Tigges M A, Bursch C J, Snustad D P
J Virol. 1977 Dec;24(3):775-85. doi: 10.1128/JVI.24.3.775-785.1977.
Most, if not all, host RNA synthesis was shut off after infection of Escherichia coli strain B/5 with a bacteriophage T4 multiple mutant defective in the abilities to induce (i) unfolding of the host nucleoid (unf-), (ii) nuclear disruption (ndd-), and (iii) host DNA degradation (denA-, denB-). The shutoff of host RNA synthesis and turn-on of phage RNA synthesis were slower after infection of E. coli with unf- phage than after infection with unf+ phage. This delay in the switchover from host RNA synthesis to phage RNA synthesis in unf- infections did not result in a measurable delay in the onset of nuclear disruption, deoxyribonucleoside monophosphate kinase synthesis, or DNA synthesis. unf39 did not complement alc (allows late transcription on cytosine-containing DNA) mutants, supporting the proposal of Sirotkin et al. [Nature (London) 265:28-32, 1977] that alc and unf are possibly the same gene.
在用噬菌体T4多重突变体感染大肠杆菌B/5菌株后,多数(即便不是全部)宿主RNA合成被关闭,该突变体在诱导(i)宿主类核解折叠(unf-)、(ii)核破坏(ndd-)和(iii)宿主DNA降解(denA-、denB-)的能力方面存在缺陷。与用unf+噬菌体感染大肠杆菌后相比,用unf-噬菌体感染后宿主RNA合成的关闭以及噬菌体RNA合成的开启更为缓慢。在unf-感染中,从宿主RNA合成向噬菌体RNA合成转换的这种延迟,并未导致在核破坏、脱氧核糖核苷单磷酸激酶合成或DNA合成起始方面出现可测量的延迟。unf39不能互补alc(允许在含胞嘧啶的DNA上进行晚期转录)突变体,这支持了西罗特金等人[《自然》(伦敦)265:28 - 32,1977]的提议,即alc和unf可能是同一个基因。