The New Role of СysB Transcription Factor in Cysteine Degradation and Production of Hydrogen Sulfide in E. coli


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Resumo

The paradoxical effect of deletion of the Escherichia coli genes cysK and cysM encoding cysteine synthase enzymes has been studied: such cysteine auxotrophs actively degrade the excess of cysteine transported from the medium to form H2S. We have shown that deletions of any of the known genes controlling the degradation of exogenous cysteine, including the genes aspC, mstA, cysK, cysM, tnaA, metC, and malY, as well as the newly discovered genes yciW, cyuA, cyuP, and cyuR, do not deprive the cysteine auxotrophs ΔcysK ΔcysM of the ability to degrade cysteine. Cysteine degradation in the ΔcysK ΔcysM mutant is positively regulated by the products of the cysB and cysE genes. It is significant that the ΔcysK ΔcysM mutant shows an increased transcription of the genes opposing the oxidative stress (sodA, catG, arcA, and cydD). We assume that oxidative stress in cells of the ΔcysK ΔcysM mutant is provoked by restriction of cysteine resynthesis, while cysB-dependent degradation of exogenous cysteine and generated H2S provide protection against oxidative stress.

Sobre autores

T. Seregina

Engelhardt Institute of Molecular Biology, Russian Academy of Sciences

Email: alexmir_98@yahoo.com
Rússia, Moscow, 119991

M. Nagornykh

Engelhardt Institute of Molecular Biology, Russian Academy of Sciences; Institute of Biochemistry and Physiology of Microorganisms,
Russian Academy of Sciences

Email: alexmir_98@yahoo.com
Rússia, Moscow, 119991; Pushchino, Moscow oblast, 142290

K. Lobanov

Engelhardt Institute of Molecular Biology, Russian Academy of Sciences

Email: alexmir_98@yahoo.com
Rússia, Moscow, 119991

R. Shakulov

State Research Institute of Genetics and Selection of Industrial Microorganisms

Email: alexmir_98@yahoo.com
Rússia, Moscow, 117545

A. Mironov

Engelhardt Institute of Molecular Biology, Russian Academy of Sciences

Autor responsável pela correspondência
Email: alexmir_98@yahoo.com
Rússia, Moscow, 119991


Declaração de direitos autorais © Pleiades Publishing, Inc., 2018

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