RPA-ChIP Track Settings

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RPA-ChIP (All R-loopBase Data tracks)

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All	*Cell Line*	HeLa
*Technology*
pRPA2-ChIP
RPA2-ChIP
RPA1-ChIP

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	Cell Line^↓1	Technology^↓2	Replicate^↓3	Track Name^↓4
hide	HeLa	pRPA2-ChIP	1	bigwig_HeLa_Control_pRPA2ChIP_1	Schema
hide Configure	HeLa	pRPA2-ChIP	1	bigwig_HeLa_Control_pRPA2ChIP_1	Schema
hide	HeLa	RPA1-ChIP	1	bigwig_HeLa_Control_RPA1ChIP_1	Schema
hide Configure	HeLa	RPA1-ChIP	1	bigwig_HeLa_Control_RPA1ChIP_1	Schema
hide	HeLa	RPA2-ChIP	1	bigwig_HeLa_Control_RPA2ChIP_1	Schema
hide Configure	HeLa	RPA2-ChIP	1	bigwig_HeLa_Control_RPA2ChIP_1	Schema
hide	HeLa	RPA2-ChIP	2	bigwig_HeLa_Control_RPA2ChIP_2	Schema
hide Configure	HeLa	RPA2-ChIP	2	bigwig_HeLa_Control_RPA2ChIP_2	Schema

Description

This track integrates RPA1, RPA2 and pRPA2 ChIP-seq datasets. The RPA complex (RPA1/RPA2/RPA3) has high affinity for ssDNA and is recruited to the displaced strand of R-loops, therefore providing a complementary readout to direct RNA:DNA hybrid mapping. In contrast, pRPA2 (the ATR-phosphorylated form of RPA2 at serine 33) specifically reports the activation of the replication stress response. Phosphorylation of RPA2 by ATR occurs when R-loops physically interfere with replication fork progression, primarily at transcription termination sites (TTS) that are replicated in a head-on orientation relative to transcription. Thus, while RPA1/RPA2 indicate the presence of R-loop-associated ssDNA, pRPA2 distinguishes which R-loop regions cause replication fork stalling and ATR activation.