Disease relevance of Hic1

• Here we show that mice disrupted in the germ line for only one allele of Hic1 develop many different spontaneous malignant tumors, including a predominance of epithelial cancers in males and lymphomas and sarcomas in females [1].
• We isolated the murine homologue Hic1, encoding a zinc-finger protein with a poxvirus and zinc-finger (POZ) domain and mapped it to mouse chromosome 11 in a region exhibiting conserved synteny to human chromosome 17 [2].

High impact information on Hic1

• Homozygous disruption of Hic1 impairs development and results in embryonic and perinatal lethality in mice [1].
• The complete loss of Hic1 function in the heterozygous mice seems to involve dense methylation of the promoter of the remaining wild-type allele [1].
• HIC1 encodes a zinc-finger transcription factor that acts as a transcriptional repressor [3].
• Mice deficient in the candidate tumor suppressor gene Hic1 exhibit developmental defects of structures affected in the Miller-Dieker syndrome [4].
• Comparison of genomic and cDNA sequences predicts two exons for the murine Hic1 [2].

Biological context of Hic1

• During fetal development, Hic1 additionally is expressed in mesenchymes apposed to precartilaginous condensations, at many interfaces to budding epithelia of inner organs, and weakly in muscles [2].
• During embryonic development, Hic1 is expressed in mesenchymes of the sclerotomes, lateral body wall, limb and cranio-facial regions embedding the outgrowing peripheral nerves during their differentiation [2].

References