Identification of ZBTB24 protein domains and motifs for heterochromatin localization and transcriptional activation.
Sharmin AktarHiroyuki SasakiMotoko UnokiPublished in: Genes to cells : devoted to molecular & cellular mechanisms (2019)
Immunodeficiency, centromeric instability, facial anomalies (ICF) syndrome is a rare autosomal recessive disorder caused by mutations in either DNMT3B, ZBTB24, CDCA7, HELLS or an unknown gene(s). Among the known causative genes, ZBTB24 encodes a member of the BTB-zinc finger (ZF) transcription factor family. The protein possesses a BTB domain, an AT-hook and eight C2H2 ZF motifs. All ZBTB24 mutations reported in ICF patients are predicted to disrupt at least one ZF motif. Here, we show that both AT-hook and distinct ZF motifs, particularly the 6th motif, of human and mouse ZBTB24 proteins are important for their heterochromatin localization. On the other hand, the 6th and 7th ZF motifs, and not the AT-hook or the BTB domain, of the human and mouse proteins are essential for transcriptional activation of CDCA7, another ICF causative gene and a known target of ZBTB24. By deletion analysis of the human CDCA7 promoter, we show that two motifs for ZBTB24 binding are important for transcriptional activation of this gene. These results reveal the evolutionarily conserved domains and motifs important for the biological function of ZBTB24, which provides a basis for understanding the molecular mechanisms underlying the pathogenesis of ICF syndrome.
Keyphrases
- transcription factor
- genome wide identification
- endothelial cells
- genome wide
- gene expression
- dna methylation
- induced pluripotent stem cells
- copy number
- end stage renal disease
- pluripotent stem cells
- newly diagnosed
- ejection fraction
- chronic kidney disease
- protein protein
- binding protein
- oxidative stress
- peritoneal dialysis
- amino acid
- case report
- bioinformatics analysis