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G2-seq: A High Throughput Sequencing-based Technique for Identifying Late Replicating Regions of the Genome

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The Heritability of Replication Problems.

Jean-Sébastien Hoffmann¹

¹Laboratoire de Pathologie, Laboratoire d'Excellence Toulouse Cancer, CHU Toulouse, Institut Universitaire du Cancer-Toulouse, Oncopole, 1 Avenue Irène-Joliot-Curie, CEDEX, 31059 Toulouse, France.

|July 2, 2021

Summary

DNA replication stress can be transmitted to daughter cells, impacting their genome and replication timing. This transmission may alert subsequent cell generations to genomic instability, aiding adaptive responses, particularly in cancer therapy resistance.

Keywords:

DNA damage DNA replication replication timing replicative stress

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Area of Science:

Genetics
Cell Biology
Molecular Biology

Background:

DNA replication is crucial for genetic material duplication, but replication stress can cause genomic instability and disease, including cancer.
While cellular responses to replication stress are studied, the transmission of genomic modifications through mitosis to daughter cells, especially under low stress, is less understood.

Purpose of the Study:

To investigate the heritability of DNA damage and altered replication timing programs across cell divisions following low replication stress.
To explore the potential adaptive advantages of transmitting replication problems to subsequent cell generations.

Main Methods:

Utilizing advanced molecular biology techniques to track DNA damage propagation.
Analyzing changes in replication timing programs in daughter cells after parental cell exposure to replication stress.

Main Results:

DNA damage incurred by low replication stress can be transmitted to daughter cells.
Replication timing programs in specific chromosomal domains are altered in the next generation of cells.
This intergenerational transmission of replication stress can occur without triggering G2/M checkpoint responses.

Conclusions:

Replication problems, including DNA damage and altered replication timing, can be inherited by daughter cells.
This heritability may represent an adaptive mechanism, preparing cells for future genomic challenges, potentially influencing cancer therapy resistance.