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Mining of putative cis ‐acting elements for chromatin mediated regulation of Hox genes in mammals by in‐silico analysis
Author(s) -
Bengani Hemant,
Ganapathi Mythily,
Singh Gajinder Pal,
Brahmachari Vani
Publication year - 2007
Publication title -
journal of experimental zoology part b: molecular and developmental evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 63
eISSN - 1552-5015
pISSN - 1552-5007
DOI - 10.1002/jez.b.21162
Subject(s) - hox gene , biology , homeotic gene , chromatin , genetics , gene , transcription factor , epigenetics , enhancer , in silico , cis regulatory module , regulation of gene expression , transcription (linguistics) , computational biology , linguistics , philosophy
The remarkable conservation in developmental strategies across phyla is well reflected in the conservation of the homeotic gene complexes responsible for establishing the body plan in embryonic development. On the other hand, changes in the strategy of transcription regulation are believed to form one of the major factors in the evolution of developmental mechanisms and phenotypic evolution of species. Apart from transcription regulation by gene specific transcription factors, the role of regulators mediating modifications of chromatin proteins, especially of HOX gene clusters in Drosophila is well documented. By comparative genomics we have identified novel motifs conserved in mouse, chimpanzee and human in the noncoding upstream/intronic sequences of Hox genes by in silico analysis. These motifs lack the binding sites for known transcription factors and are significantly over represented in the target genes of one of the core components of Polycomb Repressive Complex namely Supressor of zeste 12 (SUZ12) in human embryonic cells reported by Lee et al. [2006a. Cell 125:301–313]. Therefore, we predict that they could be the sites of interaction of chromatin modifying complexes for epigenetic regulation. J. Exp. Zool. (Mol. Dev. Evol.) 308B:384–395, 2007 . © 2007 Wiley‐Liss, Inc.