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Published July 1984 | Published
Journal Article Open

Differentiation of murine erythroleukemia cells results in the rapid repression of vimentin gene expression


We show that vimentin filaments are present in undifferentiated Friend murine erythroleukemia cells, but are lost progressively to undetectable levels by 96 h of dimethyl sulfoxide-mediated differentiation. The amount of newly synthesized cytoskeletal vimentin is decreased dramatically by 24 h of induction, and is paralleled by a rapid loss of vimentin mRNA (approximately 25-fold reduction at 96 h). Hence, disappearance of vimentin filaments in these cells appears to be regulated at the level of vimentin mRNA abundance. On the other hand, the levels of actin synthesis and actin mRNA remain essentially unchanged. The kinetics of vimentin mRNA reduction during dimethyl sulfoxide-mediated differentiation, and the levels of vimentin mRNA observed in the presence of hexamethylene-bisacetamide or hemin as inducers suggest that the cessation of vimentin expression precedes, but may be associated with commitment to terminal differentiation. Our results demonstrate the dynamic regulation of vimentin expression in mammalian erythropoiesis.

Additional Information

© 1984 by The Rockefeller University Press. RUP grants the public the non-exclusive right to copy, distribute, or display the Work under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/ and http://creativecommons.org/licenses/by-nc-sa/3.0/legalcode. Received for publication 28 March 1984, and in revised form 20 April 1984. We thank Dr. Barbara J. Wold for providing the murine erythroleukemia cells used in this study, Drs. Moses V. Chao and Richard Axel for their gift of pMB-βG2 plasmid DNA, Dr. W. James Nelson for supplying purified bovine lens vimentin standards, Dr. Bruce L. Granger for his advice regarding immunofluorescence microscopy, and Dr. Jean-Paul Revel for the use of his computer facilities. Drs. Wold, Nelson, Granger, and Dr. Randall T. Moon provided stimulating discussion throughout the course of this study. We are grateful to Drs. Granger and Moon for their comments on the manuscript. Ilga Lielausis and Adriana Cortenbach provided expert technical assistance. This work was supported by grants from the National Institutes of Health, the National Science Foundation, the Muscular Dystrophy Association, and a grant-in-aid from the American Heart Association Greater Los Angeles Affiliate. J. Ngai was supported by a Gordon Ross Foundation Predoctoral Fellowship and Y.G. Capetanaki by a Postdoctoral Fellowship from the Muscular Dystrophy Association of America. E. Lazarides is a recipient of a Research Career Development Award from the National Institutes of Health.

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