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Identification and characterization of retinoic acid‐responsive genes in mouse kidney development
Author(s) -
Takayama Mami,
Miyatake Koichi,
Nishida Eisuke
Publication year - 2014
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/gtc.12163
Subject(s) - biology , retinoic acid , ureteric bud , kidney development , gene , morphogenesis , microbiology and biotechnology , in situ hybridization , retinoic acid receptor , stromal cell , gene expression , embryonic stem cell , signal transduction , cancer research , genetics
Retinoic acid ( RA ) signaling regulates a variety of developmental processes through controlling the expression of numerous genes. Here, we have identified and characterized RA ‐responsive genes in mouse kidney development. Analysis of isolated embryonic kidneys cultured in the presence and absence of RA identified 33 candidates of RA ‐responsive genes. Most of these candidate genes were down‐regulated by treatment with the RA receptor antagonist. Many of them have potential binding sites for E lf5, one of the RA ‐responsive genes, in their promoter region. Whole‐mount in situ hybridization showed that specific expression of E lf5 in the ureteric trunk depends on RA . RA ‐dependent expression in the ureteric trunk was also showed for the sodium channel subunit S cnn1b, which has been shown to be the marker gene of the collecting duct. In contrast, the expression of E cm1 , T nfsf13b and IL ‐33 was detected in the stromal mesenchymal cells. Both T nfsf13b and IL ‐33 were previously shown to cause nuclear factor κB ( NF ‐κ B ) activation. We have showed that the inhibition of NF ‐κ B signaling with specific inhibitors suppresses branching morphogenesis of the ureteric bud. Our study thus identifies and characterizes RA ‐dependent up‐regulated genes in kidney development, and suggests an involvement of NF ‐κ B signaling in the branching morphogenesis.