Schleissner C, Olivera E R, Fernández-Valverde M, Luengo J M
Departamento de Bioquímica y Biología Molecular, Facultad de Veterinaria, León, Spain.
J Bacteriol. 1994 Dec;176(24):7667-76. doi: 10.1128/jb.176.24.7667-7676.1994.
The phenylacetic acid transport system (PATS) of Pseudomonas putida U was studied after this bacterium was cultured in a chemically defined medium containing phenylacetic acid (PA) as the sole carbon source. Kinetic measurement was carried out, in vivo, at 30 degrees C in 50 mM phosphate buffer (pH 7.0). Under these conditions, the uptake rate was linear for at least 3 min and the value of Km was 13 microM. The PATS is an active transport system that is strongly inhibited by 2,4-dinitrophenol, 4-nitrophenol (100%), KCN (97%), 2-nitrophenol (90%), or NaN3 (80%) added at a 1 mM final concentration (each). Glucose or D-lactate (10 mM each) increases the PATS in starved cells (140%), whereas arsenate (20 mM), NaF, or N,N'-dicyclohexylcarbodiimide (1 mM) did not cause any effect. Furthermore, the PATS is insensitive to osmotic shock. These data strongly suggest that the energy for the PATS is derived only from an electron transport system which causes an energy-rich membrane state. The thiol-containing compounds mercaptoethanol, glutathione, and dithiothreitol have no significant effect on the PATS, whereas thiol-modifying reagents such as N-ethylmaleimide and iodoacetate strongly inhibit uptake (100 and 93%, respectively). Molecular analogs of PA with a substitution (i) on the ring or (ii) on the acetyl moiety or those containing (iii) a different ring but keeping the acetyl moiety constant inhibit uptake to different extents. None of the compounds tested significantly increase the PA uptake rate except adipic acid, which greatly stimulates it (163%). The PATS is induced by PA and also, gratuitously, by some phenyl derivatives containing an even number of carbon atoms on the aliphatic moiety (4-phenyl-butyric, 6-phenylhexanoic, and 8-phenyloctanoic acids). However, similar compounds with an odd number of carbon atoms (benzoic, 3-phenylpropionic, 5-phenylvaleric, 7-phenylheptanoic, and 9-phenylnonanoic acids) as well as many other PA derivatives do not induce the system, suggesting that the true inducer molecule is phenylacetyl-coenzyme A (PA-CoA). Furthermore, after P. putida U is cultured in the same medium containing other carbon sources (glucose or octanoic, benzoic, or 4-hydroxyphenylacetic acid) in the place of PA, the PATS and PA-CoA are not detected; neither the PATS nor PA-CoA is found in cases in which mutants (PA- and PCL-) lacking the enzyme which catalyzed the initial step of the PA degradation (phenylacetyl-CoA ligase) are used. PA-CoA has been extracted from bacteria and identified as a true PA catabolite by high-performance liquid chromatography and also enzymatically with pure acyl-CoA:6-aminopenicillanic acid acyltransferase from Penicillium chrysogenum.
在恶臭假单胞菌U在含有苯乙酸(PA)作为唯一碳源的化学限定培养基中培养后,对其苯乙酸转运系统(PATS)进行了研究。在30℃下于50mM磷酸盐缓冲液(pH 7.0)中进行体内动力学测量。在这些条件下,摄取速率至少3分钟呈线性,Km值为13μM。PATS是一种主动转运系统,最终浓度为1mM的2,4-二硝基苯酚、4-硝基苯酚(100%)、KCN(97%)、2-硝基苯酚(90%)或NaN3(80%)可强烈抑制该系统。葡萄糖或D-乳酸(各10mM)可使饥饿细胞中的PATS增加(140%),而砷酸盐(20mM)、NaF或N,N'-二环己基碳二亚胺(1mM)则无任何影响。此外,PATS对渗透压休克不敏感。这些数据强烈表明,PATS的能量仅来源于导致富含能量的膜状态的电子传递系统。含硫醇的化合物巯基乙醇、谷胱甘肽和二硫苏糖醇对PATS无显著影响,而诸如N-乙基马来酰亚胺和碘乙酸等硫醇修饰试剂则强烈抑制摄取(分别为100%和93%)。在环上(i)或乙酰基部分(ii)有取代的PA分子类似物,或那些含有不同环但乙酰基部分保持不变的类似物(iii),对摄取有不同程度的抑制。除己二酸能极大地刺激PA摄取速率(163%)外,所测试的化合物均未显著提高PA摄取速率。PATS由PA诱导,也可由脂肪族部分含有偶数个碳原子的一些苯基衍生物(4-苯基丁酸、6-苯基己酸和8-苯基辛酸)诱导产生。然而,具有奇数个碳原子的类似化合物(苯甲酸、3-苯基丙酸、5-苯基戊酸、7-苯基庚酸和9-苯基壬酸)以及许多其他PA衍生物不会诱导该系统,这表明真正的诱导分子是苯乙酰辅酶A(PA-CoA)。此外,在恶臭假单胞菌U在含有其他碳源(葡萄糖或辛酸、苯甲酸或4-羟基苯乙酸)而非PA的相同培养基中培养后,未检测到PATS和PA-CoA;在使用缺乏催化PA降解第一步的酶(苯乙酰辅酶A连接酶)的突变体(PA-和PCL-)的情况下,也未发现PATS和PA-CoA。已从细菌中提取出PA-CoA,并通过高效液相色谱以及用来自产黄青霉的纯酰基辅酶A:6-氨基青霉烷酸酰基转移酶进行酶促鉴定,确认为真正的PA分解代谢物。