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A Seminiferous Tubule Squash Technique for the Cytological Analysis of Spermatogenesis Using the Mouse Model
Published on: February 6, 2018
Mice deficient for spermatid perinuclear RNA-binding protein show neurologic, spermatogenic, and sperm morphological
A Pires-daSilva1, K Nayernia, W Engel
1Department of Molecular Cell Biology, Max-Planck for Biophysical Chemistry, D-37077 Göttingen, Germany.
Abstract:
Spermatid perinuclear RNA-binding protein (SPNR) is a microtubule-associated RNA-binding protein that localizes to the manchette in developing spermatids. The Spnr mRNA is expressed at high levels in testis, ovary, and brain and is present in these tissues in multiple forms. We have generated a gene trap allele of the murine Spnr, named Spnr(+/GT). Spnr(GT/GT) mutants show a high rate of mortality, reduced weight, and an abnormal clutching reflex. In addition to minor anatomical abnormalities in the brain, males exhibit defects in spermatogenesis that include a thin seminiferous epithelium and disorganization of spermatogenesis. Most of the sperm from mutant males display defects in the flagellum and consequently show decreased motility and transport within the oviducts. Furthermore, sperm from mutant males achieve in vitro fertilization less frequently. Our findings suggest that SPNR plays an important role in normal spermatogenesis and sperm function. Thus, the Spnr(GT/GT) mutant male mouse provides a unique model for some human male infertility cases.
Insights
Spermatid perinuclear RNA-binding protein (SPNR) is crucial for male fertility. SPNR gene disruption in mice causes severe defects in sperm development, motility, and fertilization, offering a model for male infertility.
Area of Science:
- Reproductive Biology
- Molecular Genetics
Background:
- Spermatid perinuclear RNA-binding protein (SPNR) is a microtubule-associated protein involved in spermatogenesis.
- SPNR mRNA is expressed in testis, ovary, and brain, with multiple forms present.
Purpose of the Study:
- To investigate the role of SPNR in spermatogenesis and sperm function.
- To characterize the phenotype of a gene trap mutant for SPNR.
Main Methods:
- Generation of a gene trap allele of murine Spnr (Spnr(+/GT)).
- Analysis of Spnr(GT/GT) mutant mice for mortality, weight, reflexes, anatomical abnormalities, and reproductive defects.
Main Results:
- Spnr(GT/GT) mutants exhibited high mortality, reduced weight, and abnormal reflexes.
- Male mutants displayed thin seminiferous epithelium, disorganized spermatogenesis, and sperm flagellar defects.
- Mutant sperm showed decreased motility, impaired oviductal transport, and reduced in vitro fertilization rates.
Conclusions:
- SPNR plays a critical role in normal spermatogenesis and sperm function.
- The Spnr(GT/GT) mutant mouse serves as a valuable model for studying human male infertility.

