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FACS-sorted Six2-positive nephron progenitor cells at embryonic day 15.5: wildtype (WT) vs. conditional HDAC1&2-null (MUT)

ABSTRACT: Transcriptional profiling of FACS-sorted Six2-positive nephron progenitor cells from Six2CreEGFP mice without (WT) or with (MUT) homozygously floxed HDAC1 and HDAC2 alleles at the age of embryonic day 15.5. This experiment aimed to uncover the genome-wide alternation in gene expression resulting from the removal of HDAC1&2 in the nephron progenitor population and successive changes to the series of events in kidney development.

ORGANISM(S): Mus musculus

PROVIDER: GSE84305 | GEO | 2018/05/08

REPOSITORIES: GEO

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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.

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Whole kidneys at embryonic day 17.5: wildtype (WT) vs. various combinations of the conditional homozygous Ezh2-knockout (Ezh2-KO) from Six2-positive nephron progenitor cells (NPC) and/or germline Ezh1-knockout (Ezh1-KO)

Project description:Transcriptional profiling of whole kidneys from Six2CreEGFP mice without (WT) or with (KO) homozygously floxed Ezh2 alleles at the age of embryonic day 17.5. This experiment aimed to uncover the genome-wide alternation in gene expression resulting from the removal of Ezh2 gene in the nephron progenitor population (Six2 positive) in combination with the removal of Ezh1 gene from germline, and successive changes to the series of events in kidney development.

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

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Haploinsufficiency for SIX2 increases nephron progenitor proliferation leading to elevated branching and nephron number

Project description:The regulation of final nephron number in the kidney is poorly understood. However, cessation of nephron formation occurs when the self-renewing nephron progenitor population commits to differentiation. Transcription factors within this progenitor population, such as SIX2, are assumed to control expression of genes promoting self-renewal such that homozygous Six2 deletion results in premature commitment and an early halt to kidney development. In contrast, Six2 heterozygotes were assumed to be unaffected. Using quantitative morphometry, we demonstrate here a paradoxical 18% increase in ureteric branching and final nephron number in Six2 heterozygotes, despite evidence for reduced levels of SIX2 protein and transcript. This is accompanied by a clear shift in nephron progenitor identity with a distinct subset of progenitor genes, including Cited1 and Meox1, downregulated, while others were unaffected. The net result was an increase in nephron progenitor proliferation, as assessed by elevated EDU labelling, an increase in MYC protein and transcriptional upregulation of MYC target genes. Reducing proliferation by introducing Six2 heterozygosity onto the Fgf20-/- background resulted in premature differentiation of the progenitor population. Overall, this data demonstrates a unique dose response of the nephron progenitors to the level of SIX2 protein in which the role of SIX2 in progenitor proliferation versus self-renewal is separable.

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Genome-wide map of SIX2 and SIX1 binding in human embryonic kidney cortex

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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

FACS-sorted ureteric bud-derivative cells at postnatal day one: wildtype (WT) vs. conditional null (MUT) for Bdkrb2

Project description:Transcriptional profiling of FACS-sorted ureteric bud-derivative cells from Hoxb7CreGFP mice without floxed Bdkrb2 allele (WT) or with homozygously floxed Bdkrb2 alleles (MUT) at the age of postnatal one. Both WT and MUT mice have R26RTdTomato allele as a recombinase efficiency indicator, which allows the FACS to sort cells according to both GFP and TdTomato. This experiment aimed to uncover the genome-wide alternation in gene expression resulting from the removal of Bdkrb2 in the ureteric buds and their derivative collecting ducts.

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Chromatin remodelers interact with Eya1 and Six2 to control nephron progenitor cell self-renewal maintenance

Project description:Eya1 interacts with Six1/2 to induce nephron fate and promote nephron progenitor self-renewal. Haploinsufficiency for these genes in humans causes kidney agenesis or hypoplasia. However, how the Eya1-centered network operates remains elusive. Here we identify Eya1's interacting factors via mass-spectrometry and show that Eya1 and Six2 interact with Brg1-based SWI/SNF chromatin-remodeling complex in the kidney. Depletion of Brg1 results in lack of metanephric mesenchyme and depletion of nephron progenitor cells, which is linked to loss of Eya1 expression. Transcriptional profiling reveals conspicuous downregulation of the proto-oncogene Pbx1 and the Dchs1/Fat4 signaling but premature upregulation of a large subset of genes for podocyte lineages and aberrant activation of oncogenic factors in Brg1-deficent cell. ChIP-seq identifies Brg1-occupancy to enhancers at Pbx1 to a distal enhancer of Eya1 that drives nephron progenitor-specific expression. We demonstrate Six2-dependent Brg1 enrichment to the proximal-promoter of Mycn and two distal enhancers of Pbx1, all of which govern nephron progenitor-specific expression in response to binding to Six2. Together, our results suggest a possible mechanism through which the functional specificity of Brg1-BAFs and Eya1-Six2 in cell cycle regulation and self-renewal of the nephron progenitors may be in part achieved.

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