Mitochondrial recombination? (continued)
Mitochondrial recombination? (continued)
复制标题
线粒体重组？
DOI：
10.1126/science.285.5429.835g
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发表时间：
1999
期刊：
影响因子：
56.9
通讯作者：
Kaestle Fa
中科院分区：
文献类型：
--
作者：
Merriweather Da;Kaestle Fa
在她的文章“线粒体时钟能保持时间吗？”(News 3月5日，第1435页），伊夫林·施特劳斯参考E. Hagelberg等人(1)为人类线粒体DNA（mtDNA）重组提供了证据。这些作者认为，在恩古纳岛民的研究人群中，在所有三个单倍群中发现的基因突变（HVS I的16076位）最好解释为“线粒体DNA的父系泄漏和随后的重组”（1，第490页）。他们还认为，先前发现的“高变”mtDNA位点实际上是多个单倍群中存在的古老替换，是与父系mtDNA重组的结果，我们同意Peter Arctander（Letters，25 June，p. 2090）的观点，即这些都是不可能的。据我们所知，人类中的父系mtDNA传播尚未得到证实。在小鼠种间杂交中，父本mtDNA在早期胚胎发生中明显消失（2）;“泄漏仅限于第一次种间杂交，不会溢出到随后的回交”（3，第885页）。
In her article “Can mitochondrial clocks keep time?”(News of the Week, 5 Mar., p. 1435), Evelyn Strauss references E. Hagelberg et al.(1) as providing evidence for recombination in human mitochondrial DNA (mtDNA). Those authors suggest that a genetic mutation (at 16076 in HVS I) found in all three haplogroups among a study population of Nguna islanders is best explained “by paternal leakage of mtDNA and subsequent recombination”(1, p. 490). They also suggest that previously identified “hypervariable” mtDNA sites are actually ancient substitutions present in multiple haplogroups that result from recombination with paternal mtDNA.We agree with Peter Arctander (Letters, 25 June, p. 2090) that these are improbable suggestions. Paternal mtDNA transmission in humans has not, to our knowledge, been confirmed. Paternal mtDNA in interspecific crosses of mice is apparently eliminated in early embryogenesis (2);“leakage [is] restricted to the first interspecific cross, and it did not spill over to subsequent backcrossing”(3, p. 885).