Fassler J S, Tessman I
J Virol. 1981 Mar;37(3):955-62. doi: 10.1128/JVI.37.3.955-962.1981.
The suppression of polarity by UV irradiation was similar to the suppression by rho mutants. This was demonstrated for a polar nonsense mutant of phage phi X174. Treatment of the host for 30 min with 100 micrograms of the radiomimetic drug mitomycin C per ml was about as effective as 550 J of UV irradiation per m2 in relieving polarity. The shape of the UV survival curves for rho mutants could be linked to a proposed mechanism of UV relief of polarity. Host cell reactivation of phage lambda and W-reactivation of phage G4 were unaffected by rho mutations. UV suppression of polarity is independent of the Hcr- and RecA- phenotypes. An explanation for the UV sensitivity of rho mutants is provided, and several ways are considered in which UV irradiation may deplete cellular rho activity and thereby cause UV relief of polarity. We propose a novel theory that relates the UV inactivation of normal repair-proficient cells to a decrease in rho activity.
紫外线照射对极性的抑制作用与rho突变体引起的抑制作用相似。这在噬菌体phi X174的极性无义突变体中得到了证明。用每毫升100微克的放射模拟药物丝裂霉素C处理宿主30分钟，在缓解极性方面的效果与每平方米550焦耳的紫外线照射效果相当。rho突变体的紫外线存活曲线形状可能与紫外线缓解极性的一种推测机制有关。噬菌体lambda的宿主细胞复活和噬菌体G4的W复活不受rho突变的影响。紫外线对极性的抑制与Hcr和RecA表型无关。本文提供了对rho突变体紫外线敏感性的解释，并考虑了几种紫外线照射可能耗尽细胞rho活性从而导致紫外线缓解极性的方式。我们提出了一种新理论，将正常修复能力细胞的紫外线失活与rho活性的降低联系起来。
