Abstract
The fundamental underlying paradigm of sexual reproduction is the production of male and female gametes of sufficient genetic difference and quality that, following syngamy, they result in embryos with genomic potential to allow for future adaptive change and the ability to respond to selective pressure. The fusion of dissimilar gametes resulting in the formation of a normal and viable embryo is known as anisogamy, and is concomitant with precise structural, physiological, and molecular control of gamete function for species survival. However, along the reproductive life cycle of all organisms, both male and female gametes can be exposed to an array of “stressors” that may adversely affect the composition and biological integrity of their proteins, lipids and nucleic acids, that may consequently compromise their capacity to produce normal embryos. The aim of this review is to highlight gamete genome organization, differences in the chronology of gamete production between the male and female, the inherent DNA protective mechanisms in these reproductive cells, the aetiology of DNA damage in germ cells, and the remarkable DNA repair mechanisms, pre- and post-syngamy, that function to maintain genome integrity.
Highlights
The role of sexual reproduction in conferring the potential for adaptive changes in a population relies on the phenomenon of anisogamy, or the fusion of dissimilar gametes
The condensation of the DNA with protamines instead of histones gives the sperm cell some unique characteristics when compared to somatic cells [8] and this is no doubt related to the fact that the spermatozoon is biologically prepared for a short autonomous subsistence before fertilization is accomplished. This singular purpose of the sperm cell is reflected in its peculiarity and there are substantial contributions of protamines to this process, such as: (i) DNA condensation to achieve a smaller and more hydrodynamic nucleus to facilitate sperm movement and transport; (ii) extra DNA protection and stability against the negative effects of external agents such as free radicals or radiations; (iii) competition with other transcriptional factors to eliminate some of the somatic epigenetic information from the sperm nucleus, leaving it free to be reprogrammed by the oocyte after fertilization; (iv) paternal imprinting; (v) a check point in spermiogenesis; and (vi) post-fertilization functions in the oocyte [3]
Oogenesis can be divided into three phases [134]: firstly, primordial germ cells (PGCs) initiate their differentiation into female germ cells in the early post-implantation embryo; secondly, oogonia divide through mitosis and enter meiosis I until they stop developing at the diplotene stage, in prophase I and thirdly, oocytes complete the first division of meiosis I during ovulation
Summary
The role of sexual reproduction in conferring the potential for adaptive changes in a population relies on the phenomenon of anisogamy, or the fusion of dissimilar gametes. Gamete production in female is substantially different; PGCs migrate into the embryonic gonad and proliferate to form a resident population of primary oocytes that remain in meiotic arrest in prophase 1 until the female reaches puberty. Following commencement of her first menstrual cycle, oocytes are periodically released from the follicular pool, and under the appropriate endocrine control, a proportion of oocytes are recruited, selected, until typically, one becomes dominant and recommences meiosis 1. DNA damage response mechanisms in the different developmental phases of the spermatozoon, oocyte and zygote to conserve the genome integrity will be reviewed
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