Ultrastructural study of mitochondria and their cristae in embryonic rats and primate (N. nemistrina)

Abstract

Information on the morphology of mitochondria during embryogenesis is scattered in the literature but there appears to be a developmental pattern characterized by vesiculation of the mitochondrial cristae. During early organogenesis, the embryo is in a relative state of hypoxia and this is associated with decrease of terminal electron transport system activity and a marked increase in glycolysis. Ultrastructural studies of a 14 somite monkey embryo, and day 10 and 12 rat embryos, along with a review of the literature led us to determine that this hypoxic stage is characterized by vesiculation of the mitochondrial cristae. Starting in the late morula stage and continuing during early postimplantation embryogenesis the cristae increase and appear tubular or vesicular. After the end of neurulation, and with onset of vascular perfusion, the cristae gradually become lamellated and by the limb bud stage appear more mature. We suggest that new cristae form from blebs of the inner mitochondrial membrane and that subsequently with maturation these blebs collapse giving them a lamelliform appearance. The delamellated state of the cristae may protect the embryo from toxic respiratory end-products of oxidative respiration which could accumulate in an embryo lacking vascular perfusion. In the heart of monkey and rat embryos, the mitochondria had diameters which were approximately twice those found in skin and neural tube. Anat.

Hypoxia promotes production of neural crest cells in the embryonic head

“…1D). This is in agreement with the commencement of blood circulation by this stage and subsequent aerobic glycolysis (Mackler et al, 1973;Shepard et al, 1998).…”

“…The inability of the old neural tube to produce additional neural crest cells at late stages in the head might be partly because of the progressive neural tube development and commitment in differentiation. In addition to this, we propose that it might also be due to the high oxygen demand for oxidative metabolism in response to rapid growth and increasing energy consumption (Mackler et al, 1971(Mackler et al, , 1973Shepard et al, 1998Shepard et al, , 2000, which may not allow the HIF pathway to function. This is in contrast to young embryos that successfully produce a large number of neural crest cells in the head region thanks to the hypoxic conditions.…”

“…At the subcellular level, oxygen consumption is reflected in the morphology of mitochondria. In mammalian and chick embryos of ∼10-somite stage, mitochondria show poorly developed cristae of the inner membrane, suggesting that aerobic respiration is not very active (Bancroft and Bellairs, 1975;de Paz et al, 1986;Mackler et al, 1971;Shepard et al, 1998). The cristae become more laminated at later stages, which correlates with the changes from anaerobic to aerobic glycolysis (Mackler et al, 1973;Shepard et al, 1997).…”

Mitochondrial differentiation and oxidative phosphorylation system capacity in rat embryo during placentation period

“…In middle pregnancy, rat embryo mitochondria undergo considerable morphofunctional changes (Mackler et al 1973, Shepard et al 1998, Yang et al 1998 coinciding with the switch from glycolytic to oxidative metabolism that takes place on gestational day 12 (Akazawa et al 1994, Shepard et al 1997, just when the placentary circulation is established and oxygen becomes more available to the embryo (Jollie 1986, Akazawa 2005. In addition, a previous study in our laboratory reported the activation of mitochondrial gene expression throughout the placentation period, suggesting that mitochondrial biogenesis is an active process in rat embryo during this developmental stage (Alcolea et al 2006).…”

Research Article: Expression pattern of deoxyguanosine kinase3 during mouse development

“…In yeast, this switch is accompanied by major changes in gene expression (Johnston and Carlson, 1992), an expected result since metabolic pathways need to be activated or deactivated to carry out such a shift. In mammalian embryos, this change lasts from GD7 to GD10 (Mackler et al, 1971;Shepard et al, 1998). To successfully accomplish this alteration, a high level of ATP, which is now produced by aerobic respiration in the mitochondria, must be generated.…”