Analysis and characterisation of the mouse Hic2 gene - podcast episode cover

Analysis and characterisation of the mouse Hic2 gene

Feb 13, 20040
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5.1 Analysis and characterization of the mouse Hic2 gene Like Hic1 and γFBP (chicken), Hic2 cDNA coded five Krüppel-type C2H2 zinc finger domain. Through the sequencing and comparation with different protein sequences from the homolog proteins from different species (HIC1, Hic1, HIC2, γFBP, and Hypothetical protein), Hic2 protein shares more than 80% homology with HIC1 through the BTB/POZ and zinc finger domains, and both proteins have identical GLDLSKK/R motifs. A new part of Hic2 gene coding, exon two, and new exon one deduced full-length Hic2 protein contains 601 amino acids. Hic2 gene has two Exons (240 and 1842 bp), with one Intron (2182 bp). The location of the gene is mouse chromosome 16 (B1, UniGene Cluster Mm.103787 Mus musculus). The human gene HIC2 maps to chromosome 22q11.2, and is a homolog of the HIC1 candidate tumor suppressor gene located at 17p 13.3. (Deltour et al. 2001). Upstream from the TATA box MatInspector predicted different transcription binding sites. Between them Wilms Tumor Suppressor and p53 are most interesting transcription sites for the Hic2 gene. That’s why the Hic2 promoter activity was checked. A 1.2 kb promoter fragment of Hic2 has been characterized in a gene reporter assay system. The peak activity of the Hic2 promoter is associated with the total fragment, the next higher activity is in the fragment which included Wilms Tumor Suppressor and p53 transcription sites. The expression of the mouse Hic2 was investigated by in situ hybridisations (ISHs) of whole mount embryos and paraffin sections. Hic2 expression was detected in restricted territories of the brain, sinus centralis, olfactory bulb, canallis centralis medullae spinalis, embryonic ectoderm (neuroepithelium of neural tube), and small intestine. Because of its expression in the central nervous system, and mapping position of its human homolog HIC2, Hic2 could be involved in some syndromes. Patients with a 22q11 deletion have disrupted brain development which may involve abnormal neural crest cell migration, (Van Amelsvoort et al., 2001). It is now recognized that the 22q11.2 deletion syndrome encompasses the phenotypes previously described as DiGeorge syndrome (DGS) and velocardiofacial syndrome (Shprintzen syndrome),(Thomas and Graham 1997).
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Analysis and characterisation of the mouse Hic2 gene | Tierärztliche Fakultät - Digitale Hochschulschriften der LMU - Teil 01/07 podcast - Listen or read transcript on Metacast