A test of the role of meiotic drive in fixing a pericentric inversion.
A test of the role of meiotic drive in fixing a pericentric inversion.
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减数分裂驱动在修复中心周倒位中的作用的测试。
DOI：
10.1093/genetics/123.1.241
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发表时间：
1989
期刊：
影响因子：
3.3
通讯作者：
Coyne,JA
中科院分区：
文献类型：
--
作者：
Coyne,JA
一些染色体重排，包括易位和着丝粒周围倒位，使它们的杂合携带者变得半静止，因为排列内的重组产生了非整倍体配子。这种杂合劣势(显性不足)在种群中产生了不稳定的平衡，因此新出现的重排通常会很快被消除。这些核型的劣势的其他证据来自果蝇物种，它们在着丝粒旁倒位(不是欠显性的)方面经常是多态的，但在着丝粒周围倒位和易位方面几乎从来没有多态。然而，近缘关系密切的果蝇物种往往通过固定的着丝点周围倒置和易位而不同(斯通1955)。这意味着，当许多个体是杂合子时，一些进化谱系经历了一个不适应阶段。很难解释这些转变，因为它们会遭到自然选择的反对。这个问题的通常解决方案是遗传漂移或近亲交配，这可以在面临选择时修复不显性的染色体排列。然而，这通常需要非常少的人口(兰德1979；海德里克198 L)，并寻求其他解释。一种建议是，这种排列可能与导致正减数分裂驱动的等位基因有关，如果足够强，这种力量可以引起固定(Hiraizumi，Sandler和Crow 1960；White 1978；Hedrick 198 1)。这一解释很难检验。因为减数分裂驱动只出现在杂合子中，所以当驱动等位基因固定时，无论它是否与新的染色体排列相关联，它都变得不可检测。有几种方法可以克服这个问题。例如，人们可以确定新的染色体排列是否在杂合子中显示异常分离。尽管这看起来似乎不太可能，但在醋酸模中新出现的杂合子易位和倒位(Wilby和Parker 1988)中，有六个描述了扭曲的分离比，尽管这些作者并不排除生活力选择是偏离孟德尔比的原因。因此，这种重排有可能以非孟德尔式的方式分离，但这并不能告诉我们这种分离是否导致了新核型的进化固定。或者，可以通过杂交相关物种和检查种间杂种的分离比率来检测固定的减数分裂驱动等位基因。这些都是-
Some chromosome rearrangements, including translocations and pericentric inversions, make their heterozygous carriers semisterile because recombination within the arrangement yields aneuploid gametes. This heterozygous disadvantage (underdominance) produces an unstable equilibrium in a population, so that a newly arising rearrangement is usually eliminated quickly. Other evidence for the disadvantage of these karyotypes comes from Drosophila species, which are frequently polymorphic for paracentric inversions (these are not underdominant), but almost never polymorphic for pericentric inversions and translocations. Closely related Drosophila species, however, often differ by fixed pericentric inversions and translocations (STONE 1955). This implies that some evolutionary lineages passed through a maladaptive phase when many individuals were heterozygous. It is difficult to explain these transitions because they would be opposed by natural selection. The usual solution to this problem invokes genetic drift or inbreeding, which can fix underdominant chromosome arrangements in the face of selection. This often requires very small populations, however (LANDE 1979; HEDRICK 198 l), and other explanations have been sought. One suggestion is that such arrangements could be linked to alleles causing positive meiotic drive, a force that can cause fixation if sufficiently strong (HIRAIZUMI, SANDLER and CROW 1960; WHITE 1978; HEDRICK 198 1). This explanation is difficult to test. Because meiotic drive is seen only in heterozygotes, a drive allele becomes undetectable when it is fixed regardless of whether it is linked to a new chromosome arrangement. There are several ways to overcome this problem. One could determine, for example, whether new chromosome arrangements show abnormal segregation in heterozygotes. Although this may seem unlikely, distorted segregation ratios were described for six out of ten newly arising heterozygous translocations and inversions in Rumex acetosa (WILBY and PARKER 1988), although these authors did not rule out viability selection as a cause of the deviations from Mendelian ratios. It is thus possible for such rearrangements to segregate in a non-Mendelian way, but this does not tell us whether such segregation caused the evolutionary fixation of new karyotypes. Alternatively, fixed meiotic drive alleles might be detected by crossing related species and examining segregation ratios in interspecific hybrids. These hy-
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DOI：
--
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期刊：
Surgery, gynecology & obstetrics
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