Mitochondrial DNA turnover occurs during preimplantation development and can be modulated by environmental factors

被引:91
作者
McConnell, JML [1 ]
Petrie, L [1 ]
机构
[1] Rowett Res Inst, Aberdeen AB21 9SB, Scotland
关键词
disease; fetal programming; in-vitro culture; mtDNA replication; preimplantation embryos;
D O I
10.1016/S1472-6483(10)61277-1
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
There is increasing evidence in humans that abnormal mitochondrial DNA (mtDNA) is associated, with common degenerative disorders of the twenty-first century. MtDNA is exclusively female in origin and abnormalities in mtDNA can either be inherited, or generated de novo by adverse environmental factors that disturb mitochondrial DNA synthesis or destabilize mtDNA. The preimplantation period of development in mammals was thought to be relatively immune from environmentally induced changes to mtDNA, since no replication of mtDNA was thought to occur at this stage. This study demonstrates that there is a very short period of mtDNA synthesis immediately after fertilization, which can be affected by environmental stress. Adverse culture conditions during this phase of development could therefore alter the mitochondrial genome, with possible long-term consequences for the health of the offspring. The findings have relevance for all assisted reproduction programmes and for the rapidly emerging field of stem cell technologies.
引用
收藏
页码:418 / 424
页数:7
相关论文
共 45 条
[1]   Mitochondria-to-nucleus stress signaling induces phenotypic changes, tumor progression and cell invasion [J].
Amuthan, G ;
Biswas, G ;
Zhang, SY ;
Klein-Szanto, A ;
Vijayasarathy, C ;
Avadhani, NG .
EMBO JOURNAL, 2001, 20 (08) :1910-1920
[2]  
ATTARDI G, 1988, ANNU REV CELL BIOL, V4, P289, DOI 10.1146/annurev.cb.04.110188.001445
[3]   Mitochondrial integrity and function in atherogenesis [J].
Ballinger, SW ;
Patterson, C ;
Knight-Lozano, CA ;
Burow, DL ;
Conklin, CA ;
Hu, ZY ;
Reuf, J ;
Horaist, C ;
Lebovitz, R ;
Hunter, GC ;
McIntyre, K ;
Runge, MS .
CIRCULATION, 2002, 106 (05) :544-549
[4]   Mitochondrial DNA rearrangements in human oocytes and embryos [J].
Barritt, JA ;
Brenner, CA ;
Cohen, J ;
Matt, DW .
MOLECULAR HUMAN REPRODUCTION, 1999, 5 (10) :927-933
[5]   Diabetes and nutrition: The mitochondrial part [J].
Berdanier, CD .
JOURNAL OF NUTRITION, 2001, 131 (02) :344S-353S
[6]  
BLANCATO JK, 1990, INT J FERTIL, V35, P171
[7]   Concluding remarks: The mitochondrial DNA replication bubble has not burst [J].
Bogenhagen, DF ;
Clayton, DA .
TRENDS IN BIOCHEMICAL SCIENCES, 2003, 28 (08) :404-405
[8]   Accumulation of mitochondrial DNA mutations in ageing, cancer, and mitochondrial disease: is there a common mechanism? [J].
Chinnery, PF ;
Samuels, DC ;
Elson, J ;
Turnbull, DM .
LANCET, 2002, 360 (9342) :1323-1325
[9]   In vitro methylation of nuclear respiratory factor-1 binding site suppresses the promoter activity of mitochondrial transcription factor A [J].
Choi, YS ;
Kim, S ;
Lee, HK ;
Lee, KU ;
Pak, YK .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2004, 314 (01) :118-122
[10]  
Cummins J M, 2002, Reprod Biomed Online, V4, P176