model for chromatin opening: stimulation of topoisomerase II and restriction enzyme cleavage of chromatin by distamycin

Histone H1 preferentially and cooperatively binds scaffold-associated regions (SARs) in vitro via specific interactions with the numerous short A + T-rich tracts (A-tracts) contained in these sequences. Selective titration of A-tracts by the oligopeptide distamycin abolishes this interaction and res...

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Bibliographic Details
Published in:The EMBO journal 1993, Vol.12 (1), p.115-126
Main Authors: Kas, E, Poljak, L, Adachi, Y, Laemmli, U.K
Format: Article
Language:English
Subjects:
a-tracts
Animals
antibiotics
antineoplastic agents
binding sites
Biological and medical sciences
Cell Fractionation
Cell Nucleus - metabolism
Cell Nucleus - ultrastructure
chromatin
Chromatin - drug effects
Chromatin - metabolism
Chromatin. Chromosome
Chromosomes, Human - metabolism
Chromosomes, Human - ultrastructure
Distamycins - pharmacology
DNA
DNA conformation
dna modification
DNA Restriction Enzymes - metabolism
DNA topoisomerase
DNA Topoisomerases, Type II - metabolism
Drosophila melanogaster
enzyme activity
Fundamental and applied biological sciences. Psychology
HeLa Cells
histones
Histones - metabolism
Humans
isomerases
Metaphase
Molecular and cellular biology
Molecular genetics
Restriction Mapping
scaffold-associated regions
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Summary:Histone H1 preferentially and cooperatively binds scaffold-associated regions (SARs) in vitro via specific interactions with the numerous short A + T-rich tracts (A-tracts) contained in these sequences. Selective titration of A-tracts by the oligopeptide distamycin abolishes this interaction and results in a redistribution of H1. Similarly, treatment of intact cells and isolated nuclei with distamycin specifically enhances cleavage of internucleosomal linkers of SARs by topoisomerase II and restriction enzymes. The increased accessibility of these linkers is thought to result from the unfolding (or opening) of the chromatin fiber and to be due to a reduced occupancy by histone H1. Chromatin extraction and H1 assembly experiments support this view. We discuss a model whereby open, H1-depleted chromatin regions may be generated by titration of A-tracts by putative distamycin analogues; this local opening may spread to adjacent regions assuming highly cooperative H1-H1 interactions in chromatin.
ISSN:0261-4189
1460-2075
DOI:10.1002/j.1460-2075.1993.tb05637.x