Role of <scp>HemF</scp> and <scp>HemN</scp> in the heme biosynthesis of <scp><i>V</i></scp><i>ibrio vulnificus</i> under <scp>S</scp>‐adenosylmethionine‐limiting conditions

Kim, Eui-Jin; Oh, Eun Kyoung; Lee, Chang Kyu

doi:10.1111/mmi.12951

Cited by 8 publications

(9 citation statements)

References 57 publications

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“…Some trypanosomatids ( Trypanosoma and Kentomonas ), have lost the heme biosynthetic pathway completely, while others retained genes encoding the last three enzymes (Leishmaniinae, Angomonas and Strigomonas ), or only ferrochelatase ( Phytomonas and Herpetomonas ) [97–101]. Protoporphyrin IX, a substrate of FeCH, is synthesized by a subsequent action of coproporphyrinogen oxidase and protoporphyrinogen oxidase [102]. Both enzymes were readily identifiable in the genomes of L. ( Mundinia ) spp., except for L .…”

Section: Resultsmentioning

confidence: 99%

Comparative genomics of Leishmania (Mundinia)

et al. 2019

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Background Trypanosomatids of the genus Leishmania are parasites of mammals or reptiles transmitted by bloodsucking dipterans. Many species of these flagellates cause important human diseases with clinical symptoms ranging from skin sores to life-threatening damage of visceral organs. The genus Leishmania contains four subgenera: Leishmania, Sauroleishmania, Viannia, and Mundinia. The last subgenus has been established recently and remains understudied, although Mundinia contains human-infecting species. In addition, it is interesting from the evolutionary viewpoint, representing the earliest branch within the genus and possibly with a different type of vector. Here we analyzed the genomes of L. (M.) martiniquensis, L. (M.) enriettii and L. (M.) macropodum to better understand the biology and evolution of these parasites. Results All three genomes analyzed were approximately of the same size (~ 30 Mb) and similar to that of L. (Sauroleishmania) tarentolae, but smaller than those of the members of subgenera Leishmania and Viannia, or the genus Endotrypanum (~ 32 Mb). This difference was explained by domination of gene losses over gains and contractions over expansions at the Mundinia node, although only a few of these genes could be identified. The analysis predicts significant changes in the Mundinia cell surface architecture, with the most important ones relating to losses of LPG-modifying side chain galactosyltransferases and arabinosyltransferases, as well as β-amastins. Among other important changes were gene family contractions for the oxygen-sensing adenylate cyclases and FYVE zinc finger-containing proteins. Conclusions We suggest that adaptation of Mundinia to different vectors and hosts has led to alternative host-parasite relationships and, thereby, made some proteins redundant. Thus, the evolution of genomes in the genus Leishmania and, in particular, in the subgenus Mundinia was mainly shaped by host (or vector) switches.

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Section: Resultsmentioning

confidence: 99%

Comparative genomics of Leishmania (Mundinia)

et al. 2019

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“…Many respiratory enzymes require heme as a cofactor and we identified two oxygen-independent coproporphyrinogen III oxidase paralogs (HemN; BPSL2366 and BPSL2646) as part of the RegAB modulon [ 72 – 74 ]. Although at the transcriptional level BPSL2646 showed the stronger induction, a growth defect in anaerobic conditions was only observed for BPSL2366 (Tn 5 insertion, see S3 Table ).…”

Section: Discussionmentioning

confidence: 99%

RegAB Homolog of Burkholderia pseudomallei is the Master Regulator of Redox Control and involved in Virulence

