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Published September 1, 1990 | Published
Journal Article Open

Vimentin downregulation is an inherent feature of murine erythropoiesis and occurs independently of lineage


In mammalian erythropoiesis, the mature cells of the primitive lineage remain nucleated while those of the definitive lineage are anuclear. One of the molecular and structural changes that precedes enucleation in cells of the definitive lineage is the cessation in the expression of the gene for the intermediate filament (IF) protein vimentin and the removal of all vimentin filaments from the cytoplasm. We show here that in immature primitive cells vimentin is synthesized and forms a cytoplasmic network of IFs. As differentiation proceeds in vivo, vimentin gene expression is downregulated in these cells; this is accompanied by the loss of vimentin filaments from the cytoplasm. This loss temporally coincides with the nucleus becoming freely mobile within the cytoplasm, suggesting that, while IF removal is not directly linked to the physical process of enucleation, it may be a prerequisite for the initiation of nuclear mobility in both lineages. These changes are also observed in early primitive cells cultured in vitro, suggesting that they constitute an intrinsic part of the murine erythroid differentiation program independent of lineage and hematopoietic microenvironment.

Additional Information

© 1990 Company of Biologists Limited. Accepted 25 May 1990. We thank Rochelle Diamond for her expert assistance with FACS analysis, Jessica Dausman for help with mouse embryo manipulations, Drs Thomas Coleman and Michael Rodriguez for valuable comments on the manuscript, and Louise Cloutier and Dr Olivier Gandrillon for assistance with the figures. This work was supported by grants from the National Institutes of Health (AGO60 78A) and from the Lucille P. Markey Charitable Trust to the Division of Biology at the California Institute of Technology. F.S. was supported by fellowships from the Anna Fuller Fund and the American Heart Association (Greater Los Angeles Affiliate). C.W. was supported by a fellowship from the American Heart Association (Greater Los Angeles Affiliate) and by a grant from the American Cancer Society.

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