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Research Article

KATNAL1 Regulation of Sertoli Cell Microtubule Dynamics Is Essential for Spermiogenesis and Male Fertility

  • Lee B. Smith mail,

    Lee.Smith@ed.ac.uk

    Affiliation: MRC Centre for Reproductive Health, University of Edinburgh, The Queen's Medical Research Institute, Edinburgh, United Kingdom

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  • Laura Milne,

    Affiliation: MRC Centre for Reproductive Health, University of Edinburgh, The Queen's Medical Research Institute, Edinburgh, United Kingdom

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  • Nancy Nelson,

    Affiliation: MRC Centre for Reproductive Health, University of Edinburgh, The Queen's Medical Research Institute, Edinburgh, United Kingdom

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  • Sharon Eddie,

    Affiliation: MRC Centre for Reproductive Health, University of Edinburgh, The Queen's Medical Research Institute, Edinburgh, United Kingdom

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  • Pamela Brown,

    Affiliation: MRC Centre for Reproductive Health, University of Edinburgh, The Queen's Medical Research Institute, Edinburgh, United Kingdom

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  • Nina Atanassova,

    Affiliation: Institute of Experimental Morphology and Anthropology with Museum, Bulgarian Academy of Sciences, Sofia, Bulgaria

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  • Moira K. O'Bryan,

    Affiliation: The Department of Anatomy and Developmental Biology, Monash University, Melbourne, Victoria, Australia

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  • Liza O'Donnell,

    Affiliations: The Department of Anatomy and Developmental Biology, Monash University, Melbourne, Victoria, Australia, Prince Henry's Institute of Medical Research, Clayton, Victoria, Australia

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  • Danielle Rhodes,

    Affiliation: The Department of Anatomy and Developmental Biology, Monash University, Melbourne, Victoria, Australia

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  • Sara Wells,

    Affiliation: Mary Lyon Centre, Medical Research Council, Harwell Science and Innovation Campus, Harwell, Oxfordshire, United Kingdom

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  • Diane Napper,

    Affiliation: Mary Lyon Centre, Medical Research Council, Harwell Science and Innovation Campus, Harwell, Oxfordshire, United Kingdom

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  • Patrick Nolan,

    Affiliation: Mammalian Genetics Unit, Medical Research Council, Harwell Science and Innovation Campus, Harwell, Oxfordshire, United Kingdom

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  • Zuzanna Lalanne,

    Affiliation: Mammalian Genetics Unit, Medical Research Council, Harwell Science and Innovation Campus, Harwell, Oxfordshire, United Kingdom

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  • Michael Cheeseman,

    Affiliations: Mary Lyon Centre, Medical Research Council, Harwell Science and Innovation Campus, Harwell, Oxfordshire, United Kingdom, Mammalian Genetics Unit, Medical Research Council, Harwell Science and Innovation Campus, Harwell, Oxfordshire, United Kingdom

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  • Josephine Peters

    Affiliation: Mammalian Genetics Unit, Medical Research Council, Harwell Science and Innovation Campus, Harwell, Oxfordshire, United Kingdom

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  • Published: May 24, 2012
  • DOI: 10.1371/journal.pgen.1002697

Reader Comments (1)

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The Ratio of DHEA and Testosterone may Control Sperm Maturation via KATNAL1

Posted by jamesmhoward on 25 May 2012 at 11:30 GMT

It is my hypothesis that evolution selected dehydroepiandrosterone (DHEA) because it optimizes replication and transcription of DNA. Therefore DHEA levels affect all cells and tissues. DHEA naturally begins to decline around the ages of twenty to twenty-five, reaching very low levels in old age.

It is also my hypothesis that testosterone evolved to increase DHEA entrance into cells where it stimulates gene activity. That is, testosterone increases androgen receptors through DHEA enters cells. Testosterone and DHEA reach an optimal ratio during the life span which is directly involved in reproduction, therefore, overall health.

Since DHEA and testosterone both decline in ageing, then the stimulatory activity of DHEA declines significantly with age.

The findings of Smith, et al., that KATNAL1 is involved in sperm maturation produce a useful hypothesis regarding the effects of sperm from older men. Abnormal sperm characteristics are common in elderly men as well as mental disorders in their offspring. "Progenies of fathers under 20 and over 50 had higher risk for mental disorders. Factors such as immaturity in sperm of teenage fathers, mutation in germ line of older fathers, environmental and psychosocial factors could have contributed to increased prevalence of common mental disorders in the progeny." (World J Biol Psychiatry. 2009;10(4 Pt 2):518-23)

I suggest that low DHEA is involved in reduced maturation of sperm. Since testosterone and DHEA combine to increase gene activity, young men may not produce an optimal ratio of testosterone and DHEA to produce sufficiently mature sperm, that is, their testosterone may be too low. Older men, as stated above, do not produce sufficient DHEA and testosterone to produce mature sperm. It may be that lack of sperm maturation produces both the infertility of elderly men as well as the "higher risk for mental disorders" of the offspring of elderly and young men.

No competing interests declared.