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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. Whole testis mRNA profiles of embryonic day 14.5 wild type (WT) and Glis3 mutant mice were generated by deep sequencing, using Illumina HiSeq2500

ORGANISM(S): Mus musculus

SUBMITTER: Humphrey Yao

PROVIDER: E-GEOD-72808 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2016-03-01 | GSE72808 | GEO

Disease-associated mutation in SRSF2 misregulates splicing by altering RNA binding affinities

Project description:SRSF2 is an RNA binding protein that plays important roles in splicing of mRNA precursors. Mutations in SRSF2 are frequently found in patients with myelodysplastic syndromes and certain leukemias, but how they affect SRSF2 function has only begun to be examined. Here we used CRISPR/Cas9 to introduce the P95H mutation to SRSF2 in K562 leukemia cells, generating an isogenic model so that splicing alterations can be attributed solely to mutant SRSF2. We found that SRSF2 (P95H) misregulates 548 splicing events (<1% of total). Of these, 374 involve the inclusion of cassette exons, and the inclusion was either increased (206) or decreased (168). We detected a specific motif (UCCA/UG) enriched in the more included exons and a distinct motif (UGGA/UG) in the more excluded exons. RNA gel shift assays showed that a mutant SRSF2 derivative bound more tightly than its wild-type counterpart to RNA sites containing UCCAG, but less tightly to UGGAG sites. The pattern of exon inclusion or exclusion thus correlated in most cases with stronger or weaker RNA binding, respectively. We further show that the P95H mutation does not affect other functions of SRSF2, i.e., protein-protein interactions with key splicing factors. Our results thus demonstrate that the P95H mutation positively or negatively alters the binding affinity of SRSF2 for cognate RNA sites in target transcripts, leading to misregulation of exon inclusion. Our findings not only shed light on the mechanism of the disease-associated SRSF2 mutation in splicing regulation, but also reveal a group of mis-spliced mRNA isoforms for potential therapeutic targeting. Examination of differentially spliced events in K562 CRISPR cell clones (with wild-type or mutant SRSF2) by RNA sequencing

2015-08-10 | E-GEOD-71299 | biostudies-arrayexpress

Alternative RNA processing events in a double NSR mutant Arabidopsis

Project description:We analyze the effect of a double deletion mutant for alternative-splicing regulators nsra and nsrb (Nuclear Speckle RNA binding proteins), on the Arabidopsis thaliana transcriptome. RNA-seq experiments (polyA+ RNA) in triplicates for each condition WT and nsrab mutants.

2016-07-03 | E-GEOD-65717 | 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

MIWI2 and MILI have differential effects on piRNA biogenesis and DNA methylation

Project description:In developing male germ cells, prospermatogonia, two Piwi proteins, MILI and MIWI2, use piRNA guides to repress transposable element (TE) expression and ensure genome stability and proper gametogenesis. In addition to their roles in post-transcriptional TE repression, both proteins are required for DNA methylation of TE sequences. Here we analyzed the effect of Miwi2 deficiency on piRNA biogenesis and transposon repression. Miwi2-deficiency had only a minor impact on piRNA biogenesis; however, the piRNA profile of Miwi2-knockout mice indicated overexpression of several LINE1 TE families that led to activation of the ping-pong piRNA cycle. Furthermore, we found that MILI and MIWI2 have distinct functions in TE repression in the nucleus. MILI is responsible for DNA methylation of a larger subset of TE families than MIWI2 suggesting that the proteins have independent roles in establishing DNA methylation patterns. Small RNA profiles (19-30 nt range) of embryonic (E16.5) and post-natal (P10) testis of Miwi2 mutant mice and matched heterozygote controls. mRNA profiles of embryonic testis (E16.5) of heterozygote control mice and of postnatal testis (P10) of Miwi2 and Mili mutants and heterozygote controls. CpG methylation BS-seq profile of postnatal (P10) spermatocytes of Miwi2 mutant mice and matched heterozygote controls.

2015-07-11 | E-GEOD-70731 | 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 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

Mus musculus

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

| PRJNA295095 | ENA

Induction of insulin gene transcription by Gli-similar KrÃ¼ppel-like zinc finger protein 3, Glis3, in Î±TC1-9 cells

Project description:In this study, we examined the effect of Glis3 on the transcriptional activation of gene expression, including insulin gene, in pancreatic Î±-cell line, Î±TC1-9, which do not express the insulin gene. We demonstrate that Glis3 induces the transcription of the insulin and identified a number of other genes that are induced by Glis3. Using ChIP-Seq we map the genome-wide sites with which Glis3 is associated. From this the consesus Glis3 binding site was calculated. This study shows that Glis3 is recruited to the proximal promoter of the insuln gene inthe pancreatic Î±-cell line, Î±TC1-9.

2016-03-14 | E-GEOD-72566 | biostudies-arrayexpress

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