Ovum activation

Ovum activation

Ovum activation is the events which occur after fertilisation.

Sperm entry causes calcium release into the oocyte. This is caused by the presence of PLCzeta from the sperm cytoplasm. Activation of the ovum causes the following events:*Cortical reaction:*Reactivation of meiosis:*DNA synthesis

Cortical Reaction

Reactivation of meiosis

The meotic cycle of the oocyte was suspended in metaphase of the second meiotic division. Calcium release causes reactivation of the cycle. This results in the production and extrusion of the second polar body.

DNA synthesis

4 hours after fusion of sperm and ovum, DNA synthesis begins. Male and female pronuclei move to the centre of the egg and membranes break down. Male protamine and replaced with histones and the male DNA is demethylated. Chromosomes then orientate on the metaphase spindle for mitosis. This combination of the two genomes is called syngamy.

The sperm contributes a pronucleus and a centriole to the egg. Most other components and organelles are rapidly degraded. Mitochondria are rapidly ubiquinated and destroyed. Oxidative stress theory is a hypothesis that it is evolutionarily favourable for mitochondria from the father to be destroyed, as it there is a greater possibility that the mitochondrial DNA has become mutated or damaged. This is because mtDNA is not protected by histones and has poor repair mechanisms. Due to the increased metabolic activity of the sperm compared to the egg, due to its motility, there is greater production of reactive oxygen species and therefore greater chance of mutation. Furthermore, sperm are exposed to reactive oxygen species from leukocytes in the epididymis during transit. Additionally, quality control of spermatozoa is much worse than for the ovum, as many sperm are released whereas only one dominant follicle is released per cycle. This competitive selection helps to ensure the most 'fit' ova are selected for fertilisation.

References

::*Essential Reproduction, M. Johnson, 6th Edition, Blackwell Publishing


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