TGFβ superfamily signals are required for morphogenesis of the kidney mesenchyme progenitor population

Oxburgh, Leif; Chu, Gerald C.; Michael, Simon K.; Robertson, Elizabeth J.

doi:10.1242/dev.01324

Cited by 107 publications

(107 citation statements)

References 44 publications

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“…Inactivation of cMyc in early metanephric mesenchyme (e11.5) (59) showed that c-Myc plays an early and crucial role in the renal cap mesenchymal cells. Ablation of c-Myc resulted in depletion of the renal stem/progenitor cell population caused by a major decrease in proliferation that likely impaired their self-renewal potential (2).…”

Section: Role Of C-myc In Kidney Development and Homeostasismentioning

confidence: 99%

c-Myc Signalling in the Genetic Mechanism of Polycystic Kidney Disease

Trudel

2015

Polycystic Kidney Disease

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Licence: This open access article is licenced under Creative Commons Attribution 4.0 International (CC BY 4.0). http://creativecommons.org/licenses/by/4.0/ Users are allowed to share (copy and redistribute the material in any medium or format) and adapt (remix, transform, and build upon the material for any purpose, even commercially), as long as the author and the publisher are explicitly identified and properly acknowledged as the original source. AbstractThe Myc family of transcription factors regulates major biological processes such as proliferation, stem/progenitor cell pluripotency, metabolism, apoptosis, cell growth and differentiation. The most-studied member c-Myc is essential in embryonic development and cellular homeostasis. Dysregulation of c-Myc protein function is not only associated with malignant transformation and human tumors but is also implicated in autosomal dominant polycystic kidney disease (ADPKD), a human genetic disorder, considered a neoplasia in disguise. Studies from human ADPKD kidneys, caused by mutation in the

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Section: Role Of C-myc In Kidney Development and Homeostasismentioning

confidence: 99%

c-Myc Signalling in the Genetic Mechanism of Polycystic Kidney Disease

Trudel

2015

Polycystic Kidney Disease

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“…All UB cells originate from the WD. (70) However, soon after the UB emerges it becomes divided into distinct tip and trunk domains. In addition to Ret and Gfra1, there are many other genes expressed specifically in the tip domain but not in the trunks, including Wnt11, Crlf1, and CXCL14 to name a few; (71,72) conversely, different genes are expressed only in the trunks (e.g.…”

Section: The Role Of Localized Gdnf/ret Signaling In Ureter Formationmentioning

confidence: 99%

GDNF/Ret signaling and the development of the kidney

2006

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SummarySignaling by GDNF through the Ret receptor is required for normal growth of the ureteric bud during kidney development. However, the precise role of GDNF/Ret signaling in renal branching morphogenesis and the specific responses of ureteric bud cells to GDNF remain unclear. Recent studies have provided new insight into these issues. The localized expression of GDNF by the metanephric mesenchyme, together with several types of negative regulation, is important to elicit and correctly position the initial budding event from the Wolffian duct. GDNF also promotes the continued branching of the ureteric bud. However, it does not provide the positional information required to specify the pattern of ureteric bud growth and branching, as its site of synthesis can be drastically altered with minimal effects on kidney development. Cells that lack Ret are unable to contribute to the tip of the ureteric bud, apparently because GDNF-driven proliferation is required for the formation and growth of this specialized epithelial domain.

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“…Whole mount and non-radioactive section in situ hybridizations were performed as previously described (Oxburgh et al, 2004).…”

Section: In Situ Hybridizationmentioning

confidence: 99%

Developmental expression of mouse Follistatin-like 1 (Fstl1): Dynamic regulation during organogenesis of the kidney and lung

Adams

Larman

Oxburgh

2007

Gene Expression Patterns

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Follistatin-like 1 (Fstl1) is a distantly related homolog of the Activin and Bone Morphogenetic Protein antagonist Follistatin. Interestingly, this molecule also has homology with the extracellular matrix modifying protein BM-40/SPARC/osteonectin. Previous studies in chick have identified Fstl1 as a regulator of early mesoderm patterning, somitogenesis, myogenesis and neural development. In this study, we determine the developmental expression pattern of Fstl1 during mouse development. We find that Fstl1 is ubiquitously expressed in the early embryo, and that expression becomes regionalized later during development. In the majority of tissues, Fstl1 is strongly expressed in the mesenchymal component and excluded from the epithelium. Notable exceptions include the central nervous system, in which Fstl1 expression is entirely absent with the exception of the choroid plexi and floor plate, the lung, in which Fstl1 expression can be seen in airway epithelia and the kidney, in which collecting ducts and nascent nephron epithelia express the highest levels of Fstl1.

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TGFβ superfamily signals are required for morphogenesis of the kidney mesenchyme progenitor population

Cited by 107 publications

References 44 publications

c-Myc Signalling in the Genetic Mechanism of Polycystic Kidney Disease

c-Myc Signalling in the Genetic Mechanism of Polycystic Kidney Disease

GDNF/Ret signaling and the development of the kidney

Developmental expression of mouse Follistatin-like 1 (Fstl1): Dynamic regulation during organogenesis of the kidney and lung

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