et al. 2021

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Burkholderia pseudomallei, the etiological agent of melioidosis in humans and animals, often occupies environmental niches and infection sites characterized by limited concentrations of oxygen. Versatile genomic features enable this pathogen to maintain its physiology and virulence under hypoxia, but the crucial regulatory networks employed to switch from oxygen dependent respiration to alternative terminal electron acceptors (TEA) like nitrate, remains poorly understood. Here, we combined a Tn5 transposon mutagenesis screen and an anaerobic growth screen to identify a two-component signal transduction system with homology to RegAB. We show that RegAB is not only essential for anaerobic growth, but also for full virulence in cell lines and a mouse infection model. Further investigations of the RegAB regulon, using a global transcriptomic approach, identified 20 additional regulators under transcriptional control of RegAB, indicating a superordinate role of RegAB in the B. pseudomallei anaerobiosis regulatory network. Of the 20 identified regulators, NarX/L and a FNR homolog were selected for further analyses and a role in adaptation to anaerobic conditions was demonstrated. Growth experiments identified nitrate and intermediates of the denitrification process as the likely signal activateing RegAB, NarX/L, and probably of the downstream regulators Dnr or NsrR homologs. While deletions of individual genes involved in the denitrification process demonstrated their important role in anaerobic fitness, they showed no effect on virulence. This further highlights the central role of RegAB as the master regulator of anaerobic metabolism in B. pseudomallei and that the complete RegAB-mediated response is required to achieve full virulence. In summary, our analysis of the RegAB-dependent modulon and its interconnected regulons revealed a key role for RegAB of B. pseudomallei in the coordination of the response to hypoxic conditions and virulence, in the environment and the host.

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“…A number of marine organisms, included members of the genus Vibrio, are often transformed through conjugation, and resistant strains are commonly used to optimize post-conjugation selection [34]. In V. vulnificus specifically, spontaneous rifampicin-resistant strains have been widely used in the past for transformation and mutagenesis protocols [35,36], with poor consideration of the possible effects of the resistance mutation on the phenotype of the studied strains.…”

Section: Introductionmentioning

confidence: 99%

“…In V. vulnificus specifically, spontaneous rifampicin-resistant strains have been widely used in the past for transformation and mutagenesis protocols [35, 36], with poor consideration of the possible effects of the resistance mutation on the phenotype of the studied strains.…”

Section: Introductionmentioning

confidence: 99%

rpoB mutations conferring rifampicin-resistance affect growth, stress response and motility in Vibrio vulnificus

et al. 2020

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Rifampicin is a broad-spectrum antibiotic that binds to the bacterial RNA polymerase (RNAP), compromising DNA transcription. Rifampicin resistance is common in several microorganisms and it is typically caused by point mutations in the gene encoding the β subunit of RNA polymerase, rpoB. Different rpoB mutations are responsible for various levels of rifampicin resistance and for a range of secondary effects. rpoB mutations conferring rifampicin resistance have been shown to be responsible for severe effects on transcription, cell fitness, bacterial stress response and virulence. Such effects have never been investigated in the marine pathogen Vibrio vulnificus , even though rifampicin-resistant strains of V. vulnificus have been isolated previously. Moreover, spontaneous rifampicin-resistant strains of V. vulnificus have an important role in conjugation and mutagenesis protocols, with poor consideration of the effects of rpoB mutations. In this work, effects on growth, stress response and virulence of V. vulnificus were investigated using a set of nine spontaneous rifampicin-resistant derivatives of V. vulnificus CMCP6. Three different mutations (Q513K, S522L and H526Y) were identified with varying incidence rates. These three mutant types each showed high resistance to rifampicin [minimal inhibitory concentration (MIC) >800 µg ml−1], but different secondary effects. The strains carrying the mutation H526Y had a growth advantage in rich medium but had severely reduced salt stress tolerance in the presence of high NaCl concentrations as well as a significant reduction in ethanol stress resistance. Strains possessing the S522L mutation had reduced growth rate and overall biomass accumulation in rich medium. Furthermore, investigation of virulence characteristics demonstrated that all the rifampicin-resistant strains showed compromised motility when compared with the wild-type, but no major effects on exoenzyme production were observed. These findings reveal a wide range of secondary effects of rpoB mutations and indicate that rifampicin resistance is not an appropriate selectable marker for studies that aim to investigate phenotypic behaviour in this organism.

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Role of HemF and HemN in the heme biosynthesis of Vibrio vulnificus under S‐adenosylmethionine‐limiting conditions

Cited by 8 publications

References 57 publications

Comparative genomics of Leishmania (Mundinia)

Comparative genomics of Leishmania (Mundinia)

RegAB Homolog of Burkholderia pseudomallei is the Master Regulator of Redox Control and involved in Virulence

rpoB mutations conferring rifampicin-resistance affect growth, stress response and motility in Vibrio vulnificus

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