Department of Genetics; Davison Life Sciences Building; University of Georgia; Athens, Georgia USA.
Plant Signal Behav. 2008 May;3(5):333-6. doi: 10.4161/psb.3.5.5343.
The macroevolution of organs and tissues in higher plants and animals may have been contingent upon the expansion of numerous gene families encoding interacting proteins. For example, there are dozens of gene families encoding actin cytoskeletal proteins that elaborate intercellular structures influencing development. Once gene family members evolve compartmentalized expression, protein isovariants are free to coevolve new interacting partners that may be incompatible with other related protein networks. Ancient classes of actin isovariants and actin-binding proteins are clear examples of such coevolving networks. Ectopic expression and suppression studies were used to dissect these interactions. In higher plants, the ectopic expression of a reproductive actin isovariant in vegetative cell types causes aberrant reorganization of the F-actin cytoskeleton and bizarre development of most organs and tissues. In contrast, overexpression of vegetative actin in vegetative cell types has little effect. The extreme ectopic actin expression phenotypes are suppressed by the coectopic expression of reproductive profilin or actin depolymerizing factor (ADF/cofilin) isovariants, but not by the overexpression of vegetative profilin or ADF. These data provide evidence for the coevolution of organ-specific protein-protein interactions. Thus, understanding the contingent relationships between the evolution of organ-specific isovariant networks and organ origination may be key to explaining multicellular development.
高等植物和动物器官和组织的宏观进化可能取决于许多编码相互作用蛋白的基因家族的扩张。例如，有数十个基因家族编码肌动蛋白细胞骨架蛋白，这些蛋白详细阐述了影响发育的细胞间结构。一旦基因家族成员的表达发生区室化，蛋白质同工型就可以自由地共同进化新的相互作用伙伴，这些伙伴可能与其他相关的蛋白质网络不兼容。古老的肌动蛋白同工型和肌动蛋白结合蛋白类是这种共同进化网络的明显例子。通过异位表达和抑制研究来剖析这些相互作用。在高等植物中，生殖肌动蛋白同工型在营养细胞类型中的异位表达会导致 F-肌动蛋白细胞骨架的异常重组，并导致大多数器官和组织的发育异常。相比之下，在营养细胞类型中过表达营养肌动蛋白几乎没有影响。生殖肌动蛋白的极端异位表达表型被生殖前蛋白或肌动蛋白解聚因子（ADF/丝切蛋白）同工型的共异位表达所抑制，但不受营养前蛋白或 ADF 的过表达所抑制。这些数据为器官特异性蛋白质-蛋白质相互作用的共同进化提供了证据。因此，理解器官特异性同工型网络的进化与器官起源之间的偶然关系，可能是解释多细胞发育的关键。
