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神经学小鼠突变体韦弗的雄性不育表型

Male-sterile phenotype of the neurological mouse mutant weaver.

作者信息

Harrison S M, Roffler-Tarlov S

机构信息

Department of Anatomy and Cell Biology, Tufts University School of Medicine, Boston, Massachusetts 02111.

出版信息

Dev Dyn. 1994 May;200(1):26-38. doi: 10.1002/aja.1002000104.

DOI:10.1002/aja.1002000104
PMID:8081012
Abstract

The autosomal recessive murine mutation weaver (wv) affects postnatal differentiation in at least three neuronal populations in the brain: dopamine-containing neurons in the mid-brain, and granule and Purkinje cells in the cerebellum. Neuronal populations vulnerable to the actions of weaver die in the midst of development. In addition, homozygous weaver males are sterile. We show by a histological analysis of epididymides and testes that the cause of male sterility in weaver is lack of sperm. The epididymides of the adult weaver mice examined were devoid of sperm, and few seminiferous tubules in the adult weaver's testes contained elongated spermatids. Most tubules were marked by moderate to severe degeneration of the seminiferous epithelium. A developmental study showed that the mutant phenotype emerged after the third postnatal week. By postnatal day 28, the development of weaver sperm lagged behind that of the wild-type and some seminiferous tubules contained degenerating germ cells. By postnatal day 35, terminal differentiation of spermatids appeared to be arrested in many tubules and degeneration of the seminiferous epithelium was widespread. The heterozygotes were unaffected at all ages sampled. We conclude that the normal allele at the weaver locus is necessary for spermiogenesis and the maintenance of spermatogenesis.

摘要

常染色体隐性小鼠突变“织工”(wv)影响大脑中至少三个神经元群体的出生后分化:中脑中含多巴胺的神经元,以及小脑中的颗粒细胞和浦肯野细胞。易受“织工”作用影响的神经元群体在发育过程中死亡。此外,纯合的“织工”雄性小鼠不育。我们通过对附睾和睾丸的组织学分析表明,“织工”小鼠雄性不育的原因是缺乏精子。所检查的成年“织工”小鼠的附睾中没有精子,成年“织工”小鼠睾丸中的生精小管很少含有伸长的精子细胞。大多数小管的特征是生精上皮有中度至重度退化。一项发育研究表明,突变表型在出生后第三周后出现。到出生后第28天,“织工”精子的发育落后于野生型,一些生精小管含有退化的生殖细胞。到出生后第35天,许多小管中精子细胞的终末分化似乎停滞,生精上皮的退化很普遍。杂合子在所有采样年龄均未受影响。我们得出结论,“织工”基因座的正常等位基因对于精子发生和精子生成的维持是必需的。

相似文献

1
Male-sterile phenotype of the neurological mouse mutant weaver.神经学小鼠突变体韦弗的雄性不育表型
Dev Dyn. 1994 May;200(1):26-38. doi: 10.1002/aja.1002000104.
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Hypospermatogenesis is the cause of infertility in the male weaver mutant mouse.精子发生减少是雄性织布工突变小鼠不育的原因。
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Differentiation of germ cells in seminiferous tubules transplanted to testes of germ cell-deficient mice of W/Wv and Sl/Sld genotypes.移植到W/Wv和Sl/Sld基因型生殖细胞缺陷小鼠睾丸中的生精小管内生殖细胞的分化。
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Loss of sperm in juvenile spermatogonial depletion (jsd) mutant mice is ascribed to a defect of intratubular environment to support germ cell differentiation.在幼年精原细胞耗竭(jsd)突变小鼠中精子缺失归因于支持生殖细胞分化的管内环境缺陷。
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Cell death during development of testis and cerebellum in the mutant mouse weaver.突变型小鼠韦弗中睾丸和小脑发育过程中的细胞死亡。
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Targeted disruption of the estrogen receptor gene in male mice causes alteration of spermatogenesis and infertility.雄性小鼠雌激素受体基因的靶向破坏会导致精子发生改变和不育。
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The weaver gene expression affects neuronal generation patterns depending on age and encephalic region.
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Sohlh2 knockout mice are male-sterile because of degeneration of differentiating type A spermatogonia.Sohlh2基因敲除小鼠由于分化型A精原细胞的退化而导致雄性不育。
Stem Cells. 2008 Jun;26(6):1587-97. doi: 10.1634/stemcells.2007-0502. Epub 2008 Mar 13.

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Heteromultimerization of G-protein-gated inwardly rectifying K+ channel proteins GIRK1 and GIRK2 and their altered expression in weaver brain.G蛋白门控内向整流钾离子通道蛋白GIRK1和GIRK2的异源多聚化及其在weaver小鼠大脑中的表达改变
J Neurosci. 1996 Nov 15;16(22):7137-50. doi: 10.1523/JNEUROSCI.16-22-07137.1996.
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