ArticlePloS one2012
Conditional expression of Wnt9b in Six2-positive cells disrupts stomach and kidney function.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Kidney Organoids: Current Advances and Applications.Life (Basel, Switzerland) · 2025Review
- Elevated Protein Kinase A Activity in Stomach Mesenchyme Disrupts Mesenchymal-epithelial Crosstalk and Induces Preneoplasia.Cellular and molecular gastroenterology and hepatology · 2022Article
- Postnatal prolongation of mammalian nephrogenesis by excess fetal GDNF.Development (Cambridge, England) · 2021Article
- Review
- The core SWI/SNF catalytic subunit Brg1 regulates nephron progenitor cell proliferation and differentiation.Developmental biology · 2020Article
- Review
- Pharmacologic inhibition of RGD-binding integrins ameliorates fibrosis and improves function following kidney injury.Physiological reports · 2020Article
- Catalytically inactive Dnmt3b rescues mouse embryonic development by accessory and repressive functions.Nature communications · 2019Article
- Atmin modulates Pkhd1 expression and may mediate Autosomal Recessive Polycystic Kidney Disease (ARPKD) through altered non-canonical Wnt/Planar Cell Polarity (PCP) signalling.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Disparate levels of beta-catenin activity determine nephron progenitor cell fate.Developmental biology · 2018Article
- Translating Developmental Principles to Generate Human Gastric Organoids.Cellular and molecular gastroenterology and hepatology · 2018Review
- Wnt Signaling in Kidney Development and Disease.Progress in molecular biology and translational science · 2018Review
- A Sall1-NuRD interaction regulates multipotent nephron progenitors and is required for loop of Henle formation.Development (Cambridge, England) · 2017Article
- Impairment of Wnt11 function leads to kidney tubular abnormalities and secondary glomerular cystogenesis.BMC developmental biology · 2016Article
- Assessment of promoter methylation and expression of SIX2 as a diagnostic and prognostic biomarker in Wilms' tumor.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Bap1 is essential for kidney function and cooperates with Vhl in renal tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Atmin mediates kidney morphogenesis by modulating Wnt signaling.Human molecular genetics · 2014Article
- LIM homeodomain transcription factor Isl1 directs normal pyloric development by targeting Gata3.BMC biology · 2014Article
- Sall1 balances self-renewal and differentiation of renal progenitor cells.Development (Cambridge, England) · 2014Article
- Proper development of the outer longitudinal smooth muscle of the mouse pylorus requires Nkx2-5 and Gata3.Gastroenterology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
During kidney development, canonical Wnt signaling activates differentiation, while the transcription factor Six2 maintains the progenitor pool. These opposing signals help to regulate nephron formation and ensure the full complement of nephrons are formed. Since these two factors control differing fates in kidney mesenchyme, we hypothesized that overexpression of Wnt9b in Six2-expressing cells would disrupt kidney formation and may alter cell differentiation decisions in other tissues. We created a transgenic mouse that conditionally expressed the canonical Wnt ligand in the developing kidney, Wnt9b. The transgene is activated by cre recombinase and expresses GFP. We first tested its biological activity using Hoxb7-cre and found that transgenic Wnt9b was capable of inducing differentiation genes and of rescuing kidney development in Wnt9b(-/-) homozygous deficient mice. In contrast, expression of Wnt9b in cells using Six2-cre caused gastrointestinal distress and severe renal failure in adult mice. Transgenic kidneys had numerous cystic tubules and elevated creatinine values (0.652 ± 0.044) compared to wild-type mice (0.119 ± 0.002). These animals also exhibited a malformed pyloric sphincter, duodenogastric reflux, and a transformation of the distal stomach into proximal fate. The gene expression changes observed for the Wnt9b:EGFP transgene were compared to a stabilized β-catenin allele to determine that Wnt9b is activating the canonical Wnt pathway in the tissues analyzed. These results demonstrate that expression of Wnt9b in Six2-positive cells disrupts cell fate decisions in the kidney and the gastrointestinal tract.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.