Role of fibroblast growth factor receptors 1 and 2 in the ureteric bud

Zhao, Haotian; Kegg, Heather; Grady, Sandy; Truong, Hoang Trang; Robinson, Michael L.; Baum, Michel; Bates, Carlton M.

doi:10.1016/j.ydbio.2004.09.002

Cited by 198 publications

(253 citation statements)

References 36 publications

Supporting

Mentioning

242

Contrasting

Order By: Relevance

“…15 A recent conditional knockout study in which floxed Fgfr2 mice were crossed with HoxB7-Cre mice to inactivate those receptors specifically in the UB lineage reported no UB budding defect, although later kidney development was affected. 26 In the FGF receptor IgG chimera transgenic study, 15 it is possible that no relevant FGFs were available for the WD, whereas in the conditional knockout study, FGF ligands are intact and the possible presence of Fgfr3 or Fgfr4 may be able to transmit the FGF signal to WD cells. Thus, the difference in these two genetic studies might be explained by a lack of FGF signaling BASIC RESEARCH www.jasn.org (resulting in agenesis) versus the presence of FGF signaling (resulting in normal UB bud formation).…”

Section: Discussionmentioning

confidence: 99%

Glial Cell–Derived Neurotrophic Factor–Independent Ureteric Bud Outgrowth from the Wolffian Duct

Maeshima

Sakurai

Choi

et al. 2007

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

The kidney collecting duct system and the ureter derive from the ureteric bud, an outgrowth of the Wolffian duct. It is generally believed that glial cell-derived neurotrophic factor (GDNF) plays a critical role in this earliest stage of kidney development, but 30 to 50% of knockout mice that lack either Gdnf or one of its receptors, such as Ret, have normal ureters. This suggests that an alternative pathway can induce ureteric bud outgrowth from the Wolffian duct. Isolated Wolffian ducts were cultured, and it was found that a combination of fibroblast growth factor 7 (FGF7) and blockade of the TGF-␤ superfamily member activin A induced formation of buds from the Wolffian duct. This occurred even in the presence of a neutralizing anti-GDNF antibody or in Ret-knockout-derived Wolffian ducts, suggesting GDNFindependent induction of bud formation. Similar to wild-type ureteric buds or those induced by GDNF, FGF7/follistatin-induced buds were shown to be functionally competent, as they underwent branching morphogenesis and induced nephron formation upon recombination with metanephric mesenchyme. These in vitro findings suggest that modulation by FGF7 and the activin A signaling pathway, or equivalent pathways, can lead to GDNF-independent induction of ureteric bud outgrowth, possibly explaining the seemingly normal ureteric bud outgrowth in Gdnf or Ret null mice.

show abstract

Section: Discussionmentioning

confidence: 99%

Glial Cell–Derived Neurotrophic Factor–Independent Ureteric Bud Outgrowth from the Wolffian Duct

Maeshima

Sakurai

Choi

et al. 2007

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

show abstract

“…SuFu loxP ) and Gli3 ⌬699 (Böse et al, 2002) mice were maintained on a mixed background, and SuFu ϩ/ Ϫ (kindly provided by C.-C. Hui), Hoxb.7-Cre (Zhao et al, 2004), Ptc1 ϩ/ Ϫ (Goodrich et al, 1997) and Ptc1 loxP (Ellis et al, 2003) mice were maintained on a CD1/129 background. ROSA lacZ/lacZ mice (Soriano, 1999) were maintained on a C57BL/6 background.…”

Section: Methodsmentioning

confidence: 99%

Suppressor of Fused Controls Mid-Hindbrain Patterning and Cerebellar Morphogenesis via GLI3 Repressor

Kim

Gill²,

Rotin³

et al. 2011

J. Neurosci.

View full text Add to dashboard Cite

Sonic Hedgehog and its GLI transcriptional effectors control foliation complexity during cerebellar morphogenesis by promoting granule cell precursor proliferation. Here, we reveal a novel contribution of Sonic Hedgehog-GLI signaling to cerebellar patterning and cell differentiation by generating mice with targeted deletion of Suppressor of Fused (SuFu), a regulator of Sonic Hedgehog signaling, in the mid-hindbrain. Postnatal SuFu-deficient mice exhibit impaired motor coordination and severe cerebellar mispatterning. SuFu conditional knock-out embryos display abnormal mid-hindbrain morphology associated with misexpression of Fgf8, and delayed differentiation and abnormal migration of major cerebellar cell types. Sonic Hedgehog is ectopically expressed in the external granule layer and Hedgehog signaling is upregulated. While expression of full-length GLI transcriptional activators downstream of Hedgehogs is markedly reduced, a processed form of GLI3, a transcriptional repressor, is essentially lost. Genetic expression of a Gli3 allele encoding GLI3 repressor in SuFu-deficient mice largely rescues abnormal cerebellar patterning and cell differentiation observed in mice with SuFu deficiency alone. Together, our data demonstrate that SuFu controls cerebellar patterning and cell differentiation in a GLI3 repressordependent manner.

show abstract

“…This implied involvement of FGF1 and FGF7 in developmental changes between E10.5 and E13.5, despite no detected changes in levels of transcripts for these factors. Both FGF1 and FGF2 have previously been impli- cated in metanephric development (Perantoni et al, 1995;Barasch et al, 1997;Qiao et al, 2001;Zhao et al, 2004). While the FGFs are secreted via a mechanism distinct from the use of an ER signal peptide (Prudovsky et al, 2003) and hence would not have been included in the soluble/secreted class using our prediction tools, these transcripts were actually not outliers themselves, highlighting the need for parallel analyses of signalling pathways.…”

Section: Ingenuity Pathway Analysismentioning

confidence: 96%

Definition and spatial annotation of the dynamic secretome during early kidney development

et al. 2006

View full text Add to dashboard Cite

The term "secretome" has been defined as a set of secreted proteins (Grimmond et al.[2003] Genome Res 13:1350 -1359). The term "secreted protein" encompasses all proteins exported from the cell including growth factors, extracellular proteinases, morphogens, and extracellular matrix molecules. Defining the genes encoding secreted proteins that change in expression during organogenesis, the dynamic secretome, is likely to point to key drivers of morphogenesis. Such secreted proteins are involved in the reciprocal interactions between the ureteric bud (UB) and the metanephric mesenchyme (MM) that occur during organogenesis of the metanephros. Some key metanephric secreted proteins have been identified, but many remain to be determined. In this study, microarray expression profiling of E10.5, E11.5, and E13.5 kidney and consensus bioinformatic analysis were used to define a dynamic secretome of early metanephric development. In situ hybridisation was used to confirm microarray results and clarify spatial expression patterns for these genes. Forty-one secreted factors were dynamically expressed between the E10.5 and E13.5 timeframe profiled, and 25 of these factors had not previously been implicated in kidney development. A text-based anatomical ontology was used to spatially annotate the expression pattern of these genes in cultured metanephric explants.

show abstract

Role of fibroblast growth factor receptors 1 and 2 in the ureteric bud

Cited by 198 publications

References 36 publications

Glial Cell–Derived Neurotrophic Factor–Independent Ureteric Bud Outgrowth from the Wolffian Duct

Glial Cell–Derived Neurotrophic Factor–Independent Ureteric Bud Outgrowth from the Wolffian Duct

Suppressor of Fused Controls Mid-Hindbrain Patterning and Cerebellar Morphogenesis via GLI3 Repressor

Definition and spatial annotation of the dynamic secretome during early kidney development

Contact Info

Product

Resources

About