Standard

Partners in crime: Tbf1 and Vid22 promote expansions of long human telomeric repeats at an interstitial chromosome position in yeast. / Radchenko, Elina A; Aksenova, Anna Y; Volkov, Kirill V; Shishkin, Alexander A; Pavlov, Youri I; Mirkin, Sergei M.

In: PNAS Nexus, Vol. 1, No. 3, 11.07.2022.

Research output: Contribution to journalArticlepeer-review

Harvard

APA

Vancouver

Author

Radchenko, Elina A ; Aksenova, Anna Y ; Volkov, Kirill V ; Shishkin, Alexander A ; Pavlov, Youri I ; Mirkin, Sergei M. / Partners in crime: Tbf1 and Vid22 promote expansions of long human telomeric repeats at an interstitial chromosome position in yeast. In: PNAS Nexus. 2022 ; Vol. 1, No. 3.

BibTeX

@article{78e20c4c8d7c41f098292384d4bf4f01,
title = "Partners in crime: Tbf1 and Vid22 promote expansions of long human telomeric repeats at an interstitial chromosome position in yeast",
abstract = "In humans, telomeric repeats (TTAGGG)n are known to be present at internal chromosomal sites. These interstitial telomeric sequences (ITSs) are an important source of genomic instability, including repeat length polymorphism, but the molecular mechanisms responsible for this instability remain to be understood. Here, we studied the mechanisms responsible for expansions of human telomeric (Htel) repeats that were artificially inserted inside a yeast chromosome. We found that Htel repeats in an interstitial chromosome position are prone to expansions. The propensity of Htel repeats to expand depends on the presence of a complex of two yeast proteins: Tbf1 and Vid22. These two proteins are physically bound to an interstitial Htel repeat, and together they slow replication fork progression through it. We propose that slow progression of the replication fork through the protein complex formed by the Tbf1 and Vid22 partners at the Htel repeat cause DNA strand slippage, ultimately resulting in repeat expansions.",
author = "Radchenko, {Elina A} and Aksenova, {Anna Y} and Volkov, {Kirill V} and Shishkin, {Alexander A} and Pavlov, {Youri I} and Mirkin, {Sergei M}",
year = "2022",
month = jul,
day = "11",
doi = "10.1093/pnasnexus/pgac080",
language = "English",
volume = "1",
journal = "PNAS Nexus",
issn = "2752-6542",
publisher = "Oxford University Press",
number = "3",

}

RIS

TY - JOUR

T1 - Partners in crime: Tbf1 and Vid22 promote expansions of long human telomeric repeats at an interstitial chromosome position in yeast

AU - Radchenko, Elina A

AU - Aksenova, Anna Y

AU - Volkov, Kirill V

AU - Shishkin, Alexander A

AU - Pavlov, Youri I

AU - Mirkin, Sergei M

PY - 2022/7/11

Y1 - 2022/7/11

N2 - In humans, telomeric repeats (TTAGGG)n are known to be present at internal chromosomal sites. These interstitial telomeric sequences (ITSs) are an important source of genomic instability, including repeat length polymorphism, but the molecular mechanisms responsible for this instability remain to be understood. Here, we studied the mechanisms responsible for expansions of human telomeric (Htel) repeats that were artificially inserted inside a yeast chromosome. We found that Htel repeats in an interstitial chromosome position are prone to expansions. The propensity of Htel repeats to expand depends on the presence of a complex of two yeast proteins: Tbf1 and Vid22. These two proteins are physically bound to an interstitial Htel repeat, and together they slow replication fork progression through it. We propose that slow progression of the replication fork through the protein complex formed by the Tbf1 and Vid22 partners at the Htel repeat cause DNA strand slippage, ultimately resulting in repeat expansions.

AB - In humans, telomeric repeats (TTAGGG)n are known to be present at internal chromosomal sites. These interstitial telomeric sequences (ITSs) are an important source of genomic instability, including repeat length polymorphism, but the molecular mechanisms responsible for this instability remain to be understood. Here, we studied the mechanisms responsible for expansions of human telomeric (Htel) repeats that were artificially inserted inside a yeast chromosome. We found that Htel repeats in an interstitial chromosome position are prone to expansions. The propensity of Htel repeats to expand depends on the presence of a complex of two yeast proteins: Tbf1 and Vid22. These two proteins are physically bound to an interstitial Htel repeat, and together they slow replication fork progression through it. We propose that slow progression of the replication fork through the protein complex formed by the Tbf1 and Vid22 partners at the Htel repeat cause DNA strand slippage, ultimately resulting in repeat expansions.

UR - https://www.mendeley.com/catalogue/0f5bd124-8510-3525-bb93-5fe734e64a5e/

U2 - 10.1093/pnasnexus/pgac080

DO - 10.1093/pnasnexus/pgac080

M3 - Article

VL - 1

JO - PNAS Nexus

JF - PNAS Nexus

SN - 2752-6542

IS - 3

ER -

ID: 97366819