有性生殖和它所依赖的特殊细胞分裂,减数分裂,是生物过程,呈现出令人难以置信的进化保守性和分歧性。这种悖论的一个明显例子是进化上古老的PCH-2/HORMAD模块在减数分裂中的作用。一方面,复杂的,有时是完全不同的,当PCH-2和/或减数分裂HORMADS在不同模型系统中突变时观察到的减数分裂缺陷阻止了对其保守功能的直接表征。另一方面,这些功能变化证明了伴随这些因素参与的减数分裂过程的进化的令人印象深刻的分子重新布线。虽然在pch-2突变体中观察到的缺陷在不同的系统中似乎有所不同,在这次审查中,我认为PCH-2具有保守的减数分裂功能:协调减数分裂重组与突触,以确保适当的交叉数量和分布。Further,考虑到重组和突触事件在不同模型系统中如何被调节的戏剧性变化,PCH-2和减数分裂HORMAD功能的机制差异在生物学上有意义,保守的角色。
Sexual reproduction and the specialized cell division it relies upon, meiosis, are biological processes that present an incredible degree of both evolutionary conservation and divergence. One clear example of this paradox is the role of the evolutionarily ancient PCH-2/HORMAD module during meiosis. On one hand, the complex, and sometimes disparate, meiotic defects observed when PCH-2 and/or the meiotic HORMADS are mutated in different model systems have prevented a straightforward characterization of their conserved functions. On the other hand, these functional variations demonstrate the impressive molecular rewiring that accompanies evolution of the meiotic processes these factors are involved in. While the defects observed in pch-2 mutants appear to vary in different systems, in this review, I argue that PCH-2 has a conserved meiotic function: to coordinate meiotic recombination with synapsis to ensure an appropriate number and distribution of crossovers. Further, given the dramatic variation in how the events of recombination and synapsis are themselves regulated in different model systems, the mechanistic differences in PCH-2 and meiotic HORMAD function make biological sense when viewed as species-specific elaborations layered onto this fundamental, conserved role.