GSBS Student Publications


Mitotic partitioning and selective reorganization of tissue-specific transcription factors in progeny cells

UMMS Affiliation

Department of Cell Biology; Graduate School of Biomedical Sciences



Document Type


Medical Subject Headings

Animals; Cell Division; Cell Line, Tumor; Cell Nucleus; Chromatin; DNA; G2 Phase; Histones; Humans; Image Processing, Computer-Assisted; Jurkat Cells; Microscopy, Fluorescence; *Mitosis; Nuclear Proteins; Phenotype; Rats; *Ribonucleoproteins; Telophase; Time Factors; Transcription Factors


Life Sciences | Medicine and Health Sciences


Postmitotic gene expression requires restoration of nuclear organization and assembly of regulatory complexes. The hematopoietic and osteogenic Runx (Cbfa/AML) transcription factors are punctately organized in the interphase nucleus and provide a model for understanding the subnuclear organization of tissue-specific regulatory proteins after mitosis. Here we have used quantitative in situ immunofluorescence microscopy and quantitative image analysis to show that Runx factors undergo progressive changes in cellular localization during mitosis while retaining a punctate distribution. In comparison, the acetyl transferase p300 and acetylated histone H4 remain localized with DNA throughout mitosis while the RNA processing factor SC35 is excluded from mitotic chromatin. Subnuclear organization of Runx foci is completely restored in telophase, and Runx proteins are equally partitioned into progeny nuclei. In contrast, subnuclear organization of SC35 is restored subsequent to telophase. Our results show a sequential reorganization of Runx and its coregulatory proteins that precedes restoration of RNA processing speckles. Thus, mitotic partitioning and spatiotemporal reorganization of regulatory proteins together render progeny cells equivalently competent to support phenotypic gene expression.

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Citation: Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):14852-7. Epub 2003 Dec 1. Link to article on publisher's site

DOI of Published Version


Related Resources

Link to Article in PubMed

Journal Title

Proceedings of the National Academy of Sciences of the United States of America

PubMed ID