Abstract

The estrogen receptor (ER), a member of the nuclear hormone receptor superfamily recruits coactivators that modify local chromatin structure. Here we investigated the effect of the estrogen receptor and estrogen on the global chromatin structure and the local chromatin structure of the progesterone receptor gene during the process of transcriptional activation using Rat1+ER cells stably expressing the estrogen receptor. The total chromatin was more accessible to DNasel in Rat1+ER cells than in the parental estrogen receptor-negative Rat1 cells. After 18 h of estrogen treatment, total chromatin was more dispersed in Rat1+ER cells than in Rat1 cells. The chromatin structure of the progesterone receptor gene was more sensitive to DNasel in Rat1+ER cells than in Rat1 cells. However, the chromatin structure of the progesterone receptor gene did not change further on estrogen treatment. Our results suggest that under certain circumstances unoccupied estrogen receptors may play some role in reorganizing the repressive chromatin structure to induce gene activation.

Highlights

  • An estrogen-occupied estrogen receptor (ER) bound to estrogen response elements (ERE) can activate or repress transcription (Beato and Klug, 2000)

  • There are evidences to suggest that no direct correlation exists between transcription and chromatin structural remodeling: DNaseI hypersensitive sites of the prolactin gene appear early in development and do not change further with estrogen treatment (Durrin and Gorski, 1985); and transcription activation of the vitellogenin gene is poorly correlated with chromatin changes (Burch and Evans, 1986)

  • The chromatin of the Rat1+ER cells required less DNaseI to be degraded than did the chromatin of the Rat1 cells, suggesting that the chromatin was more dispersed by the presence of ER

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Summary

Introduction

An estrogen-occupied estrogen receptor (ER) bound to estrogen response elements (ERE) can activate or repress transcription (Beato and Klug, 2000). Unoccupied ERs are associated with the chromatin as determined by in vivo crosslinking experiments (Wrenn and Katzenellenbogen, 1990). It is still unclear whether there is a direct relationship between estrogeninduced transcription and changes in chromatin structure (Mao and Shapiro, 2000). There are evidences to suggest that no direct correlation exists between transcription and chromatin structural remodeling: DNaseI hypersensitive sites of the prolactin gene appear early in development and do not change further with estrogen treatment (Durrin and Gorski, 1985); and transcription activation of the vitellogenin gene is poorly correlated with chromatin changes (Burch and Evans, 1986)

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