In this paper they classify the promoters into two categories, highlighted in italics below.

Two Types of Promoters

Mammalian promoters can initiate transcription across broad or narrow genomic regions, and these promoter shapes, broad or narrow (sharp), correlate with distinct transcriptional regulatory mechanisms.33 We evaluated cardiac promoters predicted from CAGE clusters for these 2 major types of promoters by calculating the interquartile range of promoter CAGE clusters by determining the base pair distance between 10% and 90% of a promoter’s total signal. We observed the expected 2 distinct populations, defined as sharp (interquartile range <10 bp) and broad promoters (interquartile range ≥10 bp; Figure 2A). Broad promoters were those associated many different cellular functions, including housekeeping functions. In contrast, genes with sharp (narrow) promoters were those encoding proteins critical for tissue-specific functions seen by the presence myofilament, muscle tissue, and muscle contractions genes (Figure 2B). Thus, tissue-specific genes important for LV specification and function were more likely to have sharp promoters.

Now My question is can I do this only based on ATAC seq data. If yes how do i get that information of narrow and broad promoters.


Its highly unlikely that you will be able to categorize promoters on this basis using only ATAC data. This is a consequence of people using the terms "promoters" and "transcription start sites" interchangeably, when they are actaully different things. CAGE data measures transcription start sites which is the specific location where transcription starts. CAGE does not identify promoters, which are the complete region around the start of a gene that contains, at a minimum, all the sequences necessary to assemble the RNA polymerase II pre-initiation complex. Some definitions of promoter are even broader, including all regulatory sequence proximal the the gene start.

ATAC identifies regions of open chromatin, and I would expect the open chromatin regions around the starts of genes to be more like the broadest definition of promoter, and therefore to be significantly larger than the transcription starts sites they contain, whether they be broad or narrow TSSs.

You could of course look at a distribution of the peak sizes over TSSs and see if you found a bimodal distribution. If you did you could correlate the genes with broad/narrow TSS peaks with their known functions so see if it fitted the idea that narrows TSSs

  • $\begingroup$ thats a good start for me to start $\endgroup$ – krushnach Chandra Jan 13 at 5:54

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