A Molecular Genetic Basis Explaining Altered Bacterial Behavior in Space

Bacterial behavior has been observed to change during spaceflight. Higher final cell counts, enhanced biofilm formation, increased virulence, and reduced susceptibility to antibiotics have been reported to occur for cells cultured in space . Most of these phenomena are theorized as being an indirect effect of an altered extracellular environment, where the carbon source uptake is inhibited and excreted acidic byproducts buildup around the cell due to the lack of gravity-driven transport forces. However, to date neither spaceflight results, ground-based studies, physical measurement techniques nor computational approaches have provided sufficient evidence needed to confirm this model. Gene expression data from the Antibiotic Effectiveness in Space (AES-1) experiment, however, have now allowed us to look into the biomolecular processes behind these observations and showed a systematic activation of glucose starvation and acid resistance genes. These results corroborate the reduced mass transport model proposed to govern bacterial responses to spaceflight. Furthermore, the gene expression data suggests that metabolism was stimulated in space, which could play a role in causing the observed increase in bacterial cell concentrations in microgravity. Similarly, the decrease in extracellular pH may also be involved with the reported increase in virulence in space.

已有研究观测到，细菌的行为在太空飞行过程中会发生改变。据报道，在太空环境中培养的细菌可呈现更高的最终细胞密度、更强的生物膜形成能力、更高的毒力以及对抗生素更低的敏感性。目前多数此类现象被理论认为是细胞外环境改变带来的间接效应：由于缺乏重力驱动的转运力，细菌的碳源摄取受到抑制，且其排泄的酸性副产物会在细胞周围积累。然而截至目前，无论是太空飞行实验结果、地面模拟研究、物理测量技术还是计算分析方法，均未提供足以验证该模型的充分证据。不过，来自太空抗生素效力（Antibiotic Effectiveness in Space, AES-1）实验的基因表达数据，如今使我们得以探究上述观测结果背后的生物分子机制，数据显示葡萄糖饥饿与酸性抗性基因均被系统性激活。上述结果佐证了被提出用以解释细菌对太空飞行响应的质量转运减弱模型。此外，基因表达数据表明，太空环境下细菌的代谢受到激活，这可能与微重力环境中观测到的细菌细胞浓度升高存在关联。与之类似，细胞外pH值的降低也可能与已报道的太空环境中细菌毒力增强有关。