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sensitivity to the sun and increased susceptibility to skin cancers than the general
population (Cruet-Hennequart et al. 2010).
DNA duplication after UV irradiation does not uniquely depend on TLS components. Unrepaired UV-lesions can also induce double-strand breaks (DSBs) in the
DNA molecule (Fig.  4.5). DSBs are very lethal lesions for a cell as both DNA
strands are cut, and genetic material can be lost (Figueroa-González and
Fig. 4.4 Translesion DNA synthesis (TLS). (a) DNA duplication machinery proceeds normally
when no lesions are presented on the molecule. (b) When DNA is damaged by UV rays, (1) the
machinery responsible for the duplication of this molecule cannot work properly across a thymine
dimer, and the system is halted. (2) To deal with this situation, cells activate an alternative pathway
called translesion DNA synthesis (TLS) that recognizes the lesion and continuous replication
across it. TLS induce mutations on the genetic material but allow cell survival after UV radiation.
(3) When TLS is not available, DNA duplication does not restart, DNA can be broken, and cell will
probably die
Fig. 4.5 Double-strand
break (DSB) created as a
consequence of a
UV-lesion. DSBs can arise
during DNA synthesis as a
consequence of the stalling
of the DNA duplication
machinery at a pyrimidine
dimer. These kinds of
lesions are extremely toxic
for the cell and can induce
cell death or genomic
instability
4 SDG 3 Good Health and Well-Being