Matrix Attachment Regions

Kohwi‐Shigematsu, Terumi; Kohwi, Yoshinori

doi:10.1002/0471203076.emm0394.pub2

Cited by 1 publication

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References 39 publications

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“…The DEPC modification of the oligonucleotides was carried out in a buffer containing 50 mM sodium cacodylate, 40 mM NaCl, and 10 mM MgCl 2 (pH 7.0) at 25°C for 60 min (40,(62)(63)(64)(65)(66)(67). The KMnO 4 reaction was performed at 20°C for 30 min in a buffer containing 50 mM sodium cacodylate and 1 mM EDTA (pH 7.0) (65, 68 -71).…”

Section: Substrate Preparation For Chemical Modification and Enzymaticmentioning

confidence: 99%

Hairpin Structure-forming Propensity of the (CCTG·CAGG) Tetranucleotide Repeats Contributes to the Genetic Instability Associated with Myotonic Dystrophy Type 2

Dere

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Ranum

et al. 2004

Journal of Biological Chemistry

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The genetic instabilities of (CCTG⅐CAGG) n tetranucleotide repeats were investigated to evaluate the molecular mechanisms responsible for the massive expansions found in myotonic dystrophy type 2 (DM2) patients. DM2 is caused by an expansion of the repeat from the normal allele of 26 to as many as 11,000 repeats. Genetic expansions and deletions were monitored in an African green monkey kidney cell culture system (COS-7 cells) as a function of the length (30, 114, or 200 repeats), orientation, or proximity of the repeat tracts to the origin (SV40) of replication. As found for CTG⅐CAG repeats related to DM1, the instabilities were greater for the longer tetranucleotide repeat tracts. Also, the expansions and deletions predominated when cloned in orientation II (CAGG on the leading strand template) rather than I and when cloned proximal rather than distal to the replication origin. Biochemical studies on synthetic d(CAGG) 26 and d(CCTG) 26 as models of unpaired regions of the replication fork revealed that d(CAGG) 26 has a marked propensity to adopt a defined base paired hairpin structure, whereas the complementary d(CCTG) 26 lacks this capacity. The effect of orientation described above differs from all previous results with three triplet repeat sequences (including CTG⅐CAG), which are also involved in the etiologies of other hereditary neurological diseases. However, similar to the triplet repeat sequences, the ability of one of the two strands to form a more stable folded structure, in our case the CAGG strand, explains this unorthodox "reversed" behavior.

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Section: Substrate Preparation For Chemical Modification and Enzymaticmentioning

confidence: 99%

Hairpin Structure-forming Propensity of the (CCTG·CAGG) Tetranucleotide Repeats Contributes to the Genetic Instability Associated with Myotonic Dystrophy Type 2

Dere

Напиерала

Ranum

et al. 2004

Journal of Biological Chemistry

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show abstract

Matrix Attachment Regions

Abstract: Phi-Van et al.; The matrix attachment regions of the chicken lysozyme gene co-map with the boundaries of the chromatin domain,

Cited by 1 publication

References 39 publications

Hairpin Structure-forming Propensity of the (CCTG·CAGG) Tetranucleotide Repeats Contributes to the Genetic Instability Associated with Myotonic Dystrophy Type 2

Hairpin Structure-forming Propensity of the (CCTG·CAGG) Tetranucleotide Repeats Contributes to the Genetic Instability Associated with Myotonic Dystrophy Type 2

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