The role of mitochondrial function in the oocyte and embryo

被引:398
作者
Dumollard, Remi
Duchen, Michael
Carroll, John
机构
[1] UCL, Dept Physiol, London WC1E 6BT, England
[2] UPMC, CNRS, UMR 7009, Lab Biol Dev,Stn Zool,Observ, F-06230 Villefranche Sur Mer, France
来源
MITOCHONDRION IN THE GERMLINE AND EARLY DEVELOPMENT | 2007年 / 77卷
基金
英国医学研究理事会; 英国惠康基金;
关键词
D O I
10.1016/S0070-2153(06)77002-8
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Mitochondria have long been known to be the powerhouses of the cell but they also contribute to redox and Ca(2+) homeostasis, provide intermediary metabolites and store proapoptotic factors. Mitochondria have a unique behavior during development. They are maternally transmitted with little (if any) paternal contribution, and they originate from a restricted founder population, which is amplified during oogenesis. Then, having established the full complement of mitochondria in the fully grown oocyte, there is no further increase of the mitochondrial population during early development. The localization of mitochondria in the egg, during maturation and their segregation to blastomeres in the cleaving embryo are strictly regulated. Gradients in the distribution of mitochondria present in the egg have the potential to give rise to blastomeres receiving different numbers of mitochondria. Such maternally inherited differences in mitochondrial distribution are thought to play roles in defining the long-term viability of the blastomere in some cases and embryonic axes and patterning in others. Mitochondria may also regulate development by a number of other means, including modulatmig Ca(2+) signaling, and the production of ATP, reactive oxygen species, and intermediary metabolites. If the participation of mitochondria in the regulation of sperm-triggered Ca(2+) oscillations is now well established, the role of other properties of mitochondrial function during development remain largely unexplored probably due to the difficulty of accessing the mitochondrial compartment in an embryo. Maintaining a functional complement of maternally derived mitochondria is vital for the early embryo. Mitochondrial dysfunction may not only compromise developmental processes but also trigger apoptosis in the embryo. This dual role for mitochondria (to maintain life or to commit to cell death) may well represent a quality control system in the early embryo that will determine whether the embryo proceeds further into development or is quickly eliminated. (c) 2007. Elsevier Inc.
引用
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页码:21 / +
页数:32
相关论文
共 147 条
  • [71] Current concepts in Bcl-2 family member regulation of female germ cell development and survival
    Kim, MR
    Tilly, JL
    [J]. BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2004, 1644 (2-3): : 205 - 210
  • [72] The Balbiani body and germ cell determinants: 150 years later
    Kloc, M
    Bilinski, S
    Etkin, LD
    [J]. CURRENT TOPICS IN DEVELOPMENTAL BIOLOGY, VOL 59, 2004, 59 : 1 - +
  • [73] Mitochondrial control of apoptosis: an introduction
    Kroemer, G
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2003, 304 (03) : 433 - 435
  • [74] Functional imaging of mitochondria in saponin-permeabilized mice muscle fibers
    Kuznetsov, AV
    Mayboroda, O
    Kunz, D
    Winkler, K
    Schubert, W
    Kunz, WS
    [J]. JOURNAL OF CELL BIOLOGY, 1998, 140 (05) : 1091 - 1099
  • [75] Mitochondrial malate-aspartate shuttle regulates mouse embryo nutrient consumption
    Lane, M
    Gardner, DK
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (18) : 18361 - 18367
  • [76] Mitochondrial transcription factor A is necessary for mtDNA maintenance and embryogenesis in mice
    Larsson, NG
    Wang, JM
    Wilhelmsson, H
    Oldfors, A
    Rustin, P
    Lewandoski, M
    Barsh, GS
    Clayton, DA
    [J]. NATURE GENETICS, 1998, 18 (03) : 231 - 236
  • [77] Quiet please, do not disturb: a hypothesis of embryo metabolism and viability
    Leese, HJ
    [J]. BIOESSAYS, 2002, 24 (09) : 845 - 849
  • [78] Increased cell death in mouse blastocysts exposed to high D-glucose in vitro: implications of an oxidative stress and alterations in glucose metabolism
    Leunda-Casi, A
    Genicot, G
    Donnay, I
    Pampfer, S
    De Hertogh, R
    [J]. DIABETOLOGIA, 2002, 45 (04) : 571 - 579
  • [79] Levasseur M, 2000, DEVELOPMENT, V127, P631
  • [80] Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis
    Li, K
    Li, YC
    Shelton, JM
    Richardson, JA
    Spencer, E
    Chen, ZJ
    Wang, XD
    Williams, RS
    [J]. CELL, 2000, 101 (04) : 389 - 399