Title

Linkages of nuclear architecture to biological and pathological control of gene expression

UMMS Affiliation

Graduate School of Biomedical Sciences; Department of Cell Biology and Cancer Center

Date

1-20-1999

Document Type

Article

Medical Subject Headings

Animals; Cell Nucleus; Cell Transformation, Neoplastic; Gene Expression Regulation; Humans; Linkage (Genetics); Models, Biological; Nuclear Matrix

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

Functional interrelationships between components of nuclear architecture and control of gene expression are becoming increasingly evident. There is growing appreciation that multiple levels of nuclear organization integrate the regulatory cues that support activation and suppression of genes as well as the processing of gene transcripts. The linear organization of genes and promoter elements provide the potential for responsiveness to physiological regulatory signals. Parameters of chromatin structure and nucleosome organization support synergism between activities at independent regulatory sequences and render promoter elements accessible or refractory to transcription factors. Association of genes, transcription factors, and the machinery for transcript processing with the nuclear matrix facilitates fidelity of gene expression within the three-dimensional context of nuclear architecture. Mechanisms must be defined that couple nuclear morphology with enzymatic parameters of gene expression. The recent characterization of factors that mediate chromatin remodeling and intranuclear targeting signals that direct transcription factors to subnuclear domains where gene expression occurs, reflect linkage of genetic and structural components of transcriptional control. Nuclear reorganization and aberrant intranuclear trafficking of transcription factors for developmental and tissue-specific control that occurs in tumor cells and in neurological disorders provides a basis for high resolution diagnostic and targeted therapy.

Rights and Permissions

Citation: J Cell Biochem Suppl. 1998;30-31:220-31.

Related Resources

Link to Article in PubMed

PubMed ID

9893274