Mitochondrial morphology during preimplantational human embryogenesis

Abstract

The structure, distribution, and function of mitochondria during human oogenesis and early development is reported. Oogonia show a sparse and even distribution of mitochondria, which are oval or elongated. Except around nuclei, growing oocytes from small antral follicles have more dense rounded or oval mitochondria, associated with the rough endoplastic reticulum. Mitochondria in fully grown, germinal vesicle (GV) oocytes present an inert appearance, with a dense matrix and a few arch-like or transverse cristae. At this stage mitochondria are usually absent from the cortical part of the cytoplasm. Mitochondria in metaphase I and II oocytes, including fertilized oocytes, present a similar structure, but they are numerous and evenly spread in the ooplasm, associating closely with vesicles or aggregates of tubular smooth endoplasmic reticulum. The most substantial change in distribution occurs at the pronuclear stage, when there is a central conglomeration of mitochondria around the pronuclei in both monospermic and dispermic embryos, which persists up to syngamy. In structure and distribution, mitochondria in blastomeres of 2-16-cell embryos remain virtually unchanged and resemble those of mature oocytes, though perinuclear aggregation can be evident. Mitochondria are usually excluded from meiotic and mitotic spindles but locate peripherally, apparently providing energy for centrosomal, cytoskeletal, and chromosomal activity during cell division. Morphogenetic changes in mitochondrial structure occur in the 8-cell cleaving embryo, the morula and the blastocyst (apparently accompanying the onset of nuclear and mitochondrial transcription), when they become progressively less electron dense and often develop clear areas in their matrices. Elongating mitochondria with inner mitochondrial membranes arranged into transverse cristae appear in expanding blastocysts, in the trophoblast, embryoblast, and endodermal cells. These mitochondria seem to play a role in blastocyst differentiation, expansion, and hatching, with their morphological changes reflecting increased cellular activity.

Reproductive aging is associated with decreased mitochondrial abundance and altered structure in murine oocytes

“…Increased oxidative stress in aged murine oocytes has been linked to low ooplasmic ATP levels [22]. Undifferentiated appearance of mitochondria in MII oocytes has previously been described; therefore, our finding is consistent with prior reports [12,17]. In MII oocytes mitochondria have a round shape with few well defined cristae.…”

Mitochondrial oxidative metabolism is required for the cardiac differentiation of stem cells

“…Besides regulating cardiac differentiation, the increased expression of cardiac transcription factors promotes mitochondrial function and cellular organization. 12,22,23 In stem cell-derived cardiomyocytes, downregulation of genes with roles in mitochondrial fission or inhibition of fusion led to intracellular and intercellular networks facilitating expansion of the cardiogenic phenotype. These cell-to-cell connections enabling the transport of mitochondria and leading to the acquisition of a cardiomyogenic phenotype by progenitor cells had been observed previously.…”

Oviduct: roles in fertilization and early embryo development

“…However, in human, the metabolic switch is not complete until the blastocyst stage (Sathananthan & Trounson 2000). This glycolytic metabolism requires supplies of glucose and simple sugars.…”

“…2A). The mature mitochondria can now use oxygen and glucose in glycolysis to provide ATP for further embryo development (Sathananthan & Trounson 2000). In mice, this is evident with the timing of embryo oxygen consumption, which peaks at the blastocyst stage (Leese 2012 Oxidative metabolism Glycolytic metabolism…”