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Dissection and Culture of Mouse Embryonic Kidney

Dissection and Culture of Mouse Embryonic Kidney

Published on: May 17, 2017

Sema4C-Plexin B2 signalling modulates ureteric branching in developing kidney.

Nina Perälä¹, Madis Jakobson, Roxana Ola

¹Institute of Biomedicine/Medical Biochemistry and Developmental Biology, Biomedicum Helsinki, PO Box 63, FI-00014 University of Helsinki, Finland. nina.perala@helsinki.fi

Differentiation; Research in Biological Diversity

|November 2, 2010

Summary

Deletion of Plexin B2 (Plxnb2) in developing kidneys impairs ureteric branching and causes renal hypoplasia. This signaling pathway may modulate Glial-cell-line-derived neurotrophic factor (Gdnf) signaling via Ret, highlighting non-redundant roles for Plexin B1 and B2 in kidney development.

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Area of Science:

Developmental Biology
Molecular Biology
Genetics

Background:

Semaphorins are known for axon guidance but also influence angiogenesis, immunity, and cancer.
Plexin B2 (Plxnb2) is a semaphorin receptor expressed in the developing kidney's ureteric epithelium and pretubular aggregates.

Purpose of the Study:

To investigate the role of Plexin B2 (Plxnb2) in kidney development.
To elucidate the signaling mechanisms by which Plxnb2 regulates ureteric branching and kidney formation.

Main Methods:

Gene deletion studies in mice to analyze Plxnb2 knockout (Plxnb2-/-) phenotypes.
Kidney explant cultures to assess ureteric epithelial branching in response to Semaphorin 4C (Sema4C).
Co-immunoprecipitation to identify interacting proteins, specifically the Ret receptor tyrosine kinase.

Main Results:

Plxnb2 deletion leads to renal hypoplasia and double ureters.
Reduced ureteric epithelial cell proliferation and fewer ureteric tips in Plxnb2-/- kidneys.
Sema4C stimulates ureteric branching in wild-type and Plxnb2+/- explants, but not in Plxnb2-/- explants.
Plxnb2 interacts with the Ret receptor tyrosine kinase.
Plxnb2-/- ureteric buds fail to branch in response to Glial-cell-line-derived neurotrophic factor (Gdnf), but this is rescued by FGF7, Follistatin, or metanephric mesenchyme.
Nephrogenic mesenchyme differentiation, morphology, and apoptosis are unaffected by Plxnb2 deletion.
Double deficiency of Plxnb1 and Plxnb2 causes embryonic lethality, with surviving embryos showing hypoplastic kidneys.

Conclusions:

Sema4C-Plxnb2 signaling is crucial for regulating ureteric branching in kidney development.
This signaling pathway likely modulates Gdnf signaling through interaction with Ret.
Plexin B1 and Plexin B2 play distinct, non-redundant roles in kidney development.