Abstract— Photoprotection i. e. the increased resistance of the cells preilluminated with near ultraviolet light (300–380 nm) to the lethal action of 254 nm radiations is observed in wild‐type Escherichia coli B cells (which exhibits the Fil phenotype) but requires either an integrated prophage or a recA mutation to be detected in E. coli K12 strains. Here we have demonstrated that significant photoprotection occurs in an E. coli K12 recA+ cell containing the Ion allele which is responsible for filamentous growth (Fil phenotype) after 254 nm irradiation. The Fil phenotype can be suppressed by the sfiA of sfiB suppressor genes. Since the E. coli K12 recA+Ion sfiB strain exhibits no more photoprotection, these data support the conclusion that in Ion strains photoprotection is due to the abolition of the 254 nm induced filamentation by the near ultraviolet treatment. In addition, we show here that near ultraviolet illumination of the cells leads to a severe restriction of the bulk protein synthesis, as well as of the inducibility of β‐galactosidase and tryptophanase. These effects are observed only in nuv+ cells that contains 4‐thiouridine the chromophore responsible for photoprotection. We propose that in Ion (lysogenic) strains, photoprotection is due to prevention of the SOS response. During the growth lag, the low residual level of protein synthesis does not allow the induction of the SOS response and accordingly prevents filamentation (the lytic cycle). Concomitantly the SOS triggering signals are eliminated via DNA repair.