Recent chromatin immunoprecipitation-on-chip (ChIP-chip) analyses in Caenorhabditis elegans (Gassmann et al., 2012) revealed that CENP-A occupies nonrepeated regions of 10 12 kb dispersed across about half of the genome and is excluded from loci that are transcribed in the germline and early embryo (for a contrasting view, see Steiner and Henikoff, 2014).
Microarrays have been applied to genome-wide analysis of gene expression, location of transcription factor binding sites (chromatin immunoprecipitation on microarray chip, ChIP-chip), DNA replication fork progression, sister chromatid cohesion, and nucleosome phasing [1] [5].
Protein kinase A (PKA) isoforms Tpk1 and Tpk2 promote hyphal growth in a signalling pathway via the transcription factor Efg1. C. albicans strains producing epitope-tagged Tpk1 or Tpk2 were used in genome-wide chromatin immunoprecipitation on chip (ChIP chip) to reveal genomic binding sites.
Nevertheless, they remain to be challenging problems until high-throughput approaches like ChIP-seq (chromatin immunoprecipitation followed by massively parallel sequencing) [ 1, 2] and ChIP-chip (ChIP on chip) appeared.
The number of H3K4me3-enriched regions in Xenopus gastrula embryos based on ChIP-chip or ChIP-seq [9] is comparable (88% overlap).
The real data analysis we performed in this study was based on ChIP-chip data and a ChIP-seq data in 66 Mb region on the mouse chromosome 7.
As a consequence, it is particularly well suited to compare results obtained through microarray, ChIP-on-chip, ChIP-seq, CGH or protein-protein interaction experiments to those previously stored in the GEO database.
These regulatory interactions are determined according to DNA binding evidences which are obtained from wet-lab experiments, such as site-directed mutation of transcription factor binding sites in its promoter region, ChIP, ChIP-on-chip, ChIP-seq and so on.
Recently, several genome-scale techniques such as ChIP-on-chip, ChIP-seq, and, more recently, ChIP-exo, have provided us with different and largely non-overlapping maps of p53 bound sites in the human genome in response to specific stimuli [ 7– 17].
Furthermore, this year, Schupp et al. (2009) independently demonstrated through a genome-wide Chromatin Immunoprecipation on chip (ChIP-chip) assay of PPARγ an important target in intron 1 of Retsat in an adipocyte in vitro system.
