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Hox Abdominal-B Genes in the Developing Kidney

ABSTRACT: The Hox complex consists of 39 genes arranged in 4 clusters of flanking genes and 13 paralogous groups in mammals. To assess the functional redundancy of Hox abdominal-B genes during renal development, we used a modified recombineering strategy to simultaneous introduce frameshift mutations into the Hox9, Hox10, and Hox11 flanking genes of the HoxA, HoxC, and HoxD paralogous groups. We performed RNA seq on whole kidneys at E18.5 in triplicates for representative genotypes including: wild type; Hoxa9,10,11-/- HoxC9,10,11+/-, Hoxa9,10,11+/- HoxC9,10,11-/-, Hoxa9,10,11-/- HoxC9,10,11-/-. Our results suggest that the loss of Hox function results in a partial metanephric to mesonephric transformation, with tubules co-expressing markers of both proximal tubules and collecting ducts, as well as markers of mesonephric-derived epididymis tubules.

ORGANISM(S): Mus musculus

PROVIDER: GSE90816 | GEO | 2018/04/25

REPOSITORIES: GEO

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RNA-Seq expression data from the reproductive tracts of WT, Hoxa91011, and Hoxd91011 mutant mice

Project description:Hox genes are key regulators of development. In mammals, the study of these genes is greatly confounded by their large number, overlapping functions, and their interspersed shared enhancers. In this report, we describe a novel recombineering strategy that was used to introduce simultaneous frameshift mutations into the flanking Hoxa9, Hoxa10, and Hoxa11 genes, as well as their paralogs on the HoxD cluster. The resulting mutant mice displayed dramatic homeotic transformations of the reproductive tracts, with uterus anteriorized towards oviduct and the vas deferens anteriorized towards epididymis. The Hoxa9,10,11 mutant mice provided a sensitized genetic background that allowed the discovery of Hoxd9,10,11 reproductive tract patterning function. Both shared and distinct Hox functions were defined. The HoxD genes played a crucial role in the regulation of the uterine immune function. Non-coding nonpolyadenylated RNAs were among the key Hox targets. In addition we observed a surprising anti-dogmatic posteriorization of the uterine epithelium. Reproductive tracts were collected from WT and Hox mutant mice (n=3/genotype) aged 3-7 months in order to characterize the molecular changes caused by mutation of Hoxa9,10,11 and Hoxd9,10,11. Female mice were staged and collected in diestrus.

2013-08-01 | E-GEOD-42339 | biostudies-arrayexpress

Expression data from the reproductive tracts of WT, Hoxa9,10,11, and Hoxd9,10,11 mutant mice

Project description:Hox genes are key regulators of development. In mammals, the study of these genes is greatly confounded by their large number, overlapping functions, and their interspersed shared enhancers. In this report, we describe a novel recombineering strategy that was used to introduce simultaneous frameshift mutations into the flanking Hoxa9, Hoxa10, and Hoxa11 genes, as well as their paralogs on the HoxD cluster. The resulting mutant mice displayed dramatic homeotic transformations of the reproductive tracts, with uterus anteriorized towards oviduct and the vas deferens anteriorized towards epididymis. The Hoxa9,10,11 mutant mice provided a sensitized genetic background that allowed the discovery of Hoxd9,10,11 reproductive tract patterning function. Both shared and distinct Hox functions were defined. The HoxD genes played a crucial role in the regulation of the uterine immune function. Non-coding nonpolyadenylated RNAs were among the key Hox targets. In addition, we observed a surprising anti-dogmatic posteriorization of the uterine epithelium. Reproductive tracts were collected from WT and Hox mutant mice (n=3/genotype) aged 3-7 months in order to characterize the molecular changes caused by mutation of Hoxa9,10,11 and Hoxd9,10,11. Female mice were staged and collected in diestrus.

2013-08-01 | E-GEOD-41993 | biostudies-arrayexpress

RNA-Seq expression data from the reproductive tracts of WT, Hoxa91011, and Hoxd91011 mutant mice

2013-08-01 | GSE42339 | GEO

Expression data from the reproductive tracts of WT, Hoxa9,10,11, and Hoxd9,10,11 mutant mice

Project description:Hox genes are key regulators of development. In mammals, the study of these genes is greatly confounded by their large number, overlapping functions, and their interspersed shared enhancers. In this report, we describe a novel recombineering strategy that was used to introduce simultaneous frameshift mutations into the flanking Hoxa9, Hoxa10, and Hoxa11 genes, as well as their paralogs on the HoxD cluster. The resulting mutant mice displayed dramatic homeotic transformations of the reproductive tracts, with uterus anteriorized towards oviduct and the vas deferens anteriorized towards epididymis. The Hoxa9,10,11 mutant mice provided a sensitized genetic background that allowed the discovery of Hoxd9,10,11 reproductive tract patterning function. Both shared and distinct Hox functions were defined. The HoxD genes played a crucial role in the regulation of the uterine immune function. Non-coding nonpolyadenylated RNAs were among the key Hox targets. In addition, we observed a surprising anti-dogmatic posteriorization of the uterine epithelium.

