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An essential gene screening identifies yeast Mot1 as a suppressor of R-loops and genome instability

María E Soler-Oliva1,2, Rocío A Domínguez-Sierra1,2, Hélène Gaillard1,2

  • 1Centro Andaluz de Biología Molecular y Medicina Regenerativa - CABIMER, Consejo Superior de Investigaciones Científicas - Universidad de Sevilla - Universidad Pablo de Olavide, Seville, Spain.

Plos Genetics
|February 9, 2026
PubMed

Insights

The SWI/SNF-like protein Mot1 prevents genomic instability by resolving RNA-DNA hybrids called R-loops. Mot1 dysfunction impairs DNA replication during S phase, highlighting its role in mitigating transcription-replication conflicts.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Transcription can cause genetic instability via R-loop formation (RNA-DNA hybrids).
  • Accumulated R-loops are linked to DNA damage and human diseases like cancer.
  • Factors preventing R-loop accumulation are known, but roles of essential proteins are unclear.

Purpose of the Study:

  • Identify novel proteins preventing R-loop-associated genomic instability.
  • Investigate the function of the SWI/SNF-like protein Mot1 in R-loop metabolism.

Main Methods:

  • Utilized a genetic screen of over 1200 temperature-sensitive mutants in Saccharomyces cerevisiae.
  • Analyzed R-loop accumulation and R-loop-associated genomic instability.
  • Examined epistatic relationships between MOT1 and SEN1 mutations.

Main Results:

  • The SWI/SNF-like protein Mot1 is crucial for preventing R-loop accumulation and genomic instability.
  • Mot1 deficiency impairs S phase DNA replication, causing R-loop-dependent replication issues, likely due to transcription-replication conflicts (TRCs).
  • Epistasis between MOT1 and SEN1 supports Mot1's role in resolving TRCs.

Conclusions:

  • Mot1 plays a key role in maintaining genome stability by regulating R-loop homeostasis.
  • Transcriptional regulators like Mot1 are vital for mitigating TRCs and preventing R-loop-associated instability.
  • Understanding Mot1's function provides insights into disease mechanisms linked to R-loop accumulation.

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