Thymine-starvation-induced chromosomal fragmentation is not required for thymineless death in Escherichia coli,Molecular Microbiology

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Thymine-starvation-induced chromosomal fragmentation is not required for thymineless death in Escherichia coli
Molecular Microbiology ( IF 2.6 ) Pub Date : 2022-03-24 , DOI: 10.1111/mmi.14897
Sharik R Khan ₁ , Andrei Kuzminov ₁

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Thymine or thymidine starvation induces robust chromosomal fragmentation in Escherichia coli thyA deoCABD mutants and is proposed to be the cause of thymineless death (TLD). However, fragmentation kinetics challenges the idea that fragmentation causes TLD, by peaking before the onset of TLD and disappearing by the time TLD accelerates. Quantity and kinetics of fragmentation also stay unchanged in hyper-TLD-exhibiting recBCD mutant, making its faster and deeper TLD independent of fragmentation as well. Elimination of fragmentation without affecting cellular metabolism did not abolish TLD in the thyA mutant, but reduced early TLD in the thyA recBCD mutant, suggesting replication-dependent, but undetectable by pulsed-field gel, double-strand breaks contributed to TLD. Chromosomal fragmentation, but not TLD, was eliminated in both the thyA and thyA recBCD mutants harboring deoCABD operon. The expression of a single gene, deoA, encoding thymidine phosphorylase, was sufficient to abolish fragmentation, suggesting thymidine-to-thymine interconversion during T-starvation being a key factor. Overall, this study reveals that chromosomal fragmentation, a direct consequence of T-starvation, is either dispensable or redundant for the overall TLD pathology, including hyper-TLD in the recBCD mutant. Replication forks, unlike chromosomal fragmentation, may provide a minor contribution to TLD, but only in the repair-deficient thyA deoCABD recBCD mutant.

中文翻译：

胸腺嘧啶饥饿诱导的染色体断裂不是大肠杆菌中无胸腺嘧啶死亡所必需的

胸腺嘧啶或胸苷饥饿会在大肠杆菌thyA deoCABD突变体中诱导强烈的染色体片段化，并被认为是无胸腺嘧啶死亡 (TLD) 的原因。然而，碎片化动力学挑战了碎片化导致 TLD 的观点，在 TLD 开始之前达到峰值并在 TLD 加速时消失。在超 TLD 表现出的recBCD突变体中，碎片的数量和动力学也保持不变，使其更快和更深的 TLD 也独立于碎片。在不影响细胞代谢的情况下消除碎片并没有消除thyA突变体中的 TLD，但减少了thyA recBCD中的早期 TLD突变体，表明复制依赖性，但脉冲场凝胶检测不到，双链断裂有助于 TLD。在含有deoCABD操纵子的thyA和thyA recBCD突变体中消除了染色体片段化，但没有消除 TLD 。编码胸苷磷酸化酶的单个基因deoA的表达足以消除片段化，这表明在 T 饥饿期间胸苷到胸腺嘧啶的相互转换是一个关键因素。总体而言，这项研究表明，作为 T 饥饿的直接后果的染色体片段化对于整个 TLD 病理学（包括recBCD中的超 TLD）要么是可有可无的，要么是多余的突变体。与染色体碎片不同，复制叉可能对 TLD 的贡献很小，但仅限于修复缺陷的thyA deoCABD recBCD突变体。

更新日期：2022-03-24

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