Epididymal Sperm Count

Wang, Yefan

doi:10.1002/0471140856.tx1606s14

Cited by 48 publications

(37 citation statements)

References 3 publications

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“…Epididymal sperm count and sperm evaluation was as described in ref. 63 and in SI Materials and Methods. Further details about generation of transgenic mice, behavioral testing, pharmacology experiments, TUNEL staining, and qPCR techniques are described in SI Materials and Methods.…”

Section: Methodsmentioning

confidence: 99%

Genetic loss or pharmacological blockade of testes-expressed taste genes causes male sterility

Mosinger

Redding

Parker

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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TAS1R taste receptors and their associated heterotrimeric G protein gustducin are involved in sugar and amino acid sensing in taste cells and in the gastrointestinal tract. They are also strongly expressed in testis and sperm, but their functions in these tissues were previously unknown. Using mouse models, we show that the genetic absence of both TAS1R3, a component of sweet and amino acid taste receptors, and the gustducin α-subunit GNAT3 leads to malespecific sterility. To gain further insight into this effect, we generated a mouse model that expressed a humanized form of TAS1R3 susceptible to inhibition by the antilipid medication clofibrate. Sperm formation in animals without functional TAS1R3 and GNAT3 is compromised, with malformed and immotile sperm. Furthermore, clofibrate inhibition of humanized TAS1R3 in the genetic background of Tas1r3 −/− , Gnat3 −/− doubly null mice led to inducible male sterility. These results indicate a crucial role for these extraoral "taste" molecules in sperm development and maturation. We previously reported that blocking of human TAS1R3, but not mouse TAS1R3, can be achieved by common medications or chemicals in the environment. We hypothesize that even low levels of these compounds can lower sperm count and negatively affect human male fertility, which common mouse toxicology assays would not reveal. Conversely, we speculate that TAS1R3 and GNAT3 activators may help infertile men, particularly those that are affected by some of the mentioned inhibitors and/or are diagnosed with idiopathic infertility involving signaling pathway of these receptors.phenoxy compounds | spermiogenesis

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Section: Methodsmentioning

confidence: 99%

Genetic loss or pharmacological blockade of testes-expressed taste genes causes male sterility

Mosinger

Redding

Parker

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…The number of spermatozoa in the cauda epididymides of 8-week-old mice was counted based on an established method (Wang, 2003). Briefly, cauda epididymides were weighed and minced in 2 ml of PBS.…”

Section: Epididymal Sperm Countmentioning

confidence: 99%

Ttll9 −/− mice sperm flagella show shortening of doublet 7, reduction of doublet 5 polyglutamylation and a stall in beating

Konno

Ikegami

Konishi

et al. 2016

Journal of Cell Science

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Nine outer doublet microtubules in axonemes of flagella and cilia are heterogeneous in structure and biochemical properties. In mammalian sperm flagella, one of the factors to generate the heterogeneity is tubulin polyglutamylation, although the importance of the heterogeneous modification is unclear. Here, we show that a tubulin polyglutamylase Ttll9 deficiency (Ttll9) causes a unique set of phenotypes related to doublet heterogeneity. Ttll9 −/− sperm axonemes had frequent loss of a doublet and reduced polyglutamylation. Intriguingly, the doublet loss selectively occurred at the distal region of doublet 7, and reduced polyglutamylation was observed preferentially on doublet 5. Ttll9 −/− spermatozoa showed aberrant flagellar beating, characterized by frequent stalls after antihook bending. This abnormal motility could be attributed to the reduction of polyglutamylation on doublet 5, which probably occurred at a position involved in the switching of bending. These results indicate that mammalian Ttll9 plays essential roles in maintaining the normal structure and beating pattern of sperm flagella by establishing normal heterogeneous polyglutamylation patterns.

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“…Data were plotted at the 95% confidence limit. At the completion of the three mating periods, males were sacrificed and their testis weight and sperm counts from cauda epididymes determined as described (Wang, 2003). Progeny of mutant males were genotyped to determine the efficiency of conditional allele excision.…”

Section: Fertility Studiesmentioning

confidence: 99%

The DNA damage checkpoint protein RAD9A is essential for male meiosis in the mouse

Vasil’eva

Hopkins

Wang

et al. 2013

Journal of Cell Science

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SummaryIn mitotic cells, RAD9A functions in repairing DNA double-strand breaks (DSBs) by homologous recombination and facilitates the process by cell cycle checkpoint control in response to DNA damage. DSBs occur naturally in the germline during meiosis but whether RAD9A participates in repairing such breaks is not known. In this study, we determined that RAD9A is indeed expressed in the male germ line with a peak of expression in late pachytene and diplotene stages, and the protein was found associated with the XY body. As complete loss of RAD9A is embryonic lethal, we constructed and characterized a mouse strain with Stra8-Cre driven germ cell-specific ablation of Rad9a beginning in undifferentiated spermatogonia in order to assess its role in spermatogenesis. Adult mutant male mice were infertile or sub-fertile due to massive loss of spermatogenic cells. The onset of this loss occurs during meiotic prophase, and there was an increase in the numbers of apoptotic spermatocytes as determined by TUNEL. Spermatocytes lacking RAD9A usually arrested in meiotic prophase, specifically in pachytene. The incidence of unrepaired DNA breaks increased, as detected by accumulation of cH2AX and DMC1 foci on the axes of autosomal chromosomes in pachytene spermatocytes. The DNA topoisomerase IIb-binding protein 1 (TOPBP1) was still localized to the sex body, albeit with lower intensity, suggesting that RAD9A may be dispensable for sex body formation. We therefore show for the first time that RAD9A is essential for male fertility and for repair of DNA DSBs during meiotic prophase I.

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Epididymal Sperm Count

Cited by 48 publications

References 3 publications

Genetic loss or pharmacological blockade of testes-expressed taste genes causes male sterility

Genetic loss or pharmacological blockade of testes-expressed taste genes causes male sterility

Ttll9 −/− mice sperm flagella show shortening of doublet 7, reduction of doublet 5 polyglutamylation and a stall in beating

The DNA damage checkpoint protein RAD9A is essential for male meiosis in the mouse

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