Dataset Information

Male-enhanced antigen gene is phylogenetically conserved and expressed at late stages of spermatogenesis.

ABSTRACT: The male-enhanced antigen gene (Mea) was previously isolated from a mouse testicular cDNA library by using a pool of specific antisera against the serological H-Y antigen. The present studies characterize the human and mouse cDNAs and indicate that the MEA gene is conserved at both nucleic acid and protein levels. The corresponding mRNA encodes proteins of 18-20 kDa. The phylogenetic conservation could be extended to other mammalian species by Southern blot analysis. Although the Mea gene was transcribed as a 1-kilobase mRNA in most tissues, it was expressed at the highest level in adult testis. The testis-enhanced expression of the Mea gene was associated with germ cell development at late stages of spermatogenesis. Chromosome walking experiments identified two linked genes, A and B, located within 38 kilobases of human genomic sequence. Like the MEA gene, genes A and B were coordinately transcribed in the testis, which suggests that MEA and genes A and B are members of a gene family. In situ hybridization studies localized the MEA gene to the short arm of human chromosome 6 at band p21.1-21.3, close to the major histocompatibility complex locus. The genetic conservation and testis-specific expression of the MEA gene support the hypothesis that it plays an important role in mammalian spermatogenesis and/or testis development.

SUBMITTER: Lau YF

PROVIDER: S-EPMC298302 | biostudies-other | 1989 Nov

REPOSITORIES: biostudies-other

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Male-enhanced antigen gene is phylogenetically conserved and expressed at late stages of spermatogenesis.

Lau Y F YF Chan K M KM Sparkes R R

Proceedings of the National Academy of Sciences of the United States of America 19891101 21

The male-enhanced antigen gene (Mea) was previously isolated from a mouse testicular cDNA library by using a pool of specific antisera against the serological H-Y antigen. The present studies characterize the human and mouse cDNAs and indicate that the MEA gene is conserved at both nucleic acid and protein levels. The corresponding mRNA encodes proteins of 18-20 kDa. The phylogenetic conservation could be extended to other mammalian species by Southern blot analysis. Although the Mea gene was tr ...[more]

PMID: 2813404

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Project description:BackgroundDespite increasing evidence that particulate air pollution has adverse effects on human semen quality, few studies examine the impact of air pollution on clinically relevant thresholds used to diagnose male fertility problems. Furthermore, exposure is often assessed using average air pollution levels in a geographic area rather than individualized estimates. Finally, physiologically-informed exposure windows are inconsistent.ObjectivesWe sought to test the hypothesis that airborne particulate exposures during early-phase spermatogenesis will have a differential impact on spermatogenic formation compared to late-phase exposures, using an individualized model of exposure to particulate matter ≤ 2.5 µm and ≤ 10 µm (PM2.5 and PM10, respectively).MethodsFrom an original cohort of 183 couples, we conducted a retrospective analysis of 130 healthy males seeking to become parents, using spermatogenesis-relevant exposure windows of 77-34 days and 37-0 days prior to semen collection to encompass sperm development stages of mitosis/meiosis and spermiogenesis, respectively. Individualized residential exposure to PM2.5 and PM10 was estimated by selecting multiple air pollution sensors within the same geographic air basin as participants and employing inverse distance weighting to calculate mean daily exposure levels. We used multiple logistic regression to assess the association between pollution, temperature, and dichotomized World Health Organization semen parameters.ResultsDuring the early phase of spermatogenesis, air pollution exposure is associated with 1.52 (95% CI: 1.04-2.32) times greater odds of < 30% normal heads per 1-unit increase in IQR for PM2.5. In the late phase of spermatogenesis, air pollution exposure is associated with 0.35 (95% CI: 0.10-0.74) times greater odds of semen concentration < 15 million/mL per 1-unit increase in IQR for PM2.5, and 0.28 (95% CI: 0.07-0.72) for PM10.ConclusionParticulate exposure has a differential and more deleterious impact on sperm during early-phase spermatogenesis than late-phase.

Dataset Information

Male-enhanced antigen gene is phylogenetically conserved and expressed at late stages of spermatogenesis.

Publications

Male-enhanced antigen gene is phylogenetically conserved and expressed at late stages of spermatogenesis.

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