Regulation of the density of spermatogonia in the seminiferous epithelium of the Chinese hamster: I. Undifferentiated spermatogonia

Rooij, Dirk G. de; Janssen, Jasmijn

doi:10.1002/ar.1092170203

Cited by 78 publications

(39 citation statements)

References 9 publications

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“…In line with this, the numbers of clones of GFRA1C Aal4 were markedly reduced and GFRA1C Aal8 were even absent in stages VII-VIII. Since under physiological conditions apoptosis takes place in differentiating spermatogonia but not in undifferentiated spermatogonia (de Rooij & Janssen 1987, de Rooij & Lok 1987 we interpret this as a consequence of the progression of GFRA1C Aal clones into the next differentiation compartment. In addition, we found that Kit mRNA levels were significantly upregulated by GDNF during stages II-VIII.…”

Section: Discussionmentioning

confidence: 93%

Distribution of GFRA1-expressing spermatogonia in adult mouse testis

Grasso¹,

Fuso²,

Dovere³

et al. 2012

Reproduction

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In mice and other mammals, spermatogenesis is maintained by spermatogonial stem cells (SSCs), a cell population belonging to undifferentiated type A spermatogonia. In the accepted model of SSC self-renewal, Asingle (As) spermatogonia are the stem cells, whereas paired (Apaired (Apr)) and chained (Aaligned (Aal)) undifferentiated spermatogonia are committed to differentiation. This model has been recently challenged by evidence that As and chained (Apr and Aal), undifferentiated spermatogonia are heterogeneous in terms of gene expression and function. The expression profile of several markers, such as GFRA1 (the GDNF co-receptor), is heterogeneous among As, Apr and Aal spermatogonia. In this study, we have analysed and quantified the distribution of GFRA1-expressing cells within the different stages of the seminiferous epithelial cycle. We show that in all stages, GFRA1C chained spermatogonia (Apr to Aal) are more numerous than GFRA1C As spermatogonia. Numbers of chained GFRA1C spermatogonia are sharply reduced in stages VII-VIII when Aal differentiate into A1 spermatogonia. GFRA1 expression is regulated by GDNF and in cultures of isolated seminiferous tubules, we found that GDNF expression and secretion by Sertoli cells is stage-dependent, being maximal in stages II-VI and decreasing thereafter. Using qRT-PCR analysis, we found that GDNF regulates the expression of genes such as Tex14, Sohlh1 and Kit (c-Kit) known to be involved in spermatogonial differentiation. Expression of Kit was upregulated by GDNF in a stage-specific manner. Our data indicate that GDNF, besides its crucial role in the self-renewal of stem cells also functions in the differentiation of chained undifferentiated spermatogonia.

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Section: Discussionmentioning

confidence: 93%

Distribution of GFRA1-expressing spermatogonia in adult mouse testis

Grasso¹,

Fuso²,

Dovere³

et al. 2012

Reproduction

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“…This either means increased proliferative activity of the undifferentiated spermatogonia in p53 knock out mice, suggesting a role of p53 in the regulation of the normal cell cycle of these cells, or a decreased apoptosis of undifferentiated spermatogonia in p53 knock out mice. Apoptosis of differentiating type A spermatogonia in the normal testis has been described extensively by a number of groups (Rodriguez et al, 1997;Furuchi et al, 1996;Allan et al, 1992) and could be useful in removal of aberrant cells and/or regulation of cell density (De Rooij and Lok, 1987;De Rooij and Janssen, 1987). So far, no degeneration/apoptosis of undifferentiated spermatogonia in the normal testis has been observed.…”

Section: Discussionmentioning

confidence: 99%

The role of the tumor suppressor p53 in spermatogenesis

Beumer¹,

Roepers-Gajadien²,

Gademan³

et al. 1998

Cell Death Differ

205

182

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The p53 protein appeared to be involved in both spermatogonial cell proliferation and radiation response. During normal spermatogenesis in the mouse, spermatogonia do not express p53, as analyzed by immunohistochemistry. However, after a dose of 4 Gy of X-rays, a distinct p53 staining was present in spermatogonia, suggesting that, in contrast to other reports, p53 does have a role in spermatogonia. To determine the possible role of p53 in spermatogonia, histological analysis was performed in testes of both p53 knock out C57BL/6 and FvB mice. The results indicate that p53 is an important factor in normal spermatogonial cell production as well as in the regulation of apoptosis after DNA damage. First, p53 knock out mouse testes contained about 50% higher numbers of A 1 spermatogonia, indicating that the production of differentiating type spermatogonia by the undifferentiated spermatogonia is enhanced in these mice. Second, 10 days after a dose of 5 Gy of X-rays, in the p53 knock out testes, increased numbers of giant sized spermatogonial stem cells were found, indicating disturbance of the apoptotic process in these cells. Third, in the p53 knock out testis, the differentiating A 2 -B spermatogonia are more radioresistant compared to their wild-type controls, indicating that p53 is partly indispensable in the removal of lethally irradiated differentiating type spermatogonia. In accordance with our immunohistochemical data, Western analysis showed that levels of p53 are increased in total adult testis lysates after irradiation. These data show that p53 is important in the regulation of cell production during normal spermatogenesis either by regulation of cell proliferation or, more likely, by regulating the apoptotic process in spermatogonia. Furthermore, after irradiation, p53 is important in the removal of lethally damaged spermatogonia.

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“…In contrast, different areas in relevant epithelial stages contain widely variable numbers of A1 spermatogonia. Nevertheless, the density distribution of In and B spermatogonia and preleptotene spermatocytes appeared to be rather even (de Rooij and Janssen, 1987;de Rooij and Lok, 1987). The evening-out of the cell density occurs among A1-A4 spermatogonia.…”

Section: Germ Cell Density Regulation In the Spermatogonial Compartmentmentioning

confidence: 91%

Specific arrests of spermatogenesis in genetically modified and mutant mice

Rooij

Boer²

2003

Cytogenet Genome Res

152

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In naturally occurring mutant mice but also in mice genetically modified for the study of other organs, relatively often a spermatogenic arrest is seen. In a number of cases the arrests appear to be very specific causing apoptosis of germ cells at a particular step in their development, while before this step cells progress normally. These steps include: proliferation/migration of primordial germ cells, the production of differentiating spermatogonia by gonocytes, the regulation of stem cell renewal/differentiation, the differentiation of A_al into A1 spermatogonia, proliferation of A1-A4 spermatogonia, germ cell density regulation, start of meiosis, epithelial stage IV checkpoint of pachytene spermatocytes, the first meiotic division, the formation of the acrosomic vesicle in spermatids and several other steps in spermatid development. In addition, there are many mice that have not been studied in enough detail for a proper categorization. In this review an overview is given of the various mutations and genetically modified mice showing a direct effect on specific spermatogenic cell types. In addition, the relevance of these models to our understanding of the spermatogenic process is discussed.

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Regulation of the density of spermatogonia in the seminiferous epithelium of the Chinese hamster: I. Undifferentiated spermatogonia

Cited by 78 publications

References 9 publications

Distribution of GFRA1-expressing spermatogonia in adult mouse testis

Distribution of GFRA1-expressing spermatogonia in adult mouse testis

The role of the tumor suppressor p53 in spermatogenesis

Specific arrests of spermatogenesis in genetically modified and mutant mice

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