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RNA Sequencing of mouse E15.5 Six2-Cre Irx3/5(loxP/loxP) whole kidneys

ABSTRACT: RNA Sequencing of mouse E15.5 Six2-Cre Irx3/5(loxP/loxP) whole kidneys

PROVIDER: PRJNA1134083 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29761845_1.fastq.gz	Fastqsanger.gz
	SRR29761845_2.fastq.gz	Fastqsanger.gz
	SRR29761846_1.fastq.gz	Fastqsanger.gz
	SRR29761846_2.fastq.gz	Fastqsanger.gz
	SRR29761847_1.fastq.gz	Fastqsanger.gz

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RNA Sequencing of mouse E15.5 Six2-Cre; Irx3/5(loxP/loxP) whole kidneys

Project description:Transcriptional profiling of E15.5 whole kidneys with a conditional deletion of Irx3/5 in the nephron progenitor cell lineage. Irx3/5 were conditionally deleted using Six2-driven Cre-recombinase. Data will provide novel insight into the functional contributions of Irx3/5 towards nephrogenesis.

2024-07-23 | GSE271904 | GEO

Investigation of gene expression profiles in the kidneys of Cnnm2fl/fl;Six2-Cre mice.

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Transcriptional responses in SIX2 nephron progenitor cells following mitochondrial complex III subunit 7 (Qpc) inactivation

Project description:To identify novel transcriptional targets following Qpc inactivation. We deleteted Qpc in SIX2 nephron progenitor cells using a Six2-eGFP/cre BAC transgene. We compared SIX2-expressing progenitors from Six2-Qpc-/- kidneys with control (Six2-Qpc+/-) embryonic kidneys at E18.5.

2022-06-29 | GSE158299 | GEO

Genome-wide maps of Six2 and b-catenin in mesenchymal nephron progenitors

Project description:Self-renewing undifferentiated nephron progenitors express Six2, a transcription factor that is required for their maintenance as undifferentiated progenitors. Differentiation of nephron progenitors is triggered by Wnt/b-catenin signaling. In order to understand how Six2 and Wnt signaling counteract each other, we performed ChIP-seq of Six2 and b-catenin in mesenchymal nephron progenitor cells. Nephron progenitors were FACS-isolated from BAC transgenic Six2GFPcre-positive embryonic kidneys at E16.5. For Six2 ChIP, freshly FACS isolated Six2+ cells were used. For b-catenin ChIP, FACS isolated Six2+ cells were aggregated by centrifugation at 850g for 5min and incubated in 10%FBS/DMEM containing 4uM BIO for 24hrs.

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Next Generation Sequencing of BMDM overexpressing GFP, IRX3-WT, IRX3-S361A and IRX3-S389A

Project description:IRX3 is a transcriptional factor, which play important functions in developmental processes. But the role of IRX3 in immune cells are less studied. So we sequenced mRNA from BMDMs overexpressing GFP, IRX3, as well as two phosphorylation site mutants-S361A and S389A respectively, to address the roles of IRX3 in macrophages.

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Gene expression profiling of E15.5 FoxD1 Cre;Dicer and control embryonic kidneys

Project description:The aim of this study is to address the functional role of miRNAs in the FoxD1+ renal stroma progenitors and derivatives during embryonic kidney development. To achieve this, we generated transgenic mice that lack miRNAs in the renal stroma lineage (FoxD1 Cre;Dicer), and performed a microarray analysis on E15.5 whole kidneys to determine the transcriptional changes.

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Exploring Six2 distal enhancer interactome in developing mouse kidney

Project description:The Six2 distal enhancer regulates expression of the 60 kb-downstream gene Six2, but does not regulate the Six3 gene which is 70 kb further downstream. CTCF ChIP-Seq and Hi-C data points to a chromatin domain boundary between Six2 and Six3 which may intervene interaction between Six2-DE and Six3. The irradiation-induced Brachyrrhine (Br) mutant allele was found to carry a 320 kb genomic inversion that includes Six2 and Six3, but not Six2DE. This repositioned Six2 under Six3 enhancer control and Six3 under Six2 distal enhancer control. Consistent with this, Six3 is ectopically expressed in Br/+ kidneys and Six2 expression is reduced. To test whether there is a change of interaction between Six2 distal enhancer and Six2 or Six3 promoters, we performed 4C-Seq in E16.5 wildtyp or Br/+ mice nephron-genic zone cells.

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Six1 and Six2 of the sine oculis homeobox subfamily are not functionally interchangeable in mouse nephron formation

Project description:The vertebrate Six1 and Six2 arose by gene duplication from the Drosophila so (sine oculis) and have since diverged in their developmental expression patterns. Both genes are expressed in nephron progenitors of human fetal kidneys, and mutations in SIX1 or SIX2 cause branchio-oto-renal or renal hypodysplasia respectively. Since ~80% of SIX1 target sites are shared by SIX2, it is speculated that SIX1 and SIX2 may be functionally interchangeable by targeting common downstream genes. In contrast, in mouse kidneys, the expression of Six1 and Six2 only transiently overlaps in the metanephric mesenchyme before the onset of ureteric branching, and only Six2 expression is maintained in the nephron progenitors throughout development. This non-overlapping expression between Six1 and Six2 in mouse nephron progenitors promoted us to examine if Six1 can replace Six2. Surprisingly, forced expression of Six1 failed to rescue Six2-deficient kidney hypoplasia. We found that Six1 mediated Eya1 nuclear translocation and inhibited premature epithelialization of the progenitors but failed to rescue the proliferation defects and cell death caused by Six2-knockout. Genome-wide binding analyses showed that Six1 only bound to a small subset of Six2 target sites, but many Six2-bound loci that are crucial to the renewal and differentiation of nephron progenitors lacked Six1 occupancy. Thus, these data indicate that Six1 cannot substitute Six2 to drive nephrogenesis in mouse kidneys, demonstrating that these two transcription factors have not maintained equivalent biochemical properties since their divergence early in vertebrate evolution.

2022-01-27 | GSE189131 | GEO

Whole kidneys at embryonic day 16.5: wildtype (WT) vs. conditional Dot1-knockout (KO) from Six2-positive nephron progenitor cells (NPC)

Project description:Transcriptional profiling of whole kidneys from Six2CreEGFP mice without (WT) or with (KO) homozygously floxed DOT1 alleles at the age of embryonic day 16.5. This experiment aimed to uncover the genome-wide alternation in gene expression resulting from the removal of DOT1 gene in the nephron progenitor population (Six2 positive) and successive changes to the series of events in kidney development.

2019-12-31 | GSE110928 | GEO

Gene expression profiling of Six2-positive nephron progenitors from mouse embryo

Project description:Nephron progenitors in the embryonic kidney propagate while generating differentiated nephrons. However, the progenitors in mice terminally differentiate shortly after birth. We defined culture conditions to selectively propagated nephron progenitors in vitro in an undifferentiated state. To understand how expression profiles of Six2+ cells changed during culture in vitro compared with in vivo, we performed microarray analysis of Six2+ cells at E11.5 (starting material) and P0 (experiencing 8 days in vivo), and cultured Six2+ cells at E11.5 for 8 days or 19 days. Microarray analysis were performed with isolated Six2-positive nephron progenitors from transgenic mice embryo at E11.5 or P0, and cultured E11.5 Six2+ cells for 8 or 19 days in conditioned media. P0 non-progenitors represent Six2-GFP-negative cells at P0.

2016-04-14 | E-GEOD-79024 | biostudies-arrayexpress

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