Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Jan 22;10:953. doi: 10.1038/s41598-020-57587-6

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

The sir cytochrome maturation genes are not involved in maturation of the NrfA nitrite reductase. (a) Nitrite reduction was not significantly decreased in any of the sir mutants, however the ΔsirEF mutants reduced nitrite faster than the wildtype. As anticipated, ΔccmI was unable to reduce nitrite and reduction was restored by complementation. Enzymatic activity of the nitrate reductase was not affected in any of the sir mutants. There was no nitrite reductase activity in the cell lysates of ΔnrfA or ΔccmI. (b) ΔsirH, ΔsirEF and ΔsirG were all able to grow on DMSO or TMAO similar to wildtype. The ΔccmI mutant exhibited a lag in growth with either DMSO or TMAO, which was restored by complementation. Full-length gel is presented in Supplementary Fig. S4.