Fernandez Marilina, Paulucci Natalia S, Peppino Margutti Micaela, Biasutti Alicia M, Racagni Graciela E, Villasuso Ana L, Agostini Elizabeth, González Paola S
Departamento de Biología Molecular, Universidad Nacional de Río Cuarto, 5800, Río Cuarto, Córdoba, Argentina.
Departamento de Química-FCEFQyN, Universidad Nacional de Río Cuarto, 5800, Río Cuarto, Córdoba, Argentina.
Lipids. 2019 Sep;54(9):557-570. doi: 10.1002/lipd.12187. Epub 2019 Sep 2.
The remodeling of membrane lipids is a mechanism that allows microorganisms to survive in unfavorable environments such as industrial effluents, which often contain inorganic and organic pollutants, like chromium and phenol. In the present work, we evaluated the effect of Cr(VI) and phenol on the membrane of Acinetobacter guillouiae SFC 500-1A, a bacterial strain isolated from tannery sediments where such pollutants can be found. The presence of lipid kinases and phospholipases and the changes in their activities under exposure to these pollutants were determined. Cr(VI) and Cr(VI) + phenol caused the membrane to become more rigid for up to 16 h after exposure. This could be due to an increase in cardiolipin (Ptd Gro) and a decrease in phosphatidylethanolamine (PtdEtn), which are indicative of more order and rigidity in the membrane. Increased phospholipase A activity (PLA, EC 3.1.1.4) could be responsible for the decrease in PtdEtn levels. Moreover, our results indicate that Cr(VI) and Cr(VI) + phenol trigger the phosphatidic acid (PtdOH) signal. The finding of significantly increased phosphatidylinositol-4-phosphate (PtdIns-4-P) levels means this is likely achieved via PtdIns-PLC/DGK. This report provides the first evidence that A. guillouiae SFC 500-1A is able to sense Cr(VI) and phenol, transduce this signal through changes in the physical state of the membrane, and trigger lipid-signaling events.
膜脂重塑是一种使微生物能够在不利环境（如工业废水中，其通常含有无机和有机污染物，如铬和苯酚）中生存的机制。在本研究中，我们评估了六价铬（Cr(VI)）和苯酚对吉氏不动杆菌SFC 500 - 1A细胞膜的影响，该菌株是从可发现此类污染物的制革厂沉积物中分离出来的。我们测定了脂质激酶和磷脂酶的存在及其在暴露于这些污染物时的活性变化。Cr(VI)和Cr(VI) + 苯酚使细胞膜在暴露后长达16小时变得更加僵硬。这可能是由于心磷脂（Ptd Gro）增加和磷脂酰乙醇胺（PtdEtn）减少，这表明细胞膜中更有序且更僵硬。磷脂酶A活性（PLA，EC 3.1.1.4）增加可能是PtdEtn水平降低的原因。此外，我们的结果表明Cr(VI)和Cr(VI) + 苯酚触发了磷脂酸（PtdOH）信号。磷脂酰肌醇 - 4 - 磷酸（PtdIns - 4 - P）水平显著增加的发现意味着这可能是通过磷脂酰肌醇 - PLC/二酰甘油激酶（PtdIns - PLC/DGK）实现的。本报告首次证明吉氏不动杆菌SFC 500 - 1A能够感知Cr(VI)和苯酚，通过细胞膜物理状态的变化转导该信号，并触发脂质信号事件。
