Metabolism is enormously complicated, even in very simple creatures such as nematode worms. So there are any number of ways in which genetic and other changes can confound the conventional wisdom, or produce results that run contrary to the well-established pattern. In this case the well-established pattern is that loss of DNA repair capabilities shortens life: a whole class of rare diseases that have the appearance of accelerated aging result from forms of DNA repair deficiency in humans.
Nonetheless, the particular loss of function mutation noted here manages to extend life in nematodes, possibly by spurring overcompensation in other forms of cellular housekeeping, despite the fact that it has most of the other expected effects in reducing viability of cells and the organism as a whole:
Human-nucleotide-excision repair (NER) deficiency leads to different developmental and segmental progeroid symptoms of which the pathogenesis is only partially understood. To understand the biological impact of accumulating spontaneous DNA damage, we studied the phenotypic consequences of DNA-repair deficiency in Caenorhabditis elegans.
We find that DNA damage accumulation does not decrease the adult life span of post-mitotic tissue. Surprisingly, loss of functional ERCC-1/XPF even further extends the life span of long-lived daf-2 mutants, likely through an adaptive activation of stress signaling.
Contrariwise, NER deficiency leads to a striking transgenerational decline in replicative capacity and viability of proliferating cells. DNA damage accumulation induces severe, stochastic impairment of development and growth, which is most pronounced in NER mutants that are also impaired in their response to ionizing radiation and inter-strand crosslinks. These results suggest that multiple DNA-repair pathways can protect against replicative decline and indicate that there might be a direct link between the severity of symptoms and the level of DNA-repair deficiency in patients.
You might consider this in the context of the debate over whether nuclear DNA damage is actually relevant to aging over the course of a human life span, or whether it only contributes to cancer risk.