementation, in which certain mutant transposase proteins 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. There is also evidence that mariner/Tc1 elements can be mobilized in hybrid dysgenesis; in particular, certain dysgenic crosses in Drosophila virilis result in mobilization of a TLE designated Paris as well as the mobilization of other unrelated transposable elements.
转座元件的水手/Tc1超家族是最为多样且分布广泛的II类转座元件之一。在这个更大的组合中，类水手元件（MLEs）和类Tc1元件（TLEs）是不同的家族，其特征在于“D,D(35)E”阳离子结合结构域的组成不同。根据序列相似性水平，每个家族中的元件可进一步细分为几个较小的亚家族。MLEs和TLEs都具有极其广泛的宿主范围。它们在昆虫基因组和其他无脊椎动物中大量存在，甚至在一些脊椎动物物种中也能找到，就水手元件而言，在人类中也有发现，其中17号染色体短臂上的一个元件被认为是重组热点。尽管这些元件在进化上取得了非凡的成功，但关于它们在基因组中的调控模式几乎一无所知。有大量证据表明这些元件通过水平转移传播到新的宿主基因组中，并且有大量证据可用于推断其后续的种群动态。对工程化水手元件和转座酶诱导突变的研究已经确定了两种可能在水手元件调控中起作用的机制。一种机制是过量生产抑制，即过量的野生型转座酶会降低目标元件的切除率。另一种机制是显性负互补，即某些突变的转座酶蛋白会拮抗野生型转座酶的活性。后一过程可能有助于解释为什么自然界中绝大多数MLEs会通过多次突变经历“垂直失活”，并最终随机丢失。也有证据表明水手/Tc1元件可在杂种不育中被激活；特别是，果蝇中的某些不育杂交会导致一个名为巴黎的TLE以及其他不相关转座元件的激活。
