Analysis Tools
reproductive system
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• immunofluorescence of PNA (a marker of acrosome structure in round and elongating spermatids), showed no round or elongating spermatids at 2 months of age
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• massive male germ cell (GC) depletion at P15 with complete GC loss by 2 months of age
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azoospermia
(
J:268375
)
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• no spermatozoa are found in the epididymis at 2 months of age
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• increased number of apoptotic cells in the seminiferous epithelium after P10, as shown by TUNEL staining; likely contributing to GC loss and tubular degeneration
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• impaired male GC proliferation after P10, as shown by Ki67 staining
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• progressive collapse of tubular architecture with aberrant localization of the basement membrane and type I collagen layer, as shown by immunofluorescent staining of laminin alpha2 and collagen I
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• aberrant localization of peritubular myoid cells in most tubules, as shown by absence of alpha-smooth muscle actin staining from P15
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• at P15, the seminiferous epithelium shows complete loss of all cell architecture while some tubules display a Sertoli-cell-only phenotype
• disruption of cytoskeletal organization of actin, microtubules, and vimentin across the seminiferous epithelium
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• immunofluorescence of blood-testis barrier (BTB) proteins (ZO-1, ZO-2, and beta-catenin) revealed disruption of BTB integrity
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• the number of SCs is dramatically reduced from P10
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• immunofluorescence of Wilm's tumor 1 (WT1, a marker for Sertoli cell (SC) nuclei), revealed aberrant localization of SCs at P15
• many tubules with relatively intact tubular structures have a large proportion of SCs scattered over the seminiferous epithelium, rather than located along the basal membrane as in the control mice, suggesting impaired SC polarity
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• males exhibit progressive atrophy of the seminiferous tubules starting at P5
• most tubules show degeneration and loss of tubular structures by P15
• complete loss of the tubular structures by 2 months of age
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• disrupted balance of testicular cell populations at 2 months of age, with significantly decreased mRNA levels of functional markers for male germ cells and Sertoli cells and increased mRNA levels of markers for Leydig cells
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• testis weight is normal at P1 but starts to decline after P5; testis weight is reduced by 80% at P15 and is less than 10% of that in control mice at 2 months of age
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• males exhibit progressive testis degeneration
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• immunofluorescence of PNA (a marker of acrosome structure in round and elongating spermatids), showed no round or elongating spermatids at 2 months of age
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• epididymis weight is reduced to 25% of that in control mice at 2 months of age
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• males are infertile at 2 months of age
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cellular
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• immunofluorescence of PNA (a marker of acrosome structure in round and elongating spermatids), showed no round or elongating spermatids at 2 months of age
|
|
|
• massive male germ cell (GC) depletion at P15 with complete GC loss by 2 months of age
|
azoospermia
(
J:268375
)
|
|
• no spermatozoa are found in the epididymis at 2 months of age
|
|
|
• both the actin and microtubule cytoskeleton appear disorganized in Sertoli cells from P15, as shown by irregular arrangement and aberrant assembly of actin filaments and microtubules, respectively
• vimentin (a marker of the intrinsic cytoskeleton of SCs) fails to form apical extensions at P15 while its directional polarity is lost
• vimentin distribution appears disordered and its expression is completely lost in some tubules at 2 months of age
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• increased number of apoptotic cells in the seminiferous epithelium after P10, as shown by TUNEL staining; likely contributing to GC loss and tubular degeneration
|
|
|
• impaired male GC proliferation after P10, as shown by Ki67 staining
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endocrine/exocrine glands
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• increased number of apoptotic cells in the seminiferous epithelium after P10, as shown by TUNEL staining; likely contributing to GC loss and tubular degeneration
|
|
|
• progressive collapse of tubular architecture with aberrant localization of the basement membrane and type I collagen layer, as shown by immunofluorescent staining of laminin alpha2 and collagen I
|
|
|
• aberrant localization of peritubular myoid cells in most tubules, as shown by absence of alpha-smooth muscle actin staining from P15
|
|
|
• at P15, the seminiferous epithelium shows complete loss of all cell architecture while some tubules display a Sertoli-cell-only phenotype
• disruption of cytoskeletal organization of actin, microtubules, and vimentin across the seminiferous epithelium
|
|
|
• immunofluorescence of blood-testis barrier (BTB) proteins (ZO-1, ZO-2, and beta-catenin) revealed disruption of BTB integrity
|
|
|
• the number of SCs is dramatically reduced from P10
|
|
|
• immunofluorescence of Wilm's tumor 1 (WT1, a marker for Sertoli cell (SC) nuclei), revealed aberrant localization of SCs at P15
• many tubules with relatively intact tubular structures have a large proportion of SCs scattered over the seminiferous epithelium, rather than located along the basal membrane as in the control mice, suggesting impaired SC polarity
|
|
|
• males exhibit progressive atrophy of the seminiferous tubules starting at P5
• most tubules show degeneration and loss of tubular structures by P15
• complete loss of the tubular structures by 2 months of age
|
|
|
• disrupted balance of testicular cell populations at 2 months of age, with significantly decreased mRNA levels of functional markers for male germ cells and Sertoli cells and increased mRNA levels of markers for Leydig cells
|
|
|
• testis weight is normal at P1 but starts to decline after P5; testis weight is reduced by 80% at P15 and is less than 10% of that in control mice at 2 months of age
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• males exhibit progressive testis degeneration
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