Imagawa Masayoshi
Department of Molecular Biology, Graduate School of Pharmaceutical Sciences, Nagoya City University.
Yakugaku Zasshi. 2016;136(4):649-58. doi: 10.1248/yakushi.15-00260.
Obesity is a major risk factor for diabetes, hypertension, hyperlipidemia, and arteriosclerosis. Although the middle and late stages of adipocyte differentiation are well characterized, the earliest step in the differentiation process has remained largely unknown. We isolated 102 genes expressed at the beginning of the differentiation of a mouse preadipocyte cell line, 3T3-L1 cells. Because approximately half of these genes were unknown, we named them factor for adipocyte differentiation (fad) genes. I first show how these genes regulate the early stage of adipocyte differentiation. We next generated fad104-deficient mice, and demonstrated that fad104-deficient mice died due to cyanosis-associated lung dysplasia with atelectasis. We also found that fad104 positively regulated adipocyte differentiation and negatively regulated osteoblast differentiation. We then demonstrated that fad24-knockdown inhibited mitotic clonal expansion (MCE) and that FAD24 contributed to the regulation of DNA replication by recruiting histone acetyltransferase binding to ORC1 (HBO1) to DNA replication origins. In vitro culture experiments revealed that fad24-null embryos developed normally to the morula stage, but acquired growth defects in subsequent stages. These results strongly suggest that fad24 is essential for pre-implantation in embryonic development, particularly for progression to the blastocyst stage. These findings together indicate that both fad104 and fad24 contribute not only to adipogenesis but also to other physiological events. The multi-functional roles of these genes are discussed.
肥胖是糖尿病、高血压、高脂血症和动脉硬化的主要危险因素。尽管脂肪细胞分化的中晚期已得到充分表征,但分化过程的最早步骤在很大程度上仍不清楚。我们分离出了在小鼠前脂肪细胞系3T3-L1细胞分化开始时表达的102个基因。由于这些基因中约有一半是未知的,我们将它们命名为脂肪细胞分化因子(fad)基因。我首先展示这些基因如何调节脂肪细胞分化的早期阶段。接下来,我们培育出了fad104基因缺失的小鼠,并证明fad104基因缺失的小鼠因伴有肺不张的紫绀相关性肺发育不良而死亡。我们还发现fad104对脂肪细胞分化起正向调节作用,对成骨细胞分化起负向调节作用。然后,我们证明fad24基因敲低会抑制有丝分裂克隆扩增(MCE),并且FAD24通过招募与ORC1结合的组蛋白乙酰转移酶(HBO1)到DNA复制起点来促进DNA复制的调控。体外培养实验表明,fad24基因缺失的胚胎在桑椹胚阶段发育正常,但在随后的阶段出现生长缺陷。这些结果强烈表明fad24对胚胎发育的着床前阶段至关重要,尤其是对发育到囊胚阶段。这些发现共同表明,fad104和fad24不仅对脂肪生成有作用,而且对其他生理事件也有作用。本文讨论了这些基因的多功能作用。