Response characteristics of the mitochondrial DNA genome in developmental health and disease.
Response characteristics of the mitochondrial DNA genome in developmental health and disease.
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线粒体 DNA 基因组在发育健康和疾病中的反应特征。
DOI：
10.1002/bdrc.20028
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Green,MaiaL
中科院分区：
文献类型：
--
作者：
Knudsen,ThomasB;Green,MaiaL
本文综述了哺乳动物发育过程中的线粒体生物学，特别是线粒体DNA基因组表达调控中从细胞核到线粒体的信息传递动力学，以及线粒体作为对环境的适应性反应向细胞核的反向信号传递。最近的研究数据表明，胚胎细胞对氧合反应的能力涉及影响产前生长/发育和产后生长/功能的因素之间的权衡。例如，线虫中的线粒体DNA复制和代谢设定点可以通过生命早期的线粒体活性来确定。线粒体药物PK 11195是外周苯二氮卓受体的配体，在小鼠的几种发育环境中具有抗致畸和抗病作用。大鼠生命早期的蛋白质营养不良可以编程成年组织中的线粒体DNA水平，在人类中，流行病学数据表明胎儿生长受损与胰岛素抵抗之间存在关联。总而言之，这些发现提出了一个挑衅性的假设，即生命早期线粒体状态的环境编程可能与成年期出现的疾病有关。影响线粒体功能的遗传缺陷可能直接涉及线粒体DNA基因组（母系遗传）或通过核编码的线粒体蛋白间接涉及线粒体DNA基因组（孟德尔遗传）。在越来越多的情况下，线粒体DNA的耗尽或缺失被认为是继发于影响线粒体DNA复制，表达或稳定性的关键核编码线粒体蛋白的突变。这些基因组间调控的缺陷可能会破坏最终调节线粒体DNA完整性和拷贝数的信号的正常串扰或结构区室化，导致线粒体DNA的耗尽。出生缺陷研究（C部分）72：313-329，2005年。© 2005 Wiley利斯公司
This review focuses on mitochondrial biology in mammalian development; specifically, the dynamics of information transfer from nucleus to mitochondrion in the regulation of mitochondrial DNA genomic expression, and the reverse signaling of mitochondrion to nucleus as an adaptive response to the environment. Data from recent studies suggest that the capacity of embryonic cells to react to oxygenation involves a tradeoff between factors that influence prenatal growth/development and postnatal growth/function. For example, mitochondrial DNA replication and metabolic set points in nematodes may be determined by mitochondrial activity early in life. The mitochondrial drug PK11195, a ligand of the peripheral benzodiazepine receptor, has antiteratogenic and antidisease action in several developmental contexts in mice. Protein malnutrition during early life in rats can program mitochondrial DNA levels in adult tissues and, in humans, epidemiological data suggest an association between impaired fetal growth and insulin resistance. Taken together, these findings raise the provocative hypothesis that environmental programming of mitochondrial status during early life may be linked with diseases that manifest during adulthood. Genetic defects that affect mitochondrial function may involve the mitochondrial DNA genome directly (maternal inheritance) or indirectly (Mendelian inheritance) through nuclear‐coded mitochondrial proteins. In a growing number of cases, the depletion of, or deletion in, mitochondrial DNA is seen to be secondary to mutation of key nuclear‐coded mitochondrial proteins that affect mitochondrial DNA replication, expression, or stability. These defects of intergenomic regulation may disrupt the normal cross‐talk or structural compartmentation of signals that ultimately regulate mitochondrial DNA integrity and copy number, leading to depletion of mitochondrial DNA. Birth Defects Research (Part C) 72:313–329, 2005. © 2005 Wiley‐Liss, Inc.
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影响因子：
2.6
作者：
Mitsuo V. Kato
通讯作者：
Mitsuo V. Kato
DOI：
10.1016/s0021-9258(19)50527-0
发表时间：
1992-04
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Ching Man A Chau;M. J. Evans;R. Scarpulla
通讯作者：
Ching Man A Chau;M. J. Evans;R. Scarpulla
影响因子：
6.1
作者：
E. Shoubridge
通讯作者：
E. Shoubridge
良恶性乳腺组织中线粒体基因细胞色素氧化酶ii的差异表达
DOI：
10.1002/path.1711680203
发表时间：
1992
期刊：
The Journal of Pathology
影响因子：
--
作者：
M. Sharp;S. Adams;R. Walker;W. J. Brammar;J. Varley
通讯作者：
J. Varley
影响因子：
2.7
作者：
J. Weitzel;K. Iwen;H. Seitz
通讯作者：
J. Weitzel;K. Iwen;H. Seitz