Thymine Metabolism and DNA Replication Dynamics in Prokaryotes
Summary
Thymine metabolism in prokaryotes encompasses both de novo synthesis of deoxythymidine triphosphate (dTTP) via the reductive branch of pyrimidine biosynthesis and salvage pathways that recover exogenous thymidine. Tight control of dTTP pools is essential for accurate DNA replication, as imbalance or depletion of thymine precursors can stall replication fork progression, trigger checkpoint responses and compromise chromosome integrity. Within the replication machinery, coordinated action of DNA helicases, polymerases and primases ensures that leading and lagging strands are synthesised in synchrony, while accessory factors such as single-strand DNA binding proteins and recombination enzymes mitigate fork collapse. Nutrient or drug-induced perturbations of thymine availability not only inhibit DNA polymerase activity but also invoke stress pathways—most notably the SOS response—that can lead to replication origin re-licensing, aberrant initiation events at oriC and ultimately chromosomal fragmentation. Understanding how metabolic pathways intersect with replication dynamics has broad implications for the development of novel antimicrobials, for tackling antibiotic resistance and for exploiting thymineless death in cancer chemotherapy.
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Thymine Metabolism and DNA Replication Dynamics in Prokaryotes publication trend
The graph below shows the total number of articles in thymine metabolism and dna replication dynamics in prokaryotes across all publications each year (not limited to Nature Index journals).
Technical terms
Deoxythymidine triphosphate (dTTP): The nucleotide precursor required for incorporation of thymine into DNA during replication.
Replication origin (oriC): The specific chromosomal locus where bidirectional DNA synthesis is initiated in bacteria.
Thymineless death (TLD): The rapid and irreversible loss of viability in cells deprived of thymine or its precursors.
Replication fork: The Y-shaped structure formed when parental DNA strands are unwound and copied by the replication machinery.
SOS response: A global regulatory network induced by DNA damage that activates repair enzymes and cell-cycle checkpoints.
Reactive oxygen species (ROS): Chemically reactive molecules containing oxygen that can damage DNA, proteins and lipids under oxidative stress.
References
- Role of RecA and the SOS Response in Thymineless Death in Escherichia coli. PLOS Genetics (2010).
- Disintegration of Nascent Replication Bubbles during Thymine Starvation Triggers RecA- and RecBCD-dependent Replication Origin Destruction*. Journal of Biological Chemistry (2012).
- Reactive oxygen species accumulation is synchronised with growth inhibition of temperature-sensitive recAts polA Escherichia coli. Archives of Microbiology (2022).
- Intracellular acidification is a hallmark of thymineless death in E. coli.. PLOS Genetics (2022).
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