Zuckerkandl E
Institute of Molecular Medical Sciences, P.O. Box 20452, Stanford, CA 94309, USA.
J Mol Evol. 2001 Oct-Nov;53(4-5):539-54. doi: 10.1007/s002390010244.
A two-step process, previously considered in the literature, and here named coadaptational drive, is deemed to be largely responsible for both increases in the complexity of transcriptional control and increases in the total gene number, along lines of descent leading to more complex organisms. Coadaptational drive consists in a succession of modifications in the interaction among informational macromolecules, namely, structural decay spread by genetic drift and repair spread by selection. Increased genetic complexity, drawing on the opportunities offered by gene duplication, may be considered to be a secondary effect of such processes of decay and repair. The evolution toward higher regulatory complexity is thus considered to be obligatorily founded in part on random genetic drift. Increases in this complexity would represent primarily a trend intrinsic to the internal molecular environment, with the external environment having only to concur. Direct selection of mutations that increase complexity without the intervention of a phase of genetic drift is acknowledged likely to be a significant process as well, but it is claimed that a sequence of events of direct selection cannot be unlimited and will eventually stall, and that the roots of such a sequence ultimately are to be traced to an episode of coadaptational drive. Controller gene diseases, mostly mild, therefore seem to be essential for the evolution of increased biological complexity. The attempt is made to show or to confirm that (i) a conservative force (repair) provides a mechanism for the generation of novelty, (ii) a prominent part of selection, counterpart to Darwinian selection, originates from the internal environment and derives from the mechanics of genomic processes, and (iii) this selection is at times directional and leads to increases in complexity.
文献中先前曾考虑过的一个两步过程，在此称为协同适应驱动，被认为在很大程度上导致了转录控制复杂性的增加以及基因总数的增加，这是沿着导致更复杂生物体的谱系发生的。协同适应驱动包括信息大分子之间相互作用的一系列修饰，即由遗传漂变传播的结构衰变和由选择传播的修复。利用基因复制提供的机会增加遗传复杂性，可被视为这种衰变和修复过程的次要效应。因此，向更高调节复杂性的进化被认为部分必然基于随机遗传漂变。这种复杂性的增加将主要代表内部分子环境固有的一种趋势，外部环境只需协同作用。在没有遗传漂变阶段干预的情况下直接选择增加复杂性的突变也被认为可能是一个重要过程，但有人声称直接选择的一系列事件不可能是无限制的，最终会停滞，并且这种序列的根源最终可追溯到一次协同适应驱动事件。因此，大多数为轻度的调控基因疾病似乎对于生物复杂性增加的进化至关重要。本文试图表明或确认：（i）一种保守力量（修复）为新事物的产生提供了一种机制；（ii）与达尔文选择相对应的选择的一个突出部分源自内部环境，并源于基因组过程的机制；（iii）这种选择有时是定向的，会导致复杂性增加。
