Abstract：
OBJECTIVE: Some studies have indicated that the alterations in cellular morphology induced by selenite [Se(Ⅳ)] may be attributed to its inhibitory effects on cell division. However, whether the genes associated with cell division are implicated in Se(Ⅳ) metabolism remains unclear.
RESULTS: The ftsK gene in Rahnella aquatilis HX2 was mutated with an in-frame deletion strategy. The ftsK mutation strongly reduced the tolerance to selenite [Se(Ⅳ)] and the production of red elemental selenium [Se(0)] in R. aquatilis HX2, and this effect could not be attributed solely to the inhibition of cell growth. Deleting the ftsK gene also resulted in a significant decrease in bacterial growth of R. aquatilis HX2 during both exponential and stationary phases. The deletion of ftsK inhibited cell division, resulting in the development of elongated filamentous cells. Furthermore, the loss-of-function of FtsK significantly impacted the expression of seven genes linked to cell division and Se(Ⅳ) metabolism by at least 2-fold, as unveiled by real-time quantitative PCR (RT-qPCR) under Se(Ⅳ) treatment.
CONCLUSIONS: These findings suggest that FtsK is associated with Se(Ⅳ) tolerance and Se(0) generation and is a key player in coordinating bacterial growth and cell morphology in R. aquatilis HX2.
RESULTS: The ftsK gene in Rahnella aquatilis HX2 was mutated with an in-frame deletion strategy. The ftsK mutation strongly reduced the tolerance to selenite [Se(Ⅳ)] and the production of red elemental selenium [Se(0)] in R. aquatilis HX2, and this effect could not be attributed solely to the inhibition of cell growth. Deleting the ftsK gene also resulted in a significant decrease in bacterial growth of R. aquatilis HX2 during both exponential and stationary phases. The deletion of ftsK inhibited cell division, resulting in the development of elongated filamentous cells. Furthermore, the loss-of-function of FtsK significantly impacted the expression of seven genes linked to cell division and Se(Ⅳ) metabolism by at least 2-fold, as unveiled by real-time quantitative PCR (RT-qPCR) under Se(Ⅳ) treatment.
CONCLUSIONS: These findings suggest that FtsK is associated with Se(Ⅳ) tolerance and Se(0) generation and is a key player in coordinating bacterial growth and cell morphology in R. aquatilis HX2.
摘要：
目的：一些研究表明，亚硒酸盐[Se（Ⅳ）]诱导的细胞形态改变可能归因于其对细胞分裂的抑制作用。然而,与细胞分裂相关的基因是否与Se(Ⅳ)代谢有关尚不清楚。
结果：采用框内缺失策略对水痘HX2中的ftsK基因进行了突变。ftsK突变强烈降低了对亚硒酸盐[Se（Ⅳ）]的耐受性和对R.aquatilisHX2中红色元素硒[Se（0）]的产生，这种作用不能仅归因于对细胞生长的抑制。删除ftsK基因还导致在指数期和稳定期期间水草芽孢杆菌HX2的细菌生长显着降低。ftsK的缺失抑制了细胞分裂,导致细长丝状细胞的发育。此外，FtsK功能的丧失显著影响了7个与细胞分裂和Se(Ⅳ)代谢相关的基因表达至少2倍,硒（Ⅳ）处理下的实时定量PCR（RT-qPCR）揭示。
结论：这些发现表明，FtsK与Se（Ⅳ）耐受性和Se（0）生成有关，并且是协调水曲柳HX2中细菌生长和细胞形态的关键因素。
结果：采用框内缺失策略对水痘HX2中的ftsK基因进行了突变。ftsK突变强烈降低了对亚硒酸盐[Se（Ⅳ）]的耐受性和对R.aquatilisHX2中红色元素硒[Se（0）]的产生，这种作用不能仅归因于对细胞生长的抑制。删除ftsK基因还导致在指数期和稳定期期间水草芽孢杆菌HX2的细菌生长显着降低。ftsK的缺失抑制了细胞分裂,导致细长丝状细胞的发育。此外，FtsK功能的丧失显著影响了7个与细胞分裂和Se(Ⅳ)代谢相关的基因表达至少2倍,硒（Ⅳ）处理下的实时定量PCR（RT-qPCR）揭示。
结论：这些发现表明，FtsK与Se（Ⅳ）耐受性和Se（0）生成有关，并且是协调水曲柳HX2中细菌生长和细胞形态的关键因素。
