Mouse models in male fertility research

Jamsai, Duangporn; O'Bryan, Moira K

doi:10.1038/aja.2010.101

Cited by 115 publications

(90 citation statements)

References 167 publications

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“…Currently, many testis-restrictive and testis-selective genes have been screened through cDNA microarray hybridization analyses (Andrews et al, 2000;Huang et al, 2005;Wang et al, 2010), and more than 400 genes essential for male fertility had been revealed using 3 main mouse models: knockout/knockin/gene-trapped, transgenic, and chemical-induced point mutant mice (O'Bryan and de Kretser, 2006;Matzuk and Lamb, 2008;Yatsenko et al, 2010;Jamsai and O'Bryan, 2011). Most of these testis genes are mainly present in germ cells, some are present in both germ cells and interstitial cells, and a few are restricted to interstitial cells.…”

Section: Discussionmentioning

confidence: 99%

Identification of a novel human testicular interstitial gene, RNF148, and its expression regulated by histone deacetylases

Liu¹,

Tao²,

Liao³

et al. 2013

Genet. Mol. Res.

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ABSTRACT.Multiple genes are restrictively expressed in mammalian testicular tissues, and they play important roles in the complex process of spermatogenesis. Investigation of these genes and their expression regulation mechanisms is valuable to elucidate the molecular process of spermatogenesis. In this study, we identified a novel human gene, ring finger protein 148 (RNF148) that is abundantly expressed in testes and slightly expressed in pancreas. In situ hybridization analysis showed that RNF148 messenger RNA was mainly present in the interstitial cells of human testicular tissues, and immunohistochemical analysis confirmed protein levels in that location. Treatment with histone deacetylase inhibitor trichostatin A activated the expression of RNF148 messenger RNA in a time-and concentration-dependent manner in HEK293T and HeLa cells, neither of which normally express RNF148. Chromatin immunoprecipitation analysis showed that trichostatin A treatment increased the binding of acetylated histone H3 to the RNF148 gene promoter. We identified a novel human testicular interstitial gene and observed that histone deacetylases regulate RNF148 expression.

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Section: Discussionmentioning

confidence: 99%

Identification of a novel human testicular interstitial gene, RNF148, and its expression regulated by histone deacetylases

Liu¹,

Tao²,

Liao³

et al. 2013

Genet. Mol. Res.

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“…In humans, neither the frequency of meiotic mutations nor the rate of infertility due to such mutations is known, but bilateral spermatogenic arrest was observed in 12.5% of patients who underwent testicular biopsy due to infertility (87). In recent years, the identification of genes involved in infertility spanning all aspects of spermatogenesis, including meiotic defects, has been accelerated mainly by studies of mouse models (88,89). Despite the numerous knockout mouse models presenting with spermatogenic arrest, studies in humans have largely failed to identify specific gene mutations.…”

Section: Consequences Of Dysregulated Meiosis Signaling In the Testesmentioning

confidence: 99%

Regulation of meiotic entry and gonadal sex differentiation in the human: normal and disrupted signaling

Jørgensen

Meyts

2014

Biomolecular Concepts

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Meiosis is a unique type of cell division that is performed only by germ cells to form haploid gametes. The switch from mitosis to meiosis exhibits a distinct sex-specific difference in timing, with female germ cells entering meiosis during fetal development and male germ cells at puberty when spermatogenesis is initiated. During early fetal development, bipotential primordial germ cells migrate to the forming gonad where they remain sexually indifferent until the sex-specific differentiation of germ cells is initiated by cues from the somatic cells. This irreversible step in gonadal sex differentiation involves the initiation of meiosis in fetal ovaries and prevention of meiosis in the germ cells of fetal testes. During the last decade, major advances in the understanding of meiosis regulation have been accomplished, with the discovery of retinoic acid as an inducer of meiosis being the most prominent finding. Knowledge about the molecular mechanisms regulating meiosis signaling has mainly been established by studies in rodents, while this has not yet been extensively investigated in humans. In this review, the current knowledge about the regulation of meiosis signaling is summarized and placed in the context of fetal gonad development and germ cell differentiation, with emphasis on results obtained in humans. Furthermore, the consequences of dysregulated meiosis signaling in humans are briefly discussed in the context of selected pathologies, including testicular germ cell cancer and some forms of male infertility.

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“…Most of these animal models are mouse lines. Worldwide, there are more than 400 transgenic or knockout mouse lines available showing a reproductive phenotype (Matzuk & Lamb 2008, Jamsai & O'Bryan 2011, Ogorevc et al 2011. Almost all of them exhibit an infertile or at least subfertile phenotype.…”

Section: Introductionmentioning

confidence: 99%

High-fertility phenotypes: two outbred mouse models exhibit substantially different molecular and physiological strategies warranting improved fertility

Langhammer¹,

Michaelis²,

Hoeflich³

et al. 2014

Reproduction

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Animal models are valuable tools in fertility research. Worldwide, there are more than 400 transgenic or knockout mouse models available showing a reproductive phenotype; almost all of them exhibit an infertile or at least subfertile phenotype. By contrast, animal models revealing an improved fertility phenotype are barely described. This article summarizes data on two outbred mouse models exhibiting a 'high-fertility' phenotype. These mouse lines were generated via selection over a time period of more than 40 years and 161 generations. During this selection period, the number of offspring per litter and the total birth weight of the entire litter nearly doubled. Concomitantly with the increased fertility phenotype, several endocrine parameters (e.g. serum testosterone concentrations in male animals), physiological parameters (e.g. body weight, accelerated puberty, and life expectancy), and behavioral parameters (e.g. behavior in an open field and endurance fitness on a treadmill) were altered. We demonstrate that the two independently bred high-fertility mouse lines warranted their improved fertility phenotype using different molecular and physiological strategies. The fertility lines display female-as well as male-specific characteristics. These genetically heterogeneous mouse models provide new insights into molecular and cellular mechanisms that enhance fertility. In view of decreasing fertility in men, these models will therefore be a precious information source for human reproductive medicine. Translated abstractA German translation of abstract is freely available at

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Mouse models in male fertility research

Cited by 115 publications

References 167 publications

Identification of a novel human testicular interstitial gene, RNF148, and its expression regulated by histone deacetylases

Identification of a novel human testicular interstitial gene, RNF148, and its expression regulated by histone deacetylases

Regulation of meiotic entry and gonadal sex differentiation in the human: normal and disrupted signaling

High-fertility phenotypes: two outbred mouse models exhibit substantially different molecular and physiological strategies warranting improved fertility

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