Literature DB >> 17222699

The role of mitochondrial function in the oocyte and embryo.

Rémi Dumollard1, Michael Duchen, John Carroll.   

Abstract

Mitochondria have long been known to be the powerhouses of the cell but they also contribute to redox and Ca2+ 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 modulating Ca2+ signaling, and the production of ATP, reactive oxygen species, and intermediary metabolites. If the participation of mitochondria in the regulation of sperm-triggered Ca2+ 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. 2007, Elsevier Inc.

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Year:  2007        PMID: 17222699     DOI: 10.1016/S0070-2153(06)77002-8

Source DB:  PubMed          Journal:  Curr Top Dev Biol        ISSN: 0070-2153            Impact factor:   4.897


  126 in total

1.  No mitochondrial DNA deletions but more D-loop point mutations in repeated pregnancy loss.

Authors:  Seyed Mohammad Seyedhassani; Massoud Houshmand; Seyed Mehdi Kalantar; Glayol Modabber; Abbas Aflatoonian
Journal:  J Assist Reprod Genet       Date:  2010-05-25       Impact factor: 3.412

2.  Sirt3 protects in vitro-fertilized mouse preimplantation embryos against oxidative stress-induced p53-mediated developmental arrest.

Authors:  Yumiko Kawamura; Yasunobu Uchijima; Nanao Horike; Kazuo Tonami; Koichi Nishiyama; Tomokazu Amano; Tomoichiro Asano; Yukiko Kurihara; Hiroki Kurihara
Journal:  J Clin Invest       Date:  2010-07-19       Impact factor: 14.808

3.  Embryo developmental capability and pregnancy outcome are related to the mitochondrial DNA copy number and ooplasmic volume.

Authors:  Yukitaka Murakoshi; Kou Sueoka; Kaori Takahashi; Suguru Sato; Tomoyoshi Sakurai; Hiroto Tajima; Yasunori Yoshimura
Journal:  J Assist Reprod Genet       Date:  2013-07-30       Impact factor: 3.412

4.  Mitochondrial Factors and VACTERL Association-Related Congenital Malformations.

Authors:  S Siebel; B D Solomon
Journal:  Mol Syndromol       Date:  2013-02

5.  Mitochondria structural reorganization during mouse embryonic stem cell derivation.

Authors:  Lyubov A Suldina; Ksenia N Morozova; Aleksei G Menzorov; Elena A Kizilova; Elena Kiseleva
Journal:  Protoplasma       Date:  2018-03-16       Impact factor: 3.356

6.  Effects of moderate global maternal nutrient reduction on fetal baboon renal mitochondrial gene expression at 0.9 gestation.

Authors:  Susana P Pereira; Paulo J Oliveira; Ludgero C Tavares; António J Moreno; Laura A Cox; Peter W Nathanielsz; Mark J Nijland
Journal:  Am J Physiol Renal Physiol       Date:  2015-03-11

Review 7.  The subcortical maternal complex: multiple functions for one biological structure?

Authors:  D Bebbere; L Masala; D F Albertini; S Ledda
Journal:  J Assist Reprod Genet       Date:  2016-08-15       Impact factor: 3.412

Review 8.  ATP synthase c-subunit ring as the channel of mitochondrial permeability transition: Regulator of metabolism in development and degeneration.

Authors:  Nelli Mnatsakanyan; Elizabeth Ann Jonas
Journal:  J Mol Cell Cardiol       Date:  2020-05-24       Impact factor: 5.000

9.  A methyl-deficient diet fed to rats during the pre- and peri-conception periods of development modifies the hepatic proteome in the adult offspring.

Authors:  Christopher A Maloney; Susan M Hay; Martin D Reid; Gary Duncan; Fergus Nicol; Kevin D Sinclair; William D Rees
Journal:  Genes Nutr       Date:  2012-08-21       Impact factor: 5.523

Review 10.  Autologous Germline Mitochondrial Energy Transfer (AUGMENT) in Human Assisted Reproduction.

Authors:  Dori C Woods; Jonathan L Tilly
Journal:  Semin Reprod Med       Date:  2015-11-17       Impact factor: 1.303

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