Svp-3, a third polymorphic locus for mouse seminal vesicle proteins

1983 ◽  
Vol 21 (7-8) ◽  
pp. 797-800 ◽  
Author(s):  
R. Moutier ◽  
M. F. Bertrand
2012 ◽  
Vol 11 (6) ◽  
pp. M111.014993 ◽  
Author(s):  
Amy J. Claydon ◽  
Steven A. Ramm ◽  
Andrea Pennington ◽  
Jane L. Hurst ◽  
Paula Stockley ◽  
...  

Andrologia ◽  
2020 ◽  
Author(s):  
Sitthichai Iamsaard ◽  
Saranya Tongpan ◽  
Supataechasit Yannasithinon ◽  
Supatcharee Arun ◽  
Alexander T. H. Wu ◽  
...  

2019 ◽  
Vol 20 (18) ◽  
pp. 4557 ◽  
Author(s):  
Miyuki Shindo ◽  
Masafumi Inui ◽  
Woojin Kang ◽  
Moe Tamano ◽  
Cai Tingwei ◽  
...  

Multiple genes, whose functions or expression are overlapping, compensate for the loss of one gene. A gene cluster in the mouse genome encodes five seminal vesicle proteins (SVS2, SVS3, SVS4, SVS5, and SVS6). These proteins are produced by male rodents and function in formation of the copulatory plug following mating. SVS2 plays an essential role in the successful internal fertilization by protecting the sperm membrane against a uterine immune attack. We hypothesized that the four remaining seminal vesicle proteins (SVPs) of this gene cluster may partially/completely compensate for the deficiency of SVS2. For confirming our hypothesis, we generated mice lacking the entire SVP-encoding gene cluster and compared their fecundity with Svs2-deficient (Svs2−/−) mice; that is, mice deficient in Svs2 alone. A single loxP site remained after the deletion of the Svs2 gene. Therefore, we inserted another loxP site by combining the CRISPR/Cas9 system with single-stranded oligodeoxynucleotides (ssODN). Male mice lacking the entire SVP-encoding gene cluster (Svs2–6−/− mice) and thereby all five SVP proteins, generated by the deletion of 100kbp genomic DNA, showed low fecundity. However, the fecundity level was comparable with that from Svs2−/− male mice. Our results demonstrate that SVS3, SVS4, SVS5, and SVS6 do not function in the protection of sperm against a uterine immune attack in the absence of SVS2. Thus, Svs2 is the critical gene in the SVP gene cluster.


2019 ◽  
Vol 86 (11) ◽  
pp. 1682-1693
Author(s):  
Rubhadevi Balu ◽  
Shiyam Sundar Ramachandran ◽  
Sudhakar Gandhi Paramasivam

1969 ◽  
Vol 60 (4) ◽  
pp. 187-192 ◽  
Author(s):  
ROBERT D. PLATZ ◽  
H. GLENN WOLFE

2020 ◽  
Vol 49 ◽  
Author(s):  
Bruna Alves Felix ◽  
Kamila de Sousa Otávio ◽  
Jorge André Matias Martins ◽  
Fágner Cavalcante Patrocínio dos Santos ◽  
Ana Luiza Malhado Cazaux de Souza Velho ◽  
...  

Reproduction ◽  
1996 ◽  
Vol 107 (2) ◽  
pp. 265-277 ◽  
Author(s):  
S. A. Robertson ◽  
V. J. Mau ◽  
K. P. Tremellen ◽  
R. F. Seamark

Author(s):  
V. F. Allison ◽  
G. C. Fink ◽  
G. W. Cearley

It is well known that epithelial hyperplasia (benign hypertrophy) is common in the aging prostate of dogs and man. In contrast, little evidence is available for abnormal epithelial cell growth in seminal vesicles of aging animals. Recently, enlarged seminal vesicles were reported in senescent mice, however, that enlargement resulted from increased storage of secretion in the lumen and occurred concomitant to epithelial hypoplasia in that species.The present study is concerned with electron microscopic observations of changes occurring in the pseudostratified epithelium of the seminal vescles of aging rats. Special attention is given to certain non-epithelial cells which have entered the epithelial layer.


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