Papagiannakis Alexandros, Yu Qiwei, Govers Sander K, Lin Wei-Hsiang, Wingreen Ned S, Jacobs-Wagner Christine
Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.
Sarafan Chemistry, Engineering, and Medicine for Human Health Institute, Stanford University, Stanford, CA 94305, USA.
bioRxiv. 2025 Mar 15:2024.10.08.617237. doi: 10.1101/2024.10.08.617237.
Chromosome segregation is essential for cellular proliferation. Unlike eukaryotes, bacteria lack cytoskeleton-based machinery to segregate their chromosomal DNA (nucleoid). The bacterial ParABS system segregates the duplicated chromosomal regions near the origin of replication. However, this function does not explain how bacterial cells partition the rest (bulk) of the chromosomal material. Furthermore, some bacteria, including , lack a ParABS system. Yet, faithfully segregates nucleoids across various growth rates. Here, we provide theoretical and experimental evidence that polysome production during chromosomal gene expression helps compact, split, segregate, and position nucleoids in through out-of-equilibrium dynamics and polysome exclusion from the DNA meshwork, inherently coupling these processes to biomass growth across nutritional conditions. Halting chromosomal gene expression and thus polysome production immediately stops sister nucleoid migration while ensuing polysome depletion gradually reverses nucleoid segregation. Redirecting gene expression away from the chromosome and toward plasmids causes ectopic polysome accumulations that are sufficient to drive aberrant nucleoid dynamics. Cell width enlargement suggest that the proximity of the DNA to the membrane along the radial axis is important to limit the exchange of polysomes across DNA-free regions, ensuring nucleoid segregation along the cell length. Our findings suggest a self-organizing mechanism for coupling nucleoid segregation to cell growth.
染色体分离对于细胞增殖至关重要。与真核生物不同，细菌缺乏基于细胞骨架的机制来分离其染色体DNA（类核）。细菌的ParABS系统在复制起点附近分离复制的染色体区域。然而，这一功能并不能解释细菌细胞如何分配染色体物质的其余部分（大部分）。此外，包括某些细菌在内，一些细菌缺乏ParABS系统。然而，这些细菌在不同生长速率下都能忠实地分离类核。在这里，我们提供了理论和实验证据，表明染色体基因表达过程中的多核糖体产生通过非平衡动力学和多核糖体从DNA网络中排除，有助于在细菌中压缩、分裂、分离和定位类核，从而将这些过程与不同营养条件下的生物量生长内在地联系起来。停止染色体基因表达从而停止多核糖体产生会立即阻止姐妹类核迁移，而随后的多核糖体消耗会逐渐逆转类核分离。将基因表达从染色体转向质粒会导致异位多核糖体积累，足以驱动异常的类核动态。细胞宽度增大表明，沿径向轴DNA与细胞膜的接近程度对于限制多核糖体在无DNA区域的交换很重要，从而确保类核沿细胞长度分离。我们的研究结果表明了一种将类核分离与细胞生长耦合的自组织机制。
