Part of the salvage pathway for purine and pyrimidine deoxyribonucleotide synthesis. Phosphorylates preferentially purines over pyrimidines (PubMed:22897443). Mediates tolerance to genotoxins, such as ultraviolet-C (UV-C) irradiation, MMC, a DNA crosslinker, and ZEO, a DNA intercalator, that induce double-strand breaks and thus contributes to several DNA repair pathways by providing deoxythymidine triphosphate that serve as precursors for DNA repair and to balance deoxyribonucleotides pools (PubMed:25537647). ATP + thymidine = ADP + dTMP + H(+) kcat is 1.5 sec(-1) with deoxyuridine (dU) as substrate. kcat is 0.48 sec(-1) with deoxythymidine (dT) as substrate. kcat is 0.13 sec(-1) with 3'-azido-3'-deoxythymidine (AZT) as substrate. Purine metabolism. Pyrimidine metabolism. Monomer and dimer. Dimerization is stimulated by ATP. Expressed ubiquitously. Strongly expressed at the early stages of germination upon testa rupture and throughout seedling development. Accumulates in the cotyledons and foliar primordia. In seedlings, highly present in almost every organ except the root meristem and secondary root primordia. In young leaves, detected in the trichomes. In mature leaves, present in the vasculature as well as in the pedicel and base. In flowers organs, mostly expressed in stigma, petals, anthers and pollen. In developing siliques, restricted to pedicels and septum. Induced by genotoxins such as ultraviolet-C radiation (UV-C), and ZEO and MMC treatments. No visible phenotype. The double mutant tk1a tk1b is seedling lethal. Belongs to the thymidine kinase family.