Repression of kit Expression by Plzf in Germ Cells

Filipponi, Doria; Hobbs, Robin M.; Ottolenghi, Sergio; Rossi, Pellegrino; Jannini, Emmanuele A.; Pandolfi, Pier Paolo; Dolci, Susanna

doi:10.1128/mcb.00479-07

Cited by 172 publications

(167 citation statements)

References 42 publications

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“…The expression of Acrosin mRNA could not be detected in the transfected spermatogonia, suggesting that spermatogonia differentiated into early spermatocyte but not spermatid. Downregulation of Plzf, a transcription factor involved in spermatogonial stem cell renewal, 32 is also supportive of the notion that Col1a1 suppression can inhibit proliferation, but enhance differentiation. This effect was confirmed in vivo by electroporation-based gene delivery of Col1a1 antisense mRNA-coding plasmids.…”

Section: Discussionsupporting

confidence: 55%

Downregulation of Col1a1 induces differentiation in mouse spermatogonia

Chen¹,

Li²,

Xu³

2012

Asian J Androl

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Col1a1 (one of the subunit of collagen type I) is a collagen, which belongs to a family of extracellular matrix (ECM) proteins that play an important role in cellular proliferation and differentiation. However, the role of Col1a1 in spermatogenesis, especially in the control of proliferation and differentiation of spermatogonial stem cells (SSCs), remains unknown. In this study, we explored effects of downregulation of Col1a1 on differentiation and proliferation of mouse spermatogonia. Loss-of-function study revealed that Oct4 and Plzf, markers of SSC self-renewal, were significantly decreased, whereas the expression of c-kit and haprin, hallmarks of SSC differentiation, was enhanced after Col1a1 knockdown. Cell cycle analyses indicated that two-thirds of spermatogonia were arrested in S phase after Col1a1 knockdown. In vivo experiments, DNA injection and electroporation of the testes showed that spermatogonia self-renewal ability was impaired remarkably with the loss-of-function of Col1a1. Our data suggest that silencing of Col1a1 can suppress spermatogonia self-renewal and promote spermatogonia differentiation.

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Section: Discussionsupporting

confidence: 55%

Downregulation of Col1a1 induces differentiation in mouse spermatogonia

Chen¹,

Li²,

Xu³

2012

Asian J Androl

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“…However, Plzf is co-expressed with kit in a subset of spermatogonial stem cells during the first wave of spermatogenesis (Naughton et al, 2006). Moreover, recent data in our laboratory indicate that one of the mechanisms through which Plzf maintains the stem cell phenotype is the suppression of kit expression (Filipponi et al, 2007). Thus, Plzf induction by KL in Plzf/kit co-expressing spermatogonia during the first wave of spermatogenesis might contribute to the definitive cessation of kit expression in these cells, which is required to establish the pool of spermatogonial stem cells in the adult testis (Naughton et al, 2006).…”

Section: Growth Factors Receptors Nucleic Acid Binding Proteins Andmentioning

confidence: 85%

Transcriptome analysis of differentiating spermatogonia stimulated with kit ligand

Rossi

Lolicato

Grimaldi

et al. 2008

Gene Expression Patterns

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Kit ligand (KL) is a survival factor and a mitogenic stimulus for differentiating spermatogonia. However, it is not known whether KL also plays a role in the differentiative events that lead to meiotic entry of these cells. We performed a wide genome analysis of difference in gene expression induced by treatment with KL of spermatogonia from 7-day-old mice, using gene chips spanning the whole mouse genome. The analysis revealed that the pattern of RNA expression induced by KL is compatible with the qualitative changes of the cell cycle that occur during the subsequent cell divisions in type A and B spermatogonia, i.e. the progressive lengthening of the S phase and the shortening of the G2/M transition. Moreover, KL up-regulates in differentiating spermatogonia the expression of early meiotic genes (for instance: Lhx8, Nek1, Rnf141, Xrcc3, Tpo1, Tbca, Xrcc2, Mesp1, Phf7, Rtel1), whereas it down-regulates typical spermatogonial markers (for instance: Pole, Ptgs2, Zfpm2, Egr2, Egr3, Gsk3b, Hnrpa1, Fst, Ptch2). Since KL modifies the expression of several genes known to be up-regulated or down-regulated in spermatogonia during the transition from the mitotic to the meiotic cell cycle, these results are consistent with a role of the KL/kit interaction in the induction of their meiotic differentiation.

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“…In addition, germ cells of the testes of the Luxoid mutants are not able to repopulate the testes of recipient W/Wv mice, suggesting that the defect is inherent to the stem cells. Interestingly, Plzf directly represses the transcription of the receptor c-kit, which is characteristic of spermatogonial differentiation (Filipponi et al, 2007). Also, undifferentiated spermatogonia isolated from plzf -/-mice exhibit a marked increase in c-kit expression.…”

Section: Etv5 and Other Transcription Factorsmentioning

confidence: 99%

Gdnf signaling pathways within the mammalian spermatogonial stem cell niche

Hofmann

2008

Molecular and Cellular Endocrinology

200

176

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SummaryMammalian spermatogenesis is a complex process in which male germ-line stem cells develop to ultimately form spermatozoa. Spermatogonial stem cells, or SSCs, are found in the basal compartment of the seminiferous epithelium. They self-renew to maintain the pool of stem cells throughout life, or they differentiate to generate a large number of germ cells. A balance between SSC self-renewal and differentiation in the adult testis is therefore essential to maintain normal spermatogenesis and fertility. Maintenance and self-renewal are tightly regulated by extrinsic signals from the surrounding microenvironment, called the spermatogonial stem cell niche. By physically supporting the SSCs and providing them with growth factors, the Sertoli cell is the main component of the niche. In addition, adhesion molecules that connect the SSCs to the basement membrane and cellular components of the interstitium between the seminiferous tubules are important regulators of the niche function. This review mainly focuses on glial cell line-derived neurotrophic factor (Gdnf), which is produced by Sertoli cells to maintain SSCs self-renewal, and the downstream signaling pathways induced by this crucial growth factor. Interactions between Gdnf and other signaling pathways that maintain self-renewal, as well as the role of novel SSC-and Sertoli cell-specific transcription factors, are also discussed.

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Repression of kit Expression by Plzf in Germ Cells

Cited by 172 publications

References 42 publications

Downregulation of Col1a1 induces differentiation in mouse spermatogonia

Downregulation of Col1a1 induces differentiation in mouse spermatogonia

Transcriptome analysis of differentiating spermatogonia stimulated with kit ligand

Gdnf signaling pathways within the mammalian spermatogonial stem cell niche

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