Allen J F
Department of Plant Cell Biology, Lund University, Sweden.
J Theor Biol. 1996 May 21;180(2):135-40. doi: 10.1006/jtbi.1996.0089.
An hypothesis is presented by which gamete specialization resolves a conflict between the function and replication of mitochondria. The function of mitochondria is to synthesize ATP by oxidative phosphorylation, which is coupled to respiratory electron transport. This requires a mitochondrial genetic system. However, "incorrect" electron transfers produce free radicals that cause mutation, and the frequency of these events is increased by mutation. Mitochondrial function is therefore detrimental to the fidelity of mitochondrial replication. Damage to somatic mitochondrial DNA may accumulate within, and indeed determine, the life span of individual organisms. Motility of one gamete is required for fertilization, and requires ATP. It is proposed that male gametes maximize energy production for motility by sacrificing mitochondrial DNA to electron transfer and its mutagenic by-products, while female gametes, which are non-motile, repress mitochondrial oxidative phosphorylation, thus protecting mitochondrial DNA for faithful transmission between generations. Male gametes then make no contribution to the mitochondrial genome of the zygote: mitochondria are maternally inherited. This testable hypothesis may help to explain the evolution of separate sexes and a number of their characteristics. Maternal inheritance of chloroplasts may be explained in a similar way, and contribute to the maintenance of separate sexes in plants.
本文提出了一个假说，即配子特化解决了线粒体功能与复制之间的冲突。线粒体的功能是通过氧化磷酸化合成ATP，这与呼吸电子传递相偶联。这需要一个线粒体遗传系统。然而，“错误”的电子传递会产生导致突变的自由基，并且这些事件的频率会因突变而增加。因此，线粒体功能对线粒体复制的保真度是有害的。体细胞线粒体DNA的损伤可能在个体生物的寿命期间累积，甚至决定其寿命。受精需要一个配子具有运动能力，而这需要ATP。有人提出，雄配子通过将线粒体DNA牺牲给电子传递及其诱变副产物来最大化用于运动的能量产生，而不具运动能力的雌配子则抑制线粒体氧化磷酸化，从而保护线粒体DNA以便在世代间忠实地传递。那么雄配子对合子的线粒体基因组没有贡献：线粒体是母系遗传的。这个可检验的假说可能有助于解释两性分离及其一些特征的进化。叶绿体的母系遗传可能也可以用类似的方式来解释，并有助于维持植物中的两性分离。
