I skimmed the paper and there really isn't any direct evidence that it's a "repair mechanism" beyond the apparent effects of knocking out the gene: cells die faster, and degradation of ribosomal RNA is faster.
The presumed mechanism here would be oxidative stress->damage to rRNA->reduced protein production/increased error rate in proteins->cell is not happy,
with the RNA ligase playing the role of repairing localized damage caused by stress thus allowing the cell to continue at its normal rate.
There also isn't any strong evidence that this system resembles the ones seen in viruses and bacteria. There are many RNA ligases that have many different roles and the variations aren't shared between all kingdoms of life.
Agreed on all counts, though it's important to note that this protein has bacterial homologs that almost definitely have the same function (5'-3' RNA ligase activity).
I skimmed the paper and there really isn't any direct evidence that it's a "repair mechanism" beyond the apparent effects of knocking out the gene: cells die faster, and degradation of ribosomal RNA is faster.
The presumed mechanism here would be oxidative stress->damage to rRNA->reduced protein production/increased error rate in proteins->cell is not happy, with the RNA ligase playing the role of repairing localized damage caused by stress thus allowing the cell to continue at its normal rate.
There also isn't any strong evidence that this system resembles the ones seen in viruses and bacteria. There are many RNA ligases that have many different roles and the variations aren't shared between all kingdoms of life.