2013-08-01 | GSE41993 | GEO

Laser capture microdissection/RNA-Seq analyses of Hoxa9,10,11/Hoxd9,10,11 mutant limb development

Project description:We used a novel recombineering method to introduce frameshift mutations into the first exons of the flanking Hoxa9,10,11 and Hoxd9,10,11 genes. By interbreeding it was possibleto make mice homozygous mutant for all six genes. These mice showed an extreme shortening of the zeugopod, with only tiny cartilaginous remnants of the ulna and radius made.We used laser capture microdissection to isolate the cells of the developing mutant zeugopods. Mutant and wild type samples were compared by RNA-seq. The results define the many downstream functional pathways perturbed by the Hox mutations, including the upregulation of many genes known to inhibit chondrocyte and osteoblast differentiation, BMP signalin, and growth arrest and apoptosis. In addition we observed the downregulation of genes required for WNT signaling and chonrdocyte maturation.

2015-06-01 | GSE66679 | GEO

Transcription profiling by array of wild type and Pcsk5 Vcc mutant mouse embryos

Project description:We have identified an ENU-induced recessive mouse mutation (Vcc) with a pleiotropic phenotype overlapping including cardiac, tracheo-esophageal, anorectal, axial skeletal antero-posterior patterning defects, limb malformations, presacral mass, renal and palatal agenesis, and pulmonary hypoplasia. It results from a C470R mutation in the proprotein convertase PCSK5 (PC5/6, SPC6) that fails to complement a null allele, which also has a similar phenotype. The mutation ablates a predicted disulfide bond in the P domain, and results in reduced secretion, abnormal cellular localisation, and loss of proprotein convertase activity. We analysed whole genome gene expression in a mouse line carrying ENU-generated point mutation in Pcsk5 gene on a mixed background : 25% C57BL6/J on C3H/HeH (mutation originally introduced into C57BL6/J). We show that GDF11, a regulator of Hox expression, anteroposterior patterning and nephrogenesis, is a PCSK5 target, and that Pcsk5 mutation results in abnormal expression of several paralogous caudal Hox genes (Hoxa, Hoxc, Hoxd), and Mnx1 (Hlxb9) that are necessary for caudal embryo development. Our data establishes novel and pleiotropic functions for Pcsk5 in mammalian development and the coordinated expression of caudal Hox genes; and identifies GDF11 as a novel cleavage target for PCSK5. We propose that Pcsk5, at least in part via GDF11, coordinately regulates the expression of caudal Hox paralogs, to control antero-posterior patterning, nephrogenesis, and skeletal and anorectal development.

2008-06-27 | E-TABM-443 | biostudies-arrayexpress

Transcription profiling of mouse rhombomere 4 at E10.5 from knockins of Hoxb1 gene expressing Hox-A1 protein

Project description:This study analyzed mRNA profiles in rhombomere 4 of E10.5 mouse knock-in embryos expressing either normal endogenous Hox-B1 protein or the paralogous Hox-A1 protein from the Hoxb1 locus. The Hox-A1 protein was found to be detectably less efficacious than Hox-B1 in promoting neurogenesis in the basal plate of rhombomere 4 and its transcriptional profile shared several similarities with the Hoxb1 mutant. Experiment Overall Design: GFP-positive cells were FACS-sorted from dissected hindbrains of entire litters of E10.5 mouse embryos expressing either normal endogenous Hox-B1 protein or the paralogous Hox-A1 protein from the Hoxb1 locus, either one tagged with IRES-tauGFP. Three independent biological replicates of each genotype were analyzed. Total RNA was isolated, amplified and hybridized to Affymetrix Mouse Genome 430 2.0 Arrays.

2008-06-13 | E-GEOD-5124 | biostudies-arrayexpress

Genome-wide mapping of Hoxa11 and Hoxa13 binding sites in the limb bud

Project description:Hox genes control domain specific cartilage pattern formation along the proximodistal axis. Hoxa11 and Hoxd11 (Hox11) show overlapping expression in the mesenchyme of the zeugopod and regulate cartilage growth and differentiation. Hoxa13 and Hoxd13 (Hox13) are expressed in the autopodal mesenchyme and are crucial for the autopodal cartilage patterning. Since both Hox11 and Hox13 are involved in the limb cartilage development, they may share the target genes. To identify common target genes among the Hoxa11 and Hoxa13, we performed ChIP-Seq analysis using specific antibody.

2019-03-28 | GSE119142 | GEO

Hoxb1 gene expressing Hox-A1 protein: Altered transcriptional profile in rhombomere 4 at E10.5

2006-08-28 | GSE5124 | GEO

Comparison of gene expression profiles between wild-type and Kdm7a mutan embryos

Project description:Temporal and spatial colinear expression of Hox genes determines the specification of positional identities of the embryo. Post-translational modifications of histones contribute to transcriptional regulation, and are required for proper control of biological processes, including differentiation and development. Lysine demethylase 7A (Kdm7a) demethylates lysine 9 di-methylation of histone H3 (H3K9me2) and participates in transcriptional activation of developmental genes. However, the role of Kdm7a during mouse embryonic development remains to be elucidated. Here, we show that Kdm7a-/- mice exhibit anterior homeotic transformation of the axial skeleton (i.e. an increase in the number of presacral elements). Importantly, posterior Hox genes (caudally from Hox9) are specifically down-regulated in Kdm7a-/- embryos, which correlate with increased levels of H3K9me2. Taken together, these data suggest that Kdm7a is able to control transcription of posterior Hox genes, likely through its demethylating activity, and thereby regulating anterior-posterior development in mice.

2019-12-23 | GSE133187 | GEO

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