DNA interstrand crosslink repair by XPF-ERCC1 homologue confers ultraviolet resistance in Neurospora crassa

Fungal Genet Biol. 2023 Jan:164:103752. doi: 10.1016/j.fgb.2022.103752. Epub 2022 Nov 23.


Ultraviolet (UV) light is a mutagen that causes DNA damage. Some UV-sensitive Neurospora crassa strains have been reported to exhibit a partial photoreactivation defect (PPD) phenotype, and the possible cause of this has been unknown for more than half a century. In this study, in the process of elucidating the possible causes of a PPD phenotype, we discovered that the XPF homologue MUS-38 is involved in repairing the UV-induced DNA interstrand crosslink (ICL) in N. crassa. Furthermore, the sensitivity of the Δmus-38 and Δmus-44 strains to ICL agents was significantly higher than that of other nucleotide excision repair (NER)-related gene knockout (KO) strains, indicating that the MUS-38/MUS-44 complex is involved in an NER-independent ICL repair mechanism. Based on reports concerning the mammalian homologues XPF and ERCC1 we obtained separation-of-function mutants defective only in NER in mus-38 and mus-44. Additionally, the photoreactivation ability of these mutants was significantly higher than that of the KO strains. These results indicate that the PPD phenotype is caused by a defect in the repair-ability of ICL induced by UV and that an NER-independent ICL repair by MUS-38 and MUS-44 confers resistance to UV in N. crassa.

Keywords: DNA repair; Interstrand crosslink repair; Neurospora crassa; Nucleotide excision repair; Photoreactivation; XPF-ERCC1.

MeSH terms

  • Animals
  • DNA
  • DNA Damage / genetics
  • DNA Repair / genetics
  • Endonucleases / genetics
  • Endonucleases / metabolism
  • Mammals / genetics
  • Mammals / metabolism
  • Mutagens
  • Neurospora crassa* / genetics
  • Neurospora crassa* / metabolism
  • Ultraviolet Rays


  • DNA
  • Mutagens
  • Endonucleases