Differential regulation of the duplicated fatty acid-binding protein genes in teleost fishes

1970年，Susumu Ohno提出了促进生命进化日益复杂的主要机制是基因复制。Allan Force和其他人在复制-退化-互补(DDC)模型中重新审视了这一观点，在DDC模型中，复制的基因通过亚功能化或新功能化保留在基因组中，在亚功能化中，祖先基因的功能在姐妹重复基因之间细分，而在新功能化中，其中一个复制基因获得新的功能。在这个模型中，保留重复基因的两个过程都是通过姐妹重复基因启动子中的调控元件的丢失或获得来实现的。然而，复制基因的共同命运是非功能化，即有害突变的积累导致功能衰退。这项研究计划的长期目标是检验DDC模型的假设，即复制的基因通过亚功能化或新功能化保留在基因组中。在这项发现拨款提案中提出的工作重点是调节细胞内脂结合蛋白(ILBP)基因的多基因家族的复制副本，该基因编码脂肪酸-(

In 1970, Susumu Ohno proposed the major mechanism that facilitates increasing complexity in the evolution of life is gene duplication. Allan Force and others revisited this idea in the Duplication-Degeneration-Complementation (DDC) model in which duplicated genes are retained in the genome either by subfunctionalization, where the functions of the ancestral gene are sub-divided between the sister duplicate genes, or by neofunctionalization, where one of the duplicates acquires a new function. In this model, both processes for retention of duplicated genes occur by either loss or gain of regulatory elements in the promoters of sister duplicate genes. The common fate of a duplicated gene, however, is nonfunctionalization, the accumulation of deleterious mutations resulting in functional decay. The long-term goal of this research program is to test the hypothesis of the DDC model that duplicated genes are retained in the genome by either sub- or neofunctionalization. The work proposed in this Discovery Grant proposal focusses on the regulation of the duplicated copies of the multigene family of the intracellular lipid-binding protein (iLBP) genes that code for the fatty acid- (