GSE63286
Kdm5b depletion in embryonic stem cells does not induce intragenic promoters or affect transcription [ChIP-Seq]
The application of massively-parallel sequencing (MPS) technology to understanding how the genome is regulated is of major importance, as we now appreciate sequence variants associated with common heritable diseases to be enriched at regulatory elements in the genome.  There is, however, an enormous challenge inherent to these studies, which are much more varied as assays and in terms of analytical approaches than the approaches  used to define the sequence variants themselves.  For example, there are a plethora of assays that test 5-methylcytosine genome-wide, numerous different analytical approaches to defineing peaks from chromatin immunoprecipitation sequencing (ChIP-seq), and increasingly diverse aspects of genomic regulation being studied.  The extremely large data sets generated do not lend themselves to distribution without some degree of pre-processing, and the hardware requirements for running these analyses are often substantial.  We have highlighted these concerns previously, but the central concern for our field is that genomics research is especially prone to poor reproducibility, and is a prime candidate for implementation of measures that could help to address this general problem. To illustrate the practical issues involved in genomics reproducibility, we sought to analyze our data and data from three previoulsy published studies of the histone demethylase KDM5B using the same analytical approaches. In particular we compared the results of our ChIP-seq experiments to previous H3K4me3 and Kdm5b ChIP-seq data in the public database: GSE31966 and GSE53087 (only samples GSM1282126, GSM1282127, GSM1282129, GSM1282131, and GSM1282132). Re-analyzed (ChIP-seq) data from GSE31966 and GSE53087 are linked below as supplementary files. Overall design: Examination of H3K4me3 localization by ChIP-seq in mES cell after the knock down of Kdm5b