Localization of estrogen receptors in uterine cells. An appraisal of translocation

Edward J. Pavlik, Susan Rutledge, Richard L. Eckert, Benita S. Katzenellenbogen

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30 Scopus citations


The nuclear localization of estrogen receptors has been examined under conditions which minimize redistribution and localization artifacts. A procedure is presented which rapidly lyses suspensions of cells from immature rat uteri by using 0.04% Triton X-100 in isotonic buffer. The 'nuclei' which are obtained after lysis have a median diameter of 1μm and are devoid of nuclear membranes. There is close agreement between the number of cells before lysis and the number of nuclear particles after lysis. Triton X-100 gave no interference with quantitative binding of estradiol to receptor and no alteration in the sedimentation behavior of receptor on sucrose gradients containing high or low salt. Using this procedure to monitor the dynamics of estrogen receptor distribution within uterine cells after exposure to estradiol, translocation of estrogen receptor to the nucleus was observed to occur at a rate slightly slower than the rate at which estradiol was specifically bound to free cells or receptors. The difference in these rates is compatible with a model in which estradiol must first bind to the receptor before the binding complex moves to the nucleus. The rate of nuclear translocation was temperature-dependent and was observed to occur at 0 °C, provided that enough time was allowed for steroid entry, receptor charging and transit to the nucleus. Two distinct phases were observed to characterize nuclear receptor localization. In the first phase after hormone exposure, estrogen receptor progressively accumulated in the nucleus; afterwards, estrogen receptor was progressively lost from the nucleus but could not be detected in other subcellular compartments in a form still binding hormone. Since high cell viability was maintained during these manipulations, loss of nuclear receptor was not due to cell damage during in vitro incubation. These studies suggest that this decline in nuclear receptor level after hormone interaction, which is known to occur in vivo, may be a normal event during estrogen interaction with target cells.

Original languageEnglish
Pages (from-to)177-189
Number of pages13
JournalExperimental Cell Research
Issue number1
StatePublished - Oct 1 1979

Bibliographical note

Funding Information:
This work was supported by NIH Grant USPH HD 06726,F ord Foundation Grant 700-0333a nd an NC1 Postdoctoral Research Fellowship to E. J. P. (1 F32 CA 06149-01).T he authors appreciate the graphic assistanceo f Martv Boatz, the diligencei n manuscriot preparationo f Nancy Oliver and Robyn Luke and the expertise of Dr Birute Jakstvs of the Center for Electron Microscopy.

ASJC Scopus subject areas

  • Cell Biology


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