Translesion Synthesis in Plants: Ultraviolet Resistance and Beyond

Plant genomes sustain various forms of DNA damage that stall replication forks. Translesion synthesis (TLS) is one of the pathways to overcome stalled replication in which specific polymerases (TLS polymerase) perform bypass synthesis across DNA damage. This article gives a brief overview of plant TLS polymerases. In Arabidopsis, DNA polymerase (Pol) zeta, eta, kappa, theta and lambda and Reversionless1 (Rev1) are shown to be involved in the TLS. For example, AtPol eta bypasses ultraviolet (UV)-induced cyclobutane pyrimidine dimers in vitro. Disruption of AtPol zeta or AtPol eta increases root stem cell death after UV irradiation. These results suggest that AtPol zeta and ATPol eta bypass UV-induced damage, prevent replication arrest, and allow damaged cells to survive and grow. In general, TLS polymerases have low fidelity and often induce mutations. Accordingly, disruption of AtPol zeta or AtRev1 reduces somatic mutation frequency, whereas disruption of AtPol eta elevates it, suggesting that plants have both mutagenic and less mutagenic TLS activities. The stalled replication fork can be resolved by a strand switch pathway involving a DNA helicase Rad5. Disruption of both AtPol zeta and AtRAD5a shows synergistic or additive effects in the sensitivity to DNA-damaging agents. Moreover, AtPol zeta or AtRev1 disruption elevates homologous recombination frequencies in somatic tissues. These results suggest that the Rad5-dependent pathway and TLS are parallel. Plants grown in the presence of heat shock protein 90 (HSP90) inhibitor showed lower mutation frequencies, suggesting that HSP90 regulates mutagenic TLS in plants. Hypersensitivities of TLS-deficient plants to.-ray and/or crosslink damage suggest that plant TLS polymerases have multiple roles, as reported in other organisms.