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精子发生减少是雄性织布工突变小鼠不育的原因。

Hypospermatogenesis is the cause of infertility in the male weaver mutant mouse.

作者信息

Vogelweid C M, Verina T, Norton J, Harruff R, Ghetti B

机构信息

Department of Pathology, Indiana University School of Medicine, Indianapolis 46202.

出版信息

J Neurogenet. 1993 Dec;9(2):89-104. doi: 10.3109/01677069309083452.

DOI:10.3109/01677069309083452
PMID:8126599
Abstract

The pathologic phenotype of the testis in both prepuberal and postpuberal male weaver mutant mice was studied by light microscopy. Morphometric analysis of seminiferous tubules was carried out. Epididymal fluid was examined for the presence of spermatozoa. The seminiferous tubules of 21-day-old prepuberal weaver mutant mice lacked patent lumina and had more degenerated cells than control mice. Fifty-six day-old weaver mutants had many germinal epithelial cells located within the adluminal compartment that were in advanced stages of degeneration. Round spermatids were enlarged and multinucleated. Round spermatids and spermatocytes had sloughed into the lumen. Compared to control mice, elongated spermatids were seen less frequently. In older weaver mice, the degenerative process involved germ cells in both the adluminal and basal compartments. In 143- and 226- day-old weaver mutants, the Sertoli cells were atrophic. Diameters of seminiferous tubules in weaver mice were significantly reduced when compared to control mice. Sperm were either absent or very low in number in the epididymal fluid of postpuberal weaver mice. We conclude that spermatogenesis is abnormal in male weaver mutant mice. The testicular phenotype is characterized by a degenerative process that affects both germ cells and supporting cells.

摘要

通过光学显微镜研究了青春期前和青春期后雄性韦弗突变小鼠睾丸的病理表型。对生精小管进行了形态计量分析。检查附睾液中是否存在精子。21日龄青春期前韦弗突变小鼠的生精小管缺乏明显的管腔,且退化细胞比对照小鼠更多。56日龄的韦弗突变体有许多位于近腔室的生殖上皮细胞处于晚期退化阶段。圆形精子细胞增大且多核。圆形精子细胞和精母细胞已脱落在管腔内。与对照小鼠相比,长形精子细胞较少见。在年龄较大的韦弗小鼠中,退化过程涉及近腔室和基底室中的生殖细胞。在143日龄和226日龄的韦弗突变体中,支持细胞萎缩。与对照小鼠相比,韦弗小鼠的生精小管直径显著减小。青春期后韦弗小鼠的附睾液中精子要么不存在,要么数量极少。我们得出结论,雄性韦弗突变小鼠的精子发生异常。睾丸表型的特征是一个影响生殖细胞和支持细胞的退化过程。

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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。
J Neurogenet. 1993 Dec;9(2):89-104. doi: 10.3109/01677069309083452.
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引用本文的文献

1
Phosphoribosyl-pyrophosphate synthetase 2 (PRPS2) depletion regulates spermatogenic cell apoptosis and is correlated with hypospermatogenesis.磷酸核糖焦磷酸合成酶 2(PRPS2)缺失可调节生精细胞凋亡,并与少精子症相关。
Asian J Androl. 2020 Sep-Oct;22(5):493-499. doi: 10.4103/aja.aja_122_19.
2
Cell death in weaver mouse cerebellum.韦弗氏小鼠小脑的细胞死亡。
Cerebellum. 2002 Jul;1(3):201-6. doi: 10.1080/14734220260418420.
3
courtless, the Drosophila UBC7 homolog, is involved in male courtship behavior and spermatogenesis.无 courtless(果蝇 UBC7 同源物)参与雄性求偶行为和精子发生。 (注:这里“courtless”根据语境推测可能是特定基因名称之类的,直接保留英文未翻译,因为不清楚其准确中文译名,如果有准确中文信息请自行替换。)
Genetics. 2000 Jul;155(3):1267-80. doi: 10.1093/genetics/155.3.1267.
4
Evidence of elevated intracellular calcium levels in weaver homozygote mice.织工纯合子小鼠细胞内钙水平升高的证据。
J Physiol. 2000 Apr 15;524 Pt 2(Pt 2):447-55. doi: 10.1111/j.1469-7793.2000.t01-2-00447.x.
5
Identification of morc (microrchidia), a mutation that results in arrest of spermatogenesis at an early meiotic stage in the mouse.鉴定小鼠中一种名为morc(微睾症)的突变,该突变导致精子发生在减数分裂早期停滞。
Proc Natl Acad Sci U S A. 1998 Nov 24;95(24):14361-6. doi: 10.1073/pnas.95.24.14361.
6
Behavioral analysis of Drosophila mutants displaying abnormal male courtship.
Invert Neurosci. 1997 Sep-Dec;3(2-3):175-83. doi: 10.1007/BF02480372.
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Diverse cell death pathways result from a single missense mutation in weaver mouse.在韦弗小鼠中,单个错义突变导致了多种细胞死亡途径。
Am J Pathol. 1997 Dec;151(6):1629-38.
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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
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cDNA approaches to isolation of the mouse mutant weaver gene.采用互补DNA方法分离小鼠突变体韦弗基因。
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