Mycobacterium tuberculosis expresses methionine sulphoxide reductases A and B that protect from killing by nitrite and hypochlorite.
Mycobacterium tuberculosis expresses methionine sulphoxide reductases A and B that protect from killing by nitrite and hypochlorite.
复制标题
DOI:
10.1111/j.1365-2958.2008.06548.x
复制
发表时间:
2009-02
影响因子:
3.6
通讯作者:
Nathan C
中科院分区:
文献类型:
--
作者:
Lee WL;Gold B;Darby C;Brot N;Jiang X;de Carvalho LP;Wellner D;St John G;Jacobs WR Jr;Nathan C
Methionine sulfoxide reductases (Msr’s) reduce methionine sulfoxide to methionine and protect bacteria against reactive oxygen intermediates (ROI) and reactive nitrogen intermediates (RNI). Many organisms express both MsrA, active against methionine-(S)-sulfoxide, and MsrB, active against methionine-(R)-sulfoxide. Mycobacterium tuberculosis (Mtb) expresses MsrA, which protects ΔmsrA-E. coli from ROI and RNI. However, the function of MsrA in Mtb has not been defined, and it is unknown whether Mtb expresses MsrB. We identified MsrB as the protein encoded by Rv2674 in Mtb and confirmed the distinct stereospecificities of recombinant Mtb MsrA and MsrB. We generated strains of Mtb deficient in MsrA, MsrB or both and complemented the mutants. Lysates of singly deficient strains displayed half as much Msr activity as wild type against N-acetyl methionine sulfoxide. However, in contrast to other bacteria, single mutants were no more vulnerable than wild type to killing by ROI/RNI. Only Mtb lacking both MsrA and MsrB was more readily killed by nitrite or hypochlorite. Thus, MsrA and MsrB contribute to the enzymatic defenses of Mtb against ROI and RNI.
登录
查看更多内容
影响因子:
56.9
作者:
Darwin, KH;Ehrt, S;Nathan, CF
通讯作者:
Nathan, CF
影响因子:
82.9
作者:
Gandotra, Sheetal;Schnappinger, Dirk;Ehrt, Sabine
通讯作者:
Ehrt, Sabine
DOI:
10.1073/pnas.0406133102
发表时间:
2005-01-11
影响因子:
11.1
作者:
Rhee, KY;Erdjument-Bromage, H;Nathan, CF
通讯作者:
Nathan, CF
DOI:
10.1164/rccm.2201023
发表时间:
2002-07-15
影响因子:
24.7
作者:
Choi, HS;Rai, PR;Chan, ED
通讯作者:
Chan, ED
影响因子:
2.8
作者:
Bardarov, S;Bardarov, S;Jacobs, WR
通讯作者:
Jacobs, WR