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Glis3 plays a crucial role in spermatogenesis [923]

ABSTRACT: We show that Glis3 is expressed in gonocytes, SSCs and SPCs, but not in differentiated spermatogonia or subsequent stages of spermatogenesis nor in Sertoli or Leydig cells. We further demonstrate that Glis3-deficiency causes a severe impairment in spermatogenesis in mice. Although the number of gonocytes was slightly diminished in Glis3KO testis, the number undifferentiated, PLZF+ spermatogonia was dramatically reduced leading to a virtual block in the progression of spermatogenesis. Gene expression profiling showed that the expression of a number of genes associated with self-renewal and differentiation of spermatogonial cells was significantly decreased in 1-week-old Glis3KO2 testis. These included a set of GDNF-dependent genes, such as Etv5, Bcl6b, Lhx1, Brachyury, Id4, and Pou3f1, and GDNF-independent genes, such as FoxO1, Oct4, and Zbtb16. Impairment of the nuclear localization of FoxO1 may be in part responsible for the reduced expression of Ret, Lhx1, and Sall4 in Glis3KO2 testis. Our study identifies Glis3 as a novel and critical regulator of early stages of spermatogenesis. Thy1+ cells were isolated from 3 WT and 3 Glis3KO2 testis at postnatal day 4, and total RNAs were purified from them. Then the samples were applied to Agilent mouse genome chip.

ORGANISM(S): Mus musculus

SUBMITTER: NIEHS Microarray Core

PROVIDER: E-GEOD-70195 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Glis3 plays a crucial role in spermatogenesis [923]

Project description:We show that Glis3 is expressed in gonocytes, SSCs and SPCs, but not in differentiated spermatogonia or subsequent stages of spermatogenesis nor in Sertoli or Leydig cells. We further demonstrate that Glis3-deficiency causes a severe impairment in spermatogenesis in mice. Although the number of gonocytes was slightly diminished in Glis3KO testis, the number undifferentiated, PLZF+ spermatogonia was dramatically reduced leading to a virtual block in the progression of spermatogenesis. Gene expression profiling showed that the expression of a number of genes associated with self-renewal and differentiation of spermatogonial cells was significantly decreased in 1-week-old Glis3KO2 testis. These included a set of GDNF-dependent genes, such as Etv5, Bcl6b, Lhx1, Brachyury, Id4, and Pou3f1, and GDNF-independent genes, such as FoxO1, Oct4, and Zbtb16. Impairment of the nuclear localization of FoxO1 may be in part responsible for the reduced expression of Ret, Lhx1, and Sall4 in Glis3KO2 testis. Our study identifies Glis3 as a novel and critical regulator of early stages of spermatogenesis.

2016-07-01 | GSE70195 | GEO

Glis3 plays a crucial role in spermatogenesis [848_827]

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Glis3 plays a crucial role in spermatogenesis [848_827]

2016-07-01 | E-GEOD-70194 | biostudies-arrayexpress

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2021-01-19 | GSE111884 | GEO

Effect of 9 days of inhibited GDNF signaling on the transcriptome of the mouse testis

Project description:In the normal adult testis GDNF specifically targets spermatogonial stem cells and early progenitor spermatogonia. Inhibition of GDNF signaling for 9 days alters only 171 of the 15,000 transcripts expressed in the mouse testis. Many of these transcripts are known to be expressed by the spermatogonial stem cells. One transcript that is affected is Kif26A, a known suppressor of GDNF signaling.

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Prepubertal Human Spermatogonia and Mouse Gonocytes Share Conserved Gene Expression of Germline Stem Cell Regulatory

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Translational activation of developmental mRNAs during neonatal mouse testis development

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Germ cell progression through zebrafish spermatogenesis declines with age

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2014-10-10 | PXD000767 | Pride

Non-cell Autonomous Regionalization of Sertoli Valve Epithelia in the Terminal Segment of the Seminiferous Tubules of Mouse Testes

Project description:In mammalian testes, undifferentiated spermatogonia undergo meiotic differentiation in high retinoic acid (RA) signaling states, while their undifferentiated states are maintained by fibroblast growth factors (FGFs) and glial cell line-derived neurotrophic factor (GDNF), the major niche factors for spermatogonial stem/progenitor cells, in the basal compartment of the convoluted seminiferous tubules (STs). In the valve-like terminal end of the STs adjacent to the rete testis (RT), the Sertoli valve (SV) epithelia constitutively lack most spermatogenesis activity due in part to high GDNF expression, leading to the SV-specific enrichment of undifferentiated spermatogonia; however, the molecular and cellular characteristics of the SV epithelia are unclear. By performing a Sertoli cell ablation/replacement experiment using a mouse diphtheria toxin receptor-mediated system, we show here that the SV epithelia are non-cell autonomously specified, together with having high AKT phosphorylation, in the Sertoli cells located adjacent to the RT epithelia. RNA analyses revealed constitutively high expression of Cyp26a1, which encodes an RA-degrading enzyme, in the SV region, together with high expression of Fgf9 in the adjacent RT. Exogenous in vivo RA treatment induced meiotic differentiation of the spermatogonia located within the SV region, leading to disruption of the SV structure by the ectopic appearance of adluminal meiotic germ cells in some severely affected STs. We therefore propose that the regionalization and inactive spermatogenesis of SV epithelia are mediated in part by low RA signaling, together with high FGF9 signals in the terminal end of the STs.

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