Transcription profiling of mouse wild type and Lim1-null renal vesicles microdissected from embryonic day 12.5 kidneys

ABSTRACT: The Lim1 gene has essential functions during several stages of kidney development. In particular, a tissue specific knockout in the early metanephric mesenchyme results in the formation of the earliest nephron precursor, the renal vesicle, but failure of this structure to progress to the next stage, the comma shaped body. To better understand the molecular nature of this developmental arrest we used a laser capture microdissection-microarray strategy to examine the perturbed gene expression pattern of the mutant renal vesicles. Among the genes found differently expressed were Chrdl2, an inhibitor of BMP signaling, the pro-apoptotic factor Bmf, as well as myob5, an atypical myosin which modulates chemokine and transferring signaling, and pdgfr1, which is important in epithelial folding. Of particular interest, the microarray data indicated that the Dkk1 gene, which encodes an inhibitor of Wnt signaling, was downregulated nine fold in mutants. This was confirmed by in situ hybridizations. It is interesting to note that Lim1 and Dkk1 mutant mice have striking similarities in phenotype. These results suggest that the Dkk1 gene might be a key downstream effector of Lim1 function. Experiment Overall Design: We compared gene expression profiles of wild type and mutant Lim1 renal vesicles, which were isolated from E12.5 kidneys by laser capture microdissection. Nine biological independent samples were examined, with four mutant and five wild type. Each sample included approximately 30-50 renal vesicles. Detailed protocols are described at GUDMAP.org

ORGANISM(S): Mus musculus

SUBMITTER: Steven Potter 

PROVIDER: E-GEOD-7257 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress