Abstract
BackgroundAlthough artificial insemination (AI) technique is an established biotechnology for bovine reproduction, the results of AI (conception rates) have a tendency to decline gradually. To our annoyance, moreover, AI‐subfertile bulls have been occasionally found in the AI centers. To resolve these serious problems, it is necessary to control the sperm quality more strictly by the examinations of sperm molecules.MethodsWe reviewed a number of recent articles regarding potentials of bovine sperm proteins as the biomarkers for bull AI‐subfertility and also showed our unpublished supplemental data on the bull AI‐subfertility associated proteins.Main findingsBull AI‐subfertility is caused by the deficiency or dysfunctions of various molecules including regulatory proteins of ATP synthesis, acrosomal proteins, nuclear proteins, capacitation‐related proteins and seminal plasma proteins.ConclusionIn order to control the bovine sperm quality more strictly by the molecular examinations, it is necessary to select suitable sperm protein biomarkers for the male reproductive problems which happen in the AI centers.
Highlights
In mammals, including the human, male infertility and subfertility are due to defects in testicular spermatogenesis, epididymal sperm maturation, sperm transportation through the male reproductive tract, functions of the sperm molecules or other functions of the male reproductive organs
Similar results were obtained for the cauda epididymal spermatozoa and cryopreserved spermatozoa. These indices on the acrosomal phosphoproteins of the epididymal, ejaculated, and cryopreserved spermatozoa were positively correlated with the conception rates in artificial insemination (AI) and the percentages of cryopreserved spermatozoa with morphologically normal acrosomes.[26,55]. These results suggest that a lack of the acrosomal phosphoproteins in ejaculated spermatozoa with normal general characteristics is linked to bull AI subfertility and lower sperm freezability
For bulls (Japanese Black cattle), the authors showed that ADCY10 was distributed in the neck and flagellar principal piece of the ejaculated spermatozoa and that both messenger RNAs that coded the full-length and truncated forms were expressed in the testes by the alternative splicing of exon 11.99 Interestingly, it was found that the splicing error yielded the other variant of ADCY10, with the aberrance in the second cyclase domain by retaining the intronic nucleotides that connect to the initial part of exon 10, and that the incidence rates of this splicing error were largely varied among individual bulls by between 0% and 54.5%
Summary
In mammals, including the human, male infertility and subfertility are due to defects in testicular spermatogenesis, epididymal sperm maturation, sperm transportation through the male reproductive tract, functions of the sperm molecules or other functions of the male reproductive organs.
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