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
收藏
页码:21 / +
页数:32
相关论文
共 147 条
  • [11] Charles Manning Child (1869-1954): The past, present, and future of metabolic signaling
    Blackstone, NW
    [J]. JOURNAL OF EXPERIMENTAL ZOOLOGY PART B-MOLECULAR AND DEVELOPMENTAL EVOLUTION, 2006, 306B (01) : 1 - 7
  • [12] STUDIES ON DEVELOPMENT OF MOUSE EMBRYOS IN VITRO .2. EFFECT OF ENERGY SOURCE
    BRINSTER, RL
    [J]. JOURNAL OF EXPERIMENTAL ZOOLOGY, 1965, 158 (01): : 59 - &
  • [13] Calcium, ATP, and ROS: a mitochondrial love-hate triangle
    Brookes, PS
    Yoon, YS
    Robotham, JL
    Anders, MW
    Sheu, SS
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2004, 287 (04): : C817 - C833
  • [14] Inhibition of NF-κB activity results in disruption of the apical ectodermal ridge and aberrant limb morphogenesis
    Bushdid, PB
    Brantley, DM
    Yull, FE
    Blaeuer, GL
    Hoffman, LH
    Niswander, L
    Kerr, LD
    [J]. NATURE, 1998, 392 (6676) : 615 - 618
  • [15] POLARIZATION OF MITOCHONDRIA IN THE UNFERTILIZED MOUSE OOCYTE
    CALARCO, PG
    [J]. DEVELOPMENTAL GENETICS, 1995, 16 (01): : 36 - 43
  • [16] Mitochondrial production of oxidants is necessary for physiological calcium oscillations
    Camello-Almaraz, MC
    Pozo, MJ
    Murphy, MP
    Camello, PJ
    [J]. JOURNAL OF CELLULAR PHYSIOLOGY, 2006, 206 (02) : 487 - 494
  • [17] Ca2+ oscillations stimulate an ATP increase during fertilization of mouse eggs
    Campbell, Karen
    Swann, Karl
    [J]. DEVELOPMENTAL BIOLOGY, 2006, 298 (01) : 225 - 233
  • [18] Apaf1 in developmental apoptosis and cancer:: how many ways to die?
    Cecconi, F
    Gruss, P
    [J]. CELLULAR AND MOLECULAR LIFE SCIENCES, 2001, 58 (11) : 1688 - 1697
  • [19] Chambon JP, 2002, DEVELOPMENT, V129, P3105
  • [20] CHASE JW, 1972, DEV BIOL, V27, P504, DOI 10.1016/0012-1606(72)90189-3