In conditions of halted or limited genome replication, like those experienced in 
sporulating cells of Bacillus subtilis, a more immediate detriment caused by DNA 
damage is altering the transcriptional programme that drives this developmental 
process. Here, we report that mfd, which encodes a conserved bacterial protein 
that mediates transcription-coupled DNA repair (TCR), is expressed together with 
uvrA in both compartments of B. subtilis sporangia. The function of Mfd was 
found to be important for processing the genetic damage during B. subtilis 
sporulation. Disruption of mfd sensitized developing spores to mitomycin-C (M-C) 
treatment and UV-C irradiation. Interestingly, in non-growing sporulating cells, 
Mfd played an anti-mutagenic role as its absence promoted UV-induced mutagenesis 
through a pathway involving YqjH/YqjW-mediated translesion synthesis (TLS). Two 
observations supported the participation of Mfd-dependent TCR in spore 
morphogenesis: (i) disruption of mfd notoriously affected the efficiency of B. 
subtilis sporulation and (ii) in comparison with the wild-type strain, a 
significant proportion of Mfd-deficient sporangia that survived UV-C treatment 
developed an asporogenous phenotype. We propose that the Mfd-dependent repair 
pathway operates during B. subtilis sporulation and that its function is 
required to eliminate genetic damage from transcriptionally active genes.