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Dear Group
I'm comparing with SICER some chip seq experiments of mouse muscles subjected to a specific treatment vs non treated samples.
I'm monitoring ACH3 and H3K4ME3 histone modifications(so they are both activator at promoter level).
For all the comparison I set up a window size of 200 and a gap size of 600 FDR threshold 0.05
In general i observ a very high number of increased islands in ACH3 and a very high number of decreased islands in H3K4ME3
The strange thing is that most of the genes that are modulated according to their gene expression(estimated by RNA seq) have at their promoter at the same time increased ACH3 islands and decreased H3K4ME3.
Do someone of you experienced a similar situation?
This could be a signal of something wrong in the experiment setup?
thank you for every tip you could pprovide to me
I'm comparing with SICER some chip seq experiments of mouse muscles subjected to a specific treatment vs non treated samples.
I'm monitoring ACH3 and H3K4ME3 histone modifications(so they are both activator at promoter level).
For all the comparison I set up a window size of 200 and a gap size of 600 FDR threshold 0.05
In general i observ a very high number of increased islands in ACH3 and a very high number of decreased islands in H3K4ME3
The strange thing is that most of the genes that are modulated according to their gene expression(estimated by RNA seq) have at their promoter at the same time increased ACH3 islands and decreased H3K4ME3.
Do someone of you experienced a similar situation?
This could be a signal of something wrong in the experiment setup?
thank you for every tip you could pprovide to me