QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Oshima, R G Articles by Ceceña, G Search for Related Content PubMed PubMed Citation Articles by Oshima, R G Articles by Ceceña, G Social Bookmarking                   What's this?

Research Papers

Identification of the gene coding for the Endo B murine cytokeratin and its methylated, stable inactive state in mouse nonepithelial cells.

La Jolla Cancer Research Foundation, California 92037.

Abstract

The Endo B type-I keratin intermediate filament protein is first expressed at the 4- to 8-cell stage of mouse development. In the adult, its expression is restricted to a variety of simple epithelial cell types. To investigate the mechanisms responsible for the restricted expression of Endo B, the gene coding for Endo B has been identified from among the five different Endo B genes found in the mouse genome by Southern hybridization analysis and cloning all or part of four of the genes. Nuclear run-on experiments demonstrate that Endo B expression is regulated at the level of transcription. The 5' end of the active gene, designated Endo beta 1, was found to be highly methylated and in a relatively nuclease-resistant chromatin conformation in fibroblasts and myoblasts that do not express Endo B, but undermethylated and relatively sensitive to nuclease digestion in endodermal cells or F9 embryonal carcinoma cells. The inactive state of the Endo B beta 1 gene in fibroblast appears to be very stable, because somatic cell hybrids formed by the fusion of HeLa cells, which express the homologous human protein, keratin 18, and mouse fibroblasts, continue to express keratin 18 but do not activate Endo B expression. Similarly, the fusion of mouse endodermal cells and fibroblasts results in hybrids that do not extinguish Endo B expression. These results suggest that Endo B transcription is limited by two different mechanisms. In somatic cells such as fibroblasts or myoblasts, expression may be restricted by methylation and a stable, nonpermissive transcriptional state. However, in embryonal carcinoma cells, the Endo B beta 1 gene is undermethylated and in a relatively nuclease-sensitive conformation, but it is restricted by an additional, negative regulatory mechanism.

CiteULike

Connotea

Del.icio.us

Digg

Reddit

Technorati

This article has been cited by other articles:

				F. M. Spagnoli, L. Amicone, M. Tripodi, and M. C. Weiss Identification of a Bipotential Precursor Cell in Hepatic Cell Lines Derived from Transgenic Mice Expressing Cyto-Met in the Liver J. Cell Biol., November 16, 1998; 143(4): 1101 - 1112. [Abstract] [Full Text] [PDF]

				K. Rhodes and R. G. Oshima A Regulatory Element of the Human Keratin 18 Gene with AP-1-dependent Promoter Activity J. Biol. Chem., October 9, 1998; 273(41): 26534 - 26542. [Abstract] [Full Text] [PDF]

				G. F. Spath and M. C. Weiss Hepatocyte Nuclear Factor 4 Provokes Expression of Epithelial Marker Genes, Acting As a Morphogen in Dedifferentiated Hepatoma Cells J. Cell Biol., February 23, 1998; 140(4): 935 - 946. [Abstract] [Full Text] [PDF]

				L Casanova, A Bravo, F Were, A Ramirez, J. Jorcano, and M Vidal Tissue-specific and efficient expression of the human simple epithelial keratin 8 gene in transgenic mice J. Cell Sci., January 2, 1995; 108(2): 811 - 820. [Abstract] [PDF]

				R. Wu, S Galvin, S. Wu, C Xu, M Blumenberg, and T. Sun A 300 bp 5'-upstream sequence of a differentiation-dependent rabbit K3 keratin gene can serve as a keratinocyte-specific promoter J. Cell Sci., January 6, 1993; 105(2): 303 - 316. [Abstract] [PDF]

				R G Oshima, L Abrams, and D Kulesh Activation of an intron enhancer within the keratin 18 gene by expression of c-fos and c-jun in undifferentiated F9 embryonal carcinoma cells. Genes & Dev., May 1, 1990; 4(5): 835 - 848. [Abstract] [PDF]