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Of stem cells and gametes: similarities and differences.: Current medicinal chemistry, Vol. 15, No. 13. (2008), pp. 1249-1256.Fusi on of a mammalian sperm cell with an oocyte will lead to the formation of a new organism. As this new organism develops, the cells that construct the organism gradually lose developmental competence and become differentiated , a process which is in part mediated via epigenetic modifications. These mechanisms include DNA methylation, histone tail modifications and association with Polycomb and Trithorax proteins. Several cells within the organism must however maintain or regain developmental competence while they are highly specialized. These are the primordial germ cells that form the gametes; the oocytes and sperm cells. In this review different epigenetic modifying mechanisms will be discussed as they occur in developing embryos. In addition, aspects of nuclear reprogramming that are likely to occur via removal of epigenetic modifications are important, and several epigenetic removal mechanisms are indeed also active in developing germ cells. In vivo, a pluripotent cell has the capacity to form gametes, but in vitro terminal gametogenesis has proven to be difficult. Although development of pluripotent cells to cells with the characteristic s of early germ cells has been unequivocally demonstrated, creating the correct culture milieu that enables further maturation of these cells has as yet been futile.BA Roelen, SM Lopes

Source: Current medicinal chemistry, Vol. 15, No. 13. (2008), pp. 1249-1256.
The stress response in gametes and embryos after paternal chemical exposures: Toxicology and Applied Pharmacology, Vol. 207, No. 2, Supplement 1. (1 September 2005), pp. 514-520.There is increasing concern that paternal exposure to toxic chemicals impacts negatively on progeny outcome. Exposure of male rats to a model male-mediated developmental toxicant and anticancer alkylating agent, cyclophosphami de, resulted in increased pre- and post-implantat ion loss, as well as in malformations. We hypothesize that the stage specificity of the effects of paternal cyclophosphami de exposure on progeny depends on the ability of germ cells to respond to stress, repair DNA or undergo apoptosis. Acute high dose exposure of male rats to cyclophosphami de increased the expression of heat shock proteins and DNA repair genes, predominantly in round spermatids. In contrast, chronic low dose treatment dramatically decreased the expression of stress response genes in pachytene spermatocytes and round spermatids, but not in elongated spermatids; this reduced ability to respond to stress may allow damage to accumulate, resulting in altered sperm function. Increased DNA damage was maximal 3 weeks after drug exposure, during spermiogenesis , a key point in sperm chromatin remodelling. Drug exposure for 9 weeks increased the frequency of spermatozoa with chromosome 4 disomy and nullisomy. DNA damage found in cyclophosphami de-exposed spermatozoa was imparted to the newly fertilized zygote. Drug-exposed spermatozoa decondensed more rapidly than control spermatozoa and male pronuclear formation was earlier. RNA synthesis was higher in 1-cell embryos sired by drug-treated fathers than in controls. Significantly, the profile of gene expression was altered in embryos sired by drug-treated males as early as the 1-cell stage. Thus, exposure of male rats to cyclophosphami de altered male germ cell quality with a consequent temporal and spatial disruption of the zygotic genome activation.Bar bara Hales, Adriana Aguilar-Mahech a, Bernard Robaire

Source: Toxicology and Applied Pharmacology, Vol. 207, No. 2, Supplement 1. (1 September 2005), pp. 514-520.
Asynchronous replication of imprinted genes is established in the gametes and maintained during development.: Nature, Vol. 401, No. 6756. (28 October 1999), pp. 929-932.Genomi c imprinting is characterized by allele-specifi c expression of multiple genes within large chromosomal domains that undergo DNA replication asynchronously during S phase. Here we show, using both fluorescence in situ hybridization analysis and S-phase fractionation techniques, that differential replication timing is associated with imprinted genes in a variety of cell types, and is already present in the pre-implantati on embryo soon after fertilization. This pattern is erased before meiosis in the germ line, and parent-specifi c replication timing is then reset in late gametogenesis in both the male and female. Thus, asynchronous replication timing is established in the gametes and maintained throughout development, indicating that it may function as a primary epigenetic marker for distinguishing between the parental alleles.I Simon, T Tenzen, BE Reubinoff, D Hillman, JR McCarrey, H Cedar

Source: Nature, Vol. 401, No. 6756. (28 October 1999), pp. 929-932.
The mouse X chromosome is enriched for multicopy testis genes showing postmeiotic expression.: Nature genetics (4 May 2008)According to the prevailing view, mammalian X chromosomes are enriched in spermatogenesi s genes expressed before meiosis and deficient in spermatogenesi s genes expressed after meiosis. The paucity of postmeiotic genes on the X chromosome has been interpreted as a consequence of meiotic sex chromosome inactivation (MSCI)-the complete silencing of genes on the XY bivalent at meiotic prophase. Recent studies have concluded that MSCI-initiated silencing persists beyond meiosis and that most genes on the X chromosome remain repressed in round spermatids. Here, we report that 33 multicopy gene families, representing approximately 273 mouse X-linked genes, are expressed in the testis and that this expression is predominantly in postmeiotic cells. RNA FISH and microarray analysis show that the maintenance of X chromosome postmeiotic repression is incomplete. Furthermore, X-linked multicopy genes exhibit a similar degree of expression as autosomal genes. Thus, not only is the mouse X chromosome enriched for spermatogenesi s genes functioning before meiosis, but in addition, approximately 18% of mouse X-linked genes are expressed in postmeiotic cells.Jacob L Mueller, Shantha K Mahadevaiah, Peter J Park, Peter E Warburton, David C Page, James M A Turner

Source: Nature genetics (4 May 2008)
Gametogenesis in Malaria Parasites Is Mediated by the cGMP-Dependent Protein Kinase: PLoS Biology, Vol. 6, No. 6. (1 June 2008), e139.Malaria parasite transmission requires differentiatio n of male and female gametocytes into gametes within a mosquito following a blood meal. A mosquito-deriv ed molecule, xanthurenic acid (XA), can trigger gametogenesis, but the signalling events controlling this process in the human malaria parasite Plasmodium falciparum remain unknown. A role for cGMP was revealed by our observation that zaprinast (an inhibitor of phosphodiester ases that hydrolyse cGMP) stimulates gametogenesis in the absence of XA. Using cGMP-dependent protein kinase (PKG) inhibitors in conjunction with transgenic parasites expressing an inhibitor-inse nsitive mutant PKG enzyme, we demonstrate that PKG is essential for XA- and zaprinast-indu ced gametogenesis. Furthermore, we show that intracellular calcium (Ca2+) is required for differentiatio n and acts downstream of or in parallel with PKG activation. This work defines a key role for PKG in gametogenesis, elucidates the hierarchy of signalling events governing this process in P. falciparum, and demonstrates the feasibility of selective inhibition of a crucial regulator of the malaria parasite life cycle.Louisa Mcrobert, Cathy Taylor, Wensheng Deng, Quinton Fivelman, Ross Cummings, Spencer Polley, Oliver Billker, David Baker

Source: PLoS Biology, Vol. 6, No. 6. (1 June 2008), e139.

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