The Lpt ABC transporter for lipopolysaccharide export to the cell surface

The surface of the outer membrane of Gram-negative bacteria is covered by a tightly packed layer of lipopolysaccharide molecules which provide a barrier against many toxic compounds and antibiotics. Lipopolysaccharide, synthesized in the cytoplasm, is assembled in the periplasmic leaflet of the inner membrane where the intermembrane Lpt system mediates its transport to the cell surface. The first step of lipopolysaccharide transport is its extraction from the outer leaflet of inner membrane powered by the atypical LptB₂FGC ABC transporter. Here we review latest advances leading to understanding at molecular level how lipopolysaccharide is transported irreversibly to the outer membrane.     

The SUF system: an ABC ATPase-dependent protein complex with a role in Fe–S cluster biogenesis

Iron-sulfur (Fe–S) clusters are considered one of the most ancient and versatile inorganic cofactors present in the three domains of life. Fe–S clusters can act as redox sensors or catalysts and are found to be used by a large number of functional and structurally diverse proteins. Here, we cover current knowledge of the SUF multiprotein machinery that synthesizes and inserts Fe–S clusters into proteins. Specific focus is put on the ABC ATPase SufC, which contributes to building Fe–S clusters, and appeared early on during evolution.     

From mitochondria to healthy aging: The role of branched-chain amino acids treatment: MATeR a randomized study

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体外抑菌试验评价核糖体表达筛选的抗菌肽活性

目的观察体外无细胞核糖体表达系统筛选得到的、能与细菌膜结合的多肽的体外抑菌活性变化,初步评价该筛选系统的可行性。方法采用核糖体展示系统和细胞膜模型筛选可结合于细胞膜的多肽,对筛选的多肽进行结构预测分析。选择形成α-螺旋结构可能性大、溶解性尚可的多肽(C13)进行合成。利用改良的微量肉汤稀释法测定C13和硫酸庆大霉素对G (金黄色葡萄球菌)和G-(大肠杆菌、伤寒杆菌)细菌的抗菌活性——最小抑菌浓度(MIC)和最小杀菌浓度(MBC)。结果C13对试验细菌的MIC均为400mg/L,但在现有浓度范围对试验菌的MBC则未测得。结论体外无细胞核糖体表达系统筛选的抗菌肽C13具有一定的抑菌活性,表明利用人工膜模型和核糖体表达进行抗菌肽筛选的方法是可行的,但有效抗菌肽的筛选需进一步的抑菌试验证实。     

Troxerutin attenuates diet‐induced oxidative stress,impairment of mitochondrial biogenesis and respiratory chain complexes in mice heart

Mitochondrial abnormality is thought to play a key role in cardiac disease originating from the metabolic syndrome (MS). We evaluated the effect of troxerutin (TX), a semi‐synthetic derivative of the natural bioflavanoid rutin, on the respiratory chain complex activity, oxidative stress, mitochondrial biogenesis and dynamics in heart of high fat, high fructose diet (HFFD) ‐induced mouse model of MS. Adult male Mus musculus mice of body weight 25‐30 g were fed either control diet or HFFD for 60 days. Mice from each dietary regimen were divided into two groups on the 16th day and were treated or untreated with TX (150 mg/kg body weight [bw], per oral) for the next 45 days. At the end of experimental period, respiratory chain complex activity, uncoupling proteins (UCP)‐2 and ‐3, mtDNA content, mitochondrial biogenesis and dynamics, oxidative stress markers and reactive oxygen species (ROS) generation were analyzed. Reduced mtDNA abundance with alterations in the expression of genes related to mitochondrial biogenesis and fission and fusion processes were observed in HFFD‐fed mice. Disorganized and smaller mitochondria, reduction in complexes I, III and IV activities (by about 55%) and protein levels of UCP‐2 (52%) and UCP‐3 (46%) were noted in these mice. TX administration suppressed oxidative stress, improved the oxidative capacity and biogenesis and restored fission/fusion imbalance in the cardiac mitochondria of HFFD‐fed mice. TX protects the myocardium by modulating the putative molecules of mitochondrial biogenesis and dynamics and by its anti‐oxidant function in a mouse model of MS.     

Mitochondrial dysfunction in neurodegenerative diseases and the potential countermeasure

Mitochondria not only supply the energy for cell function, but also take part in cell signaling. This review describes the dysfunctions of mitochondria in aging and neurodegenerative diseases, and the signaling pathways leading to mitochondrial biogenesis (including PGC‐1 family proteins, SIRT1, AMPK) and mitophagy (parkin‐Pink1 pathway). Understanding the regulation of these mitochondrial pathways may be beneficial in finding pharmacological approaches or lifestyle changes (caloric restrict or exercise) to modulate mitochondrial biogenesis and/or to activate mitophagy for the removal of damaged mitochondria, thus reducing the onset and/or severity of neurodegenerative diseases.