Difference between revisions of "De Lira 2018 Sci Rep"
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|abstract=To cope with toxic levels of H<sub>2</sub>S, the plant pathogens ''Xylella fastidiosa'' and ''Agrobacterium tumefaciens'' employ the bigR operon to oxidize H<sub>2</sub>S into sulfite. The ''bigR'' operon is regulated by the transcriptional repressor ''BigR'' and it encodes a bifunctional sulfur transferase (ST) and sulfur dioxygenase (SDO) enzyme, ''Blh'', required for H<sub>2</sub>S oxidation and bacterial growth under hypoxia. However, how ''Blh'' operates to enhance bacterial survival under hypoxia and how ''BigR'' is deactivated to derepress operon transcription is unknown. Here, we show that the ST and SDO activities of Blh are ''in vitro'' coupled and necessary to oxidize sulfide into sulfite, and that ''Blh'' is critical to maintain the oxygen flux during ''A. tumefaciens'' respiration when oxygen becomes limited to cells. We also show that H<sub>2</sub>S and polysulfides inactivate BigR leading to operon transcription. Moreover, we show that sulfite, which is produced by ''Blh'' in the ST and SDO reactions, is toxic to ''Citrus sinensis'' and that ''X. fastidiosa''-infected plants accumulate sulfite and higher transcript levels of sulfite detoxification enzymes, suggesting that they are under sulfite stress. These results indicate that ''BigR'' acts as a sulfide sensor in the H<sub>2</sub>S oxidation mechanism that allows pathogens to colonize plant tissues where oxygen is a limiting factor. | |abstract=To cope with toxic levels of H<sub>2</sub>S, the plant pathogens ''Xylella fastidiosa'' and ''Agrobacterium tumefaciens'' employ the bigR operon to oxidize H<sub>2</sub>S into sulfite. The ''bigR'' operon is regulated by the transcriptional repressor ''BigR'' and it encodes a bifunctional sulfur transferase (ST) and sulfur dioxygenase (SDO) enzyme, ''Blh'', required for H<sub>2</sub>S oxidation and bacterial growth under hypoxia. However, how ''Blh'' operates to enhance bacterial survival under hypoxia and how ''BigR'' is deactivated to derepress operon transcription is unknown. Here, we show that the ST and SDO activities of Blh are ''in vitro'' coupled and necessary to oxidize sulfide into sulfite, and that ''Blh'' is critical to maintain the oxygen flux during ''A. tumefaciens'' respiration when oxygen becomes limited to cells. We also show that H<sub>2</sub>S and polysulfides inactivate BigR leading to operon transcription. Moreover, we show that sulfite, which is produced by ''Blh'' in the ST and SDO reactions, is toxic to ''Citrus sinensis'' and that ''X. fastidiosa''-infected plants accumulate sulfite and higher transcript levels of sulfite detoxification enzymes, suggesting that they are under sulfite stress. These results indicate that ''BigR'' acts as a sulfide sensor in the H<sub>2</sub>S oxidation mechanism that allows pathogens to colonize plant tissues where oxygen is a limiting factor. | ||
|editor=[[Kandolf G]], | |editor=[[Kandolf G]], | ||
|mipnetlab=BR Campinas Vercesi AE | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
Latest revision as of 11:37, 13 April 2018
| de Lira NPV, Pauletti BA, Marques AC, Perez CA, Caserta R, de Souza AA, Vercesi AE, Paes Leme AF, Benedetti CE (2018) BigR is a sulfide sensor that regulates a sulfur transferase/dioxygenase required for aerobic respiration of plant bacteria under sulfide stress. Sci Rep 8:3508. |
de Lira NPV, Pauletti BA, Marques AC, Perez CA, Caserta R, de Souza AA, Vercesi AE, Paes Leme AF, Benedetti CE (2018) Sci Rep
Abstract: To cope with toxic levels of H2S, the plant pathogens Xylella fastidiosa and Agrobacterium tumefaciens employ the bigR operon to oxidize H2S into sulfite. The bigR operon is regulated by the transcriptional repressor BigR and it encodes a bifunctional sulfur transferase (ST) and sulfur dioxygenase (SDO) enzyme, Blh, required for H2S oxidation and bacterial growth under hypoxia. However, how Blh operates to enhance bacterial survival under hypoxia and how BigR is deactivated to derepress operon transcription is unknown. Here, we show that the ST and SDO activities of Blh are in vitro coupled and necessary to oxidize sulfide into sulfite, and that Blh is critical to maintain the oxygen flux during A. tumefaciens respiration when oxygen becomes limited to cells. We also show that H2S and polysulfides inactivate BigR leading to operon transcription. Moreover, we show that sulfite, which is produced by Blh in the ST and SDO reactions, is toxic to Citrus sinensis and that X. fastidiosa-infected plants accumulate sulfite and higher transcript levels of sulfite detoxification enzymes, suggesting that they are under sulfite stress. These results indicate that BigR acts as a sulfide sensor in the H2S oxidation mechanism that allows pathogens to colonize plant tissues where oxygen is a limiting factor.
• Bioblast editor: Kandolf G • O2k-Network Lab: BR Campinas Vercesi AE
Labels: MiParea: Respiration
Organism: Eubacteria
Preparation: Intact cells
HRR: Oxygraph-2k
Labels, 2018-04
