Dynamic Supercoiling Sponsors Transcription Amplification by MYC

MYC dysregulation occurs in most cancers provoking, profound changes in gene expression. Although sometimes considered to be an E-box-dependent transcription factor, an alternate model posits MYC to be a universal amplifier of active genes. Although MYC is associated with accelerated pause release, the full extent of its participation in the transcription cycle remains poorly illuminated. MYC also stimulates topoisomerases to resolve topological issues that complicate DNA transactions; whether and how this stimulation is coordinated with or independent of its transcriptional role has not been examined. We have developed a genetic tool that discriminates between MYC's ability to activate versus amplify reporter gene expression in any cell. This system enables the interrogation of genes, cofactors, and compounds that execute or modulate MYC activity. Using a combination of biochemical and cellular assays, we reveal the dynamic interplay between MYC-driven transcription amplification and DNA supercoiling. The early stages of transcription are highly sensitive to the level of DNA supercoiling. Reducing the activity of TOP1 either through genetic knockdown or low-dose inhibition potentiates transcription amplification by MYC. This enhancement is associated with pre-initiation complex (PIC) stabilization by DNA supercoiling. MYC helps to mobilize these stabilized PICs.

Authors

Institutions

Publication Details

Journal
bioRxiv (Cold Spring Harbor Laboratory)
Published
2026-01-19
DOI
https://doi.org/10.64898/2026.01.19.700398
Primary Topic
Cancer therapeutics and mechanisms
Type
article
Field-Weighted Citation Impact
0.00

Funders

Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Dynamic Supercoiling Sponsors Transcription Amplification by MYC

David Levens, Fedor Kouzine, Subhendu Das, Brian A. Lewis et al.
bioRxiv (Cold Spring Harbor Laboratory)
Cancer therapeutics and mechanisms
article

Dynamic Supercoiling Sponsors Transcription Amplification by MYC

David Levens, Fedor Kouzine, Subhendu Das, Brian A. Lewis, Bo Wang, James D Phelan, Rajiv K Jha
article en

Abstract

MYC dysregulation occurs in most cancers provoking, profound changes in gene expression. Although sometimes considered to be an E-box-dependent transcription factor, an alternate model posits MYC to be a universal amplifier of active genes. Although MYC is associated with accelerated pause release, the full extent of its participation in the transcription cycle remains poorly illuminated. MYC also stimulates topoisomerases to resolve topological issues that complicate DNA transactions; whether and how this stimulation is coordinated with or independent of its transcriptional role has not been examined. We have developed a genetic tool that discriminates between MYC's ability to activate versus amplify reporter gene expression in any cell. This system enables the interrogation of genes, cofactors, and compounds that execute or modulate MYC activity. Using a combination of biochemical and cellular assays, we reveal the dynamic interplay between MYC-driven transcription amplification and DNA supercoiling. The early stages of transcription are highly sensitive to the level of DNA supercoiling. Reducing the activity of TOP1 either through genetic knockdown or low-dose inhibition potentiates transcription amplification by MYC. This enhancement is associated with pre-initiation complex (PIC) stabilization by DNA supercoiling. MYC helps to mobilize these stabilized PICs.

bioRxiv (Cold Spring Harbor Laboratory)
National Cancer Institute (US), Center for Cancer Research (US)
U.S. Department of Health and Human Services, National Institutes of Health, National Cancer Institute
Reduced inequalities
Openalex Percentile: Top 84%
Cancer therapeutics and mechanisms
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.