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(Received for publication, February 28, 1996, and in revised form, May 1, 1996)
From the Institute of Biosciences and Technology, Center for Genome
Research, Department of Biochemistry and Biophysics, Texas A&M
University, Texas Medical Center, Houston, Texas 77030-3303
CTG·CAG, CGG·CCG, and AAG·CTT triplet
repeats proximal to or in disease genes expand by a non-Mendelian
genetic process to cause several human hereditary syndromes. As part of
our physical, biological, and genetic studies on the 10 possible
triplet repeats, we discovered that the TTA·TAA repeat, isolated from
the upstream region of the variant surface glycoprotein gene of
Trypanosoma brucei, shows a propensity to adopt a non-H
bonded structure under appropriate conditions. The other nine triplet
repeat sequences do not exhibit this property. (TTA·TAA)n,
where n = 90, 60, 30, and 18, cloned into pUC19 was studied
by chemical and enzymatic probes as well as two-dimensional gel
electrophoretic analyses under a variety of conditions. The helix
opening was observed for all four inserts in supercoiled plasmids as a
function of temperature, pH, metal ions, and buffer conditions using
OsO4, diethyl pyrocarbonate, and chloroacetaldehyde probes.
This unusual property of the TTA·TAA repeat suggests that it plays a
different role from the other nine triplet repeats in gene
expression.
Volume 271, Number 28,
Issue of July 12, 1996
pp. 16784-16791
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
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