Pathways for the utilization of N-acetyl-galactosamine and galactosamine in Escherichia coli
Pathways for the utilization of N-acetyl-galactosamine and galactosamine in Escherichia coli
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DOI：
10.1046/j.1365-2958.2000.01969.x
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发表时间：
2000-07-01
影响因子：
3.6
通讯作者：
Lengeler, JW
中科院分区：
文献类型：
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作者：
Brinkkötter, A;Klöss, H;Lengeler, JW
在肠道细菌中，在 N-乙酰半乳糖胺（GalNAc 或 Aga）和 d-半乳糖胺（GalN 或 Gam）上生长的能力不同。因此，大肠杆菌的菌株B、C和EC3132是Aga(+) Gam(+)，而大肠杆菌K-12是Aga(-) Gam(-)，类似于肺炎克雷伯菌KAY2026、产酸克雷伯菌M5a1和鼠伤寒沙门氏菌LT2。以前的菌株在其基因图谱的 70.5 分钟处携带完整的 aga/kba 基因簇。这些基因编码 Aga 特异性磷酸转移酶系统 (PTS) 或 IIAga (agaVWE) 和 GalN 特异性 PTS 或 IIGam (agaBCD)。两种 PTS 均属于甘露糖-山梨糖家族，即 IIB、IIC 和 IID 结构域由不同基因编码，并且它们共享 IIA 结构域 (agaF)。此外，这些基因编码Aga6P-脱乙酰酶(agaA)、GalN6P脱氨酶(agaI)、包含两种不同肽的塔格糖二磷酸醛缩酶(kbaYZ)和推定的异构酶(agaS)，即两种氨基糖的转运和降解的完整途径。这些基因由两个相邻的操纵子（kbaZagaVWEFA 和 agaS kbaYagaBCDI）组成，并由阻遏物 AgaR 控制。其基因agaR位于kbaZ上游，AgaR对培养基中的GalNAc和GalN作出反应。然而，所有 Aga(-) Gam(-) 菌株均携带覆盖基因 agaW' EF 'A 的缺失；因此，它们缺乏活性 IIAga 和 IIGam PTS，从而解释了它们无法依靠这两种氨基糖生长。在各种 Aga(-) Gam(-) 肠道细菌中，删除的 DNA 两侧都有推定重组位点的残余物。具有 Aga(+) Gam(-) 表型的衍生物可以从大肠杆菌 K-12 中分离出来。它们保留了 Delta agaW'EF'A 缺失，并分别在半乳糖醇和 N-乙酰氨基葡萄糖代谢的 gat 和 nag 基因中携带抑制突变，从而允许在 Aga 上生长，但不能在 GalN 上生长。
Among enteric bacteria, the ability to grow on N-acetyl-galactosamine (GalNAc or Aga) and on d-galactosamine (GalN or Gam) differs. Thus, strains B, C and EC3132 of Escherichia coli are Aga(+) Gam(+) whereas E. coli K-12 is Aga(-) Gam(-), similarly to Klebsiella pneumoniae KAY2026, Klebsiella oxytoca M5a1 and Salmonella typhimurium LT2. The former strains carry a complete aga/kba gene cluster at 70.5 min of their gene map. These genes encode an Aga-specific phosphotransferase system (PTS) or IIAga (agaVWE) and a GalN-specific PTS or IIGam (agaBCD). Both PTSs belong to the mannose-sorbose family, i.e. the IIB, IIC and IID domains are encoded by different genes, and they share a IIA domain (agaF). Furthermore, the genes encode an Aga6P-deacetylase (agaA), a GalN6P deaminase (agaI), a tagatose-bisphosphate aldolase comprising two different peptides (kbaYZ) and a putative isomerase (agaS), i.e. complete pathways for the transport and degradation of both amino sugars. The genes are organized in two adjacent operons (kbaZagaVWEFA and agaS kbaYagaBCDI) and controlled by a repressor AgaR. Its gene agaR is located upstream of kbaZ, and AgaR responds to GalNAc and GalN in the medium. All Aga(-) Gam(-) strains, however, carry a deletion covering genes agaW' EF 'A; consequently they lack active IIAga and IIGam PTSs, thus explaining their inability to grow on the two amino sugars. Remnants of a putative recombination site flank the deleted DNA in the various Aga(-) Gam(-) enteric bacteria. Derivatives with an Aga(+) Gam(-) phenotype can be isolated from E. coli K-12. These retain the Delta agaW' EF 'A deletion and carry suppressor mutations in the gat and nag genes for galactitol and N-acetyl-glucosamine metabolism, respectively, that allow growth on Aga but not on GalN.