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Next Generation Sequencing of Wild Type and Glis3 Mutant Fetal Testis Transcriptomes

ABSTRACT: The goals of this study are to utilize high-throughput transcriptome sequencing of mutant and control fetal testis samples to identify changes in both transcript and repeat element abundance in tissues harboring a homozygous mutation for Glis3. 672 unique genes were differentially expressed in mutant versus wild-type samples. Of the downregulated genes, there was a strong enrichment for piRNA pathway members, while upregulated genes were associated with leydig cell differentiation, meiosis, and histone cluster genes. Differential expression of several repeat elements was also detected in mutant samples. Our findings provide valuable information on the potential mechanisms underlying the fetal germ cell loss observed in Glis3 mutant testes.

ORGANISM(S): Mus musculus

PROVIDER: GSE72808 | GEO | 2016/03/01

SECONDARY ACCESSION(S): PRJNA295095

REPOSITORIES: GEO

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Next Generation Sequencing of Wild Type and Glis3 Mutant Fetal Testis Transcriptomes

Project description:The goals of this study are to utilize high-throughput transcriptome sequencing of mutant and control fetal testis samples to identify changes in both transcript and repeat element abundance in tissues harboring a homozygous mutation for Glis3. 672 unique genes were differentially expressed in mutant versus wild-type samples. Of the downregulated genes, there was a strong enrichment for piRNA pathway members, while upregulated genes were associated with leydig cell differentiation, meiosis, and histone cluster genes. Differential expression of several repeat elements was also detected in mutant samples. Our findings provide valuable information on the potential mechanisms underlying the fetal germ cell loss observed in Glis3 mutant testes. Whole testis mRNA profiles of embryonic day 14.5 wild type (WT) and Glis3 mutant mice were generated by deep sequencing, using Illumina HiSeq2500

2016-03-01 | E-GEOD-72808 | biostudies-arrayexpress

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. 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.

2016-07-01 | E-GEOD-70195 | biostudies-arrayexpress

Glis3 plays a crucial role in spermatogenesis [848_827]

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. Testis total RNAs were purified from 4 WT and 4 Glis3KO2 at 1 week old age, and 3WT and 3 Glis3KO2 at 3 week-old age. Then the samples were applied to Agilent mouse genome chip.

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

Glis3 plays a crucial role in spermatogenesis [923]

2016-07-01 | GSE70195 | GEO

Glis3 plays a crucial role in spermatogenesis [848_827]

2016-07-01 | GSE70194 | GEO

Glis3: The role in osteoblast differentiation and adipocyte differentiation

Project description:The expression of Glis3 in C3H10T1/2 cells promotes osteoblastic differentiation as indicated by the the induction of increase in alkaline phosphatase activity, an early marker of osteoblast differentiation, and increased expression of osteopontin, a late marker of osteogenesis. Glis3 acts synergistically with bone morphogenic protein 2 (BMP-2). In contrast, expression of Glis3 inhibits the induction of adipocyte differentiation. Microarray analysis identified the fibroblast growth factor 18 (FGF18) as one of the genes induced by Glis3 in C3H10T1/2 cells directly. Keywords: Glis3, osteoblast differentiation, adipocyte differentiation, FGF18, BMP2

2007-05-22 | GSE5379 | GEO

Glis3 plays a crucial role in thyroid hormone production

Project description:The serum hormone levels including T3 and T4 were dramatically decreased in Glis3-null mice due to reduced production of thyroid hormones in thyroid. Gene expression profile and EdU incorporation analysis between WT and Glis3-null mice showed that the cell proliferation was greatly reduced in Glis3-null thyroid. Goitergenic diet (low iodine diet; LID) dramatically enhanced serum TSH levels in both WT and Glis3-null mice, however thyroid goiter was observed in WT mice but not in Glis3-null mice. A subset of genes associated with thyroid hormone production including Pendrin (Slc26a4), Nis (Na+/I– symporter, Slc5a5), Duoxa2 (dualoxidase A2), Tpo (thyroperoxidase), and Dio1 (Deiodinase1) was significantly induced in WT but not in Glis3-null mice by LID feeding.

2017-11-06 | GSE86841 | GEO

Identification of GLIS3 and HNF1b target genes in kidney

Project description:Comparison of cistromes from GLIS3 and HNF1b ChIP-Seq analysis using mouse kidney was performed to examine whether there was a significant overlap in target genes between GLIS3 and HNF1b.

2023-12-31 | GSE240072 | GEO

GLIS3 is indispensable for TSH/TSHR-dependent thyroid hormone biosynthesis and follicular cell proliferation

Project description:Deficiency in Krüppel-like zinc finger transcription factor, GLI-Similar 3 (GLIS3) in humans is associated with the development of congenital hypothyroidism. However, the functions of GLIS3 in the thyroid gland and by what mechanism GLIS3-dysfunction causes hypothyroidism are unknown. In this study, we demonstrate that GLIS3 acts downstream of thyroid stimulating hormone (TSH)/TSHR and is indispensable for TSH/TSHR-mediated induction of thyroid follicular cell proliferation and thyroid hormone biosynthesis. ChIP-Seq and promoter analysis revealed that GLIS3 is critical for the transcriptional activation of several genes required for thyroid hormone biosynthesis, including the iodide transporters Nis and Pds, indicating that these genes are directly regulated by GLIS3. The repression of cell proliferation regulatory genes is due to the inhibition of TSH-mediated activation of the mTORC1/RPS6 pathway as well as direct transcriptional regulation of several cell division-related genes by GLIS3. Consequently, GLIS3-deficiency prevents the development of goiter as well as the induction of inflammatory and fibrotic genes during chronic elevation of circulating TSH. Our study identifies GLIS3 as a new and key regulator of TSH/TSHR-mediated thyroid hormone biosynthesis and proliferation of thyroid follicular cells, and uncovers a mechanism by which GLIS3-deficiency causes congenital hypothyroidism and prevents goiter development.

2017-08-30 | GSE103297 | GEO

Regulation of gene expression by GLIS3 during neonatal kidney development

Project description:Loss of transcription factor GLIS3 function in humans and mice leads to the development of neonatal polycystic kidney disease (PKD). To investigate how loss of GLIS3 function in kidney affects postnatal kidney development and PKD, we analyzed the gene expression profiles of kidneys from WT and Glis3-null mice at P7, P14, and P28 by RNA-Seq analysis using Glis3 global KO model Glis3-mCherry and kidney specific knockout model Glis3-PAX8Cre.

2023-12-31 | GSE240071 | GEO

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