Lack of mycothiol and ergothioneine induces different protective mechanisms in Mycobacterium smegmatis.

Lack of mycothiol and ergothioneine induces different protective mechanisms in Mycobacterium smegmatis.
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DOI:
10.1016/j.bbrep.2016.08.006
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发表时间:
2016-12
影响因子:
2.7
通讯作者:
Rawat M
Rawat M
中科院分区:
其他
文献类型:
--
作者:
Singh AR;Strankman A;Orkusyan R;Purwantini E;Rawat M

文献摘要

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耻垢分枝杆菌含有低分子量的硫醇,真菌硫醇(MSH)和麦角硫因(ESH)。分别参与MSH和ESH生物合成的mshC和egtA中被破坏的转座子突变体的检查表明,这两种突变体对氧化、烷基化和金属胁迫敏感。然而,mshC突变体比野生型表现出显着更多的蛋白质羰基化和脂质过氧化,而egtA突变体比野生型表现出更少的蛋白质和脂质损伤。我们进一步表明,Ohr,KatN,和AhpC,参与保护氧化应激,上调egtA突变体。在mshC突变体中,Usp和推定的巯基过氧化物酶上调。此外,与野生型相比,缺乏MSH的突变体还含有更高水平的辅酶F420,并且发现两种辅酶F420依赖性酶被上调。这些结果表明,缺乏MSH和ESH导致诱导不同的机制,以保护免受氧化应激。MSH和ESH参与耻垢分枝杆菌对金属胁迫的保护。MSH突变体具有更大的大分子损伤,而ESH突变体具有比野生型更小的损伤。与保护免受氧化应激相关的不同蛋白质在mshC和egtA突变体中上调。
Mycobacterium smegmatis contains the low molecular weight thiols, mycothiol (MSH) and ergothioneine (ESH). Examination of transposon mutants disrupted in mshC and egtA, involved in the biosynthesis of MSH and ESH respectively, demonstrated that both mutants were sensitive to oxidative, alkylating, and metal stress. However, the mshC mutant exhibited significantly more protein carbonylation and lipid peroxidation than wildtype, while the egtA mutant had less protein and lipid damage than wildtype. We further show that Ohr, KatN, and AhpC, involved in protection against oxidative stress, are upregulated in the egtA mutant. In the mshC mutant, an Usp and a putative thiol peroxidase are upregulated. In addition, mutants lacking MSH also contained higher levels of Coenzyme F420 as compared to wildtype and two Coenzyme F420 dependent enzymes were found to be upregulated. These results indicate that lack of MSH and ESH result in induction of different mechanisms for protecting against oxidative stress. MSH and ESH are involved in protection against metal stress in Mycobacterium smegmatis. MSH mutants have greater macromolecular damage while ESH mutants have lesser damage than wildtype. Different proteins associated with protection against oxidative stress are upregulated in mshC and egtA mutants.