Ishihara Takaya, Ban-Ishihara Reiko, Maeda Maki, Matsunaga Yui, Ichimura Ayaka, Kyogoku Sachiko, Aoki Hiroki, Katada Shun, Nakada Kazuto, Nomura Masatoshi, Mizushima Noboru, Mihara Katsuyoshi, Ishihara Naotada
Department of Protein Biochemistry, Institute of Life Science, Kurume University, Kurume, Japan.
Department of Protein Biochemistry, Institute of Life Science, Kurume University, Kurume, Japan Department of Physiology and Cell Biology, Tokyo Medical and Dental University, Tokyo, Japan.
Mol Cell Biol. 2015 Jan;35(1):211-23. doi: 10.1128/MCB.01054-14. Epub 2014 Oct 27.
Mitochondria are dynamic organelles, and their fusion and fission regulate cellular signaling, development, and mitochondrial homeostasis, including mitochondrial DNA (mtDNA) distribution. Cardiac myocytes have a specialized cytoplasmic structure where large mitochondria are aligned into tightly packed myofibril bundles; however, recent studies have revealed that mitochondrial dynamics also plays an important role in the formation and maintenance of cardiomyocytes. Here, we precisely analyzed the role of mitochondrial fission in vivo. The mitochondrial fission GTPase, Drp1, is highly expressed in the developing neonatal heart, and muscle-specific Drp1 knockout (Drp1-KO) mice showed neonatal lethality due to dilated cardiomyopathy. The Drp1 ablation in heart and primary cultured cardiomyocytes resulted in severe mtDNA nucleoid clustering and led to mosaic deficiency of mitochondrial respiration. The functional and structural alteration of mitochondria also led to immature myofibril assembly and defective cardiomyocyte hypertrophy. Thus, the dynamics of mtDNA nucleoids regulated by mitochondrial fission is required for neonatal cardiomyocyte development by promoting homogeneous distribution of active mitochondria throughout the cardiomyocytes.
线粒体是动态细胞器,其融合与分裂调节细胞信号传导、发育以及线粒体稳态,包括线粒体DNA(mtDNA)分布。心肌细胞具有特殊的细胞质结构,其中大的线粒体排列成紧密堆积的肌原纤维束;然而,最近的研究表明,线粒体动力学在心肌细胞的形成和维持中也起着重要作用。在此,我们精确分析了线粒体分裂在体内的作用。线粒体分裂GTP酶Drp1在发育中的新生心脏中高度表达,肌肉特异性Drp1基因敲除(Drp1-KO)小鼠因扩张型心肌病而表现出新生期致死性。心脏和原代培养心肌细胞中的Drp1缺失导致严重的mtDNA核仁聚集,并导致线粒体呼吸的镶嵌性缺陷。线粒体的功能和结构改变还导致肌原纤维组装不成熟和心肌细胞肥大缺陷。因此,通过促进活性线粒体在整个心肌细胞中的均匀分布,由线粒体分裂调节的mtDNA核仁动力学是新生心肌细胞发育所必需的。