Moving to the beat: a review of mammalian sperm motility regulation

Turner, Regina M.

doi:10.1071/rd05120

Cited by 242 publications

(196 citation statements)

References 152 publications

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“…sperm count and sperm motility, and did not reveal obvious ultrastructural sperm anomalies, we noticed a significant increase in the distance between the nuclear membrane and the capitulum when ODF1 is reduced. A larger distance between the nucleus and the capitulum most probably reflects weakening of sperm head-tail linkage that eventually might provoke decapitation potentially when hyperactivated in motility in the female oviduct (Turner 2006). In men, cases of infertility have already been reported in which spermatozoa are easily decapitated when manipulated for ICSI, but whether weakening of the HTCA is causative is not known (Kamal et al 1999).…”

Section: Discussionmentioning

confidence: 99%

Haplo-deficiency of ODF1/HSPB10 in mouse sperm causes relaxation of head-to-tail linkage

Yang¹,

Grzmil²,

Meinhardt³

et al. 2014

Reproduction

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The small heat shock protein ODF1/HSPB10 is essential for male fertility in mice. Targeted deletion of Odf1 resulted in acephalic sperm in homozygous mice of mixed background (C57BL/6J//129/Sv), whereas heterozygous animals are fully fertile. To further elucidate the function of ODF1, we generated incipient congenic mice with targeted deletion of Odf1 by successive backcrossing on the 129/Sv background. We observed that fecundity of heterozygous Odf1 C/K male mice was severely reduced over backcross generations. However, neither aberrant sperm parameters nor sperm anomalies could be observed. Ultra-structural analyses of sperm from incipient congenic heterozygous Odf1 C/K males of backcross generation N7 revealed no obvious pathological findings. However, we observed an enlargement of the distance between nuclear membrane and capitulum, indicating a weakening of the sperm head-to-tail coupling. Severe male subfertility provoked by haplo-deficiency of ODF1 is therefore most probably caused by impaired head-to-tail coupling that eventually might induce sperm decapitation on the specific conditions of in vivo fertilisation. As subfertility in haplo-deficient ODF1 male mice could not be diagnosed by semen analysis, it seems to be a paradigm for unexplained infertility that is a frequent diagnosis for male fertility impairment in humans.

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Section: Discussionmentioning

confidence: 99%

Haplo-deficiency of ODF1/HSPB10 in mouse sperm causes relaxation of head-to-tail linkage

Yang¹,

Grzmil²,

Meinhardt³

et al. 2014

Reproduction

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“…Men with poorly motile or immotile sperm are typically infertile or sterile (Turner 2006). A deeper knowledge of the role of the NO/cGMP/ PRKG1 signaling pathway in the physiopathology of sperm motility could help to pharmacologically improve the fertilization capacity of human sperm or, alternatively, could lead to the development of an effective and safe male contraceptive based on sperm motility impairment.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide stimulates human sperm motility via activation of the cyclic GMP/protein kinase G signaling pathway

Miraglia¹,

Angelis²,

Gazzano³

et al. 2011

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Nitric oxide (NO), a modulator of several physiological processes, is involved in different human sperm functions. We have investigated whether NO may stimulate the motility of human spermatozoa via activation of the soluble guanylate cyclase (sGC)/cGMP pathway. Sperm samples obtained by masturbation from 70 normozoospermic patients were processed by the swim-up technique. The kinetic parameters of the motile sperm-rich fractions were assessed by computer-assisted sperm analysis. After a 30-90 min incubation, the NO donor S-nitrosoglutathione (GSNO) exerted a significant enhancing effect on progressive motility (77, 78, and 78% vs 66, 65, and 62% of the control at the corresponding time), straight linear velocity (44, 49, and 48 mm/s vs 34, 35, and 35.5 mm/s), curvilinear velocity (81, 83, and 84 mm/s vs 68 mm/s), and average path velocity (52, 57, and 54 mm/s vs 40, 42, and 42 mm/s) at 5 mM but not at lower concentrations, and in parallel increased the synthesis of cGMP. A similar effect was obtained with the NO donor spermine NONOate after 30 and 60 min. The GSNO-induced effects on sperm motility were abolished by 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (a specific sGC inhibitor) and mimicked by 8-bromo-cGMP (8-Br-cGMP; a cell-permeating cGMP analog); the treatment with Rp-8-Br-cGMPS (an inhibitor of cGMP-dependent protein kinases) prevented both the GSNO-and the 8-Br-cGMP-induced responses. On the contrary, we did not observe any effect of the cGMP/PRKG1 (PKG) pathway modulators on the onset of hyperactivated sperm motility. Our results suggest that NO stimulates human sperm motility via the activation of sGC, the subsequent synthesis of cGMP, and the activation of cGMP-dependent protein kinases.

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“…The ability of sperm to move forward is crucial for the successful fertilization of an egg [3]. There is little information about the normal physiology of sperm motility or the proteins responsible for sperm function [4].…”

Section: Introductionmentioning

confidence: 99%

A proteomic analysis on human sperm tail: comparison between normozoospermia and asthenozoospermia

Hashemitabar

Sabbagh

Orazizadeh

et al. 2015

J Assist Reprod Genet

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Purpose Asthenozoospermia is a common cause of human male infertility characterized by reduced sperm motility. The molecular mechanism that impairs sperm motility is not fully understood. This study proposed to identify novel biomarkers by focusing on sperm tail proteomic analysis of asthenozoospermic patients. Methods Sperm were isolated from normozoospermic and asthenozoospermic semen samples. Tail fractions were obtained by sonication followed by Percoll gradient. The proteins were extracted by solubilization and subjected to two-dimensional gel electrophoresis (2-DE); then, the spots were analyzed using Image Master 2D Platinum software. The significantly increased/ decreased amounts of proteins in the two groups were exploited by matrix-assisted laser desorption-ionization time-of-flight/ time-of-flight (MALDI-TOF-TOF) mass spectrometry. Results Three hundred ninety protein spots were detected in both groups. Twenty-one protein spots that had significantly altered amounts (p<0.05) were excised and exploited using MALDI-TOF-TOF mass spectrometry. They led to the identification of the following 14 unique proteins: Tubulin beta 2B; glutathione S-transferase Mu 3; keratin, type II cytoskeletal 1; outer dense fiber protein 2; voltage-dependent anionselective channel protein 2; A-kinase anchor protein 4; cytochrome c oxidase subunit 6B; sperm protein associated with the nucleus on the X chromosome B; phospholipid hydroperoxide glutathione peroxidase-mitochondrial; isoaspartyl peptidase/L-asparaginase; heat shock-related 70 kDa protein 2; stress-70 protein, mitochondrial; glyceraldehyde-3-phosphate dehydrogenase, testis-specific and clusterin. Conclusion Fourteen proteins present in different amounts in asthenozoospermic sperm tail samples were identified, four of which are reported here for the first time. These proteins might be used as markers for the better diagnosis of sperm dysfunctions, targets for male contraceptive development, and to predict embryo quality.

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Moving to the beat: a review of mammalian sperm motility regulation

Cited by 242 publications

References 152 publications

Haplo-deficiency of ODF1/HSPB10 in mouse sperm causes relaxation of head-to-tail linkage

Haplo-deficiency of ODF1/HSPB10 in mouse sperm causes relaxation of head-to-tail linkage

Nitric oxide stimulates human sperm motility via activation of the cyclic GMP/protein kinase G signaling pathway

A proteomic analysis on human sperm tail: comparison between normozoospermia and asthenozoospermia

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