Genetics of Capsular Polysaccharides and Cell Envelope (Glyco)lipids

Daffé, Mamadou; Crick, Dean C.; Jackson, Mary

doi:10.1128/9781555818845.ch28

Cited by 19 publications

(35 citation statements)

References 346 publications

(328 reference statements)

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“…Our findings are consistent with the in vivo evidence that SL-1 is not a classic virulence factor that enhances Mtb survival. Based on our cell culture and in vivo data, and the observation that only pathogenic mycobacteria produce SL-1 (this report and reviewed in Daffe et al, 2014;Minnikin et al, 2002), we uncover a heretofore unrecognized function of SL-1 in nociceptive neuron activation and cough induction. Because cough is a major mechanism of Mtb transmission, we propose (legend continued on next page)…”

Section: Discussionmentioning

confidence: 69%

Mycobacterium tuberculosis Sulfolipid-1 Activates Nociceptive Neurons and Induces Cough

Ruhl

Pasko

Khan

et al. 2020

Cell

109

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publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. Article Mycobacterium tuberculosis Sulfolipid-1 Activates Nociceptive Neurons and Induces Cough Graphical Abstract Highlights d An Mtb organic extract activates nociceptive neurons and induces cough in guinea pigs d Mtb sulfolipid-1 is necessary and sufficient to trigger neuronal activation and cough d Guinea pigs infected with an SL-1-deficient Mtb mutant do not coughMycobacterium tuberculosis produces a glycolipid called sulfolipid-1 (SL-1) that triggers cough by activating nociceptive neurons.

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Section: Discussionmentioning

confidence: 69%

Mycobacterium tuberculosis Sulfolipid-1 Activates Nociceptive Neurons and Induces Cough

Ruhl

Pasko

Khan

et al. 2020

Cell

109

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“…Disruption of pca and pckA lead to severe in vitro and intracellular growth defects and pckA was shown to be essential for virulence in M. bovis (73, 74). Indeed, oxaloacetate, also generated from pyruvate via the activity of Pyruvate carboxylase ( pca ), feeds into the Methylcitrate cycle (75, 76). Therefore, the mutations we identified in these key Central Carbon Metabolic genes (Table 1) could disrupt energy metabolism and growth in the respective lineages they occur in.…”

Section: Resultsmentioning

confidence: 99%

Comparative Genomics Shows Differences in the Electron Transport and Carbon Metabolic Pathways ofMycobacterium africanumrelative toMycobacterium tuberculosisand suggests an adaptation to low oxygen tension

Ofori-Anyinam

Riley

Jobarteh

et al. 2019

Preprint

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Pathways of Mycobacterium africanum relative to Mycobacterium tuberculosis and suggests an 3 adaptation to low oxygen tension 4 5 Summary: 27 The geographically restricted M. africanum lineages (MAF) are primarily found in West Africa, where 28 they account for a significant proportion of tuberculosis. Despite this phenomenon, little is known 29 about the co-evolution of these ancient lineages with West Africans. MAF and M. tuberculosis sensu 30 stricto lineages (MTB) differ in their clinical, in vitro and in vivo characteristics for reasons not fully 31 understood. Therefore, we compared genomes of 289 MAF and 205 MTB clinical isolates from the 32 6 main human-adapted M. tuberculosis complex lineages, for mutations in their Electron Transport 33 Chain and Central Carbon Metabolic pathway in an attempt to explain these metabolic differences. 34 Furthermore, we determined, in silico, whether each mutation could affect the function of genes 35 encoding enzymes in these pathways. 36 We found more potentially deleterious mutations in these pathways in MAF lineages compared to 37 MTB lineages. Additionally, we found that convergent evolution in these pathways occurred 38 between MAF and some MTB lineages. 39 Generally, our findings show further differences between MAF and MTB lineages that may have 40 contributed to the MAF clinical-and growth phenotype and may indicate potential adaptation of 41 MAF lineages to a distinct ecological niche, that we suggest may include areas characterized by low 42 oxygen tension. 43 44 Running title: The M. africanum respiratory chain and carbon metabolic pathway 45 46 Transport, Carbon Metabolism 48 49 50 51 3 1 Introduction 52 The Mycobacterium tuberculosis complex (MTBC) consists of a group of human-adapted ecotypes-53 Mycobacterium tuberculosis sensu stricto, Mycobacterium africanum, Mycobacterium canetti and 54 animal-adapted ecotypes (1-4). There are seven known MTBC lineages (L) associated with particular 55 geographic regions and adapted to specific human populations. These are the five lineages that 56 make up M. tuberculosis sensu stricto (lineages 1-4 and lineage 7) and the two M. africanum lineages 57 (lineages 5 and 6). Africa uniquely has a representation of all seven lineages. 58 MTBC strains from the seven lineages differ on average by about 1200 single nucleotide 59 polymorphisms (5), with clear distinction between MAF and MTB lineages (6-8). 60 MTB Lineages 2 and 4 are more widespread geographically, more pathogenic and more 61 transmissible, while MAF Lineages are exclusively found in West Africa and less transmissible (5, 9, 62 10). Clinically, MTB L4 is relatively more virulent than MAF L6 as evidenced by significantly faster 63 progression, in contacts of infectious cases, to active disease (11). MAF lineages are associated with 64 extrapulmonary disease and MAF L6 more commonly causes disease in immunocompromised 65 persons and those with lower Body Mass Index, implying a more opportunistic pathogen (10, 12). 66 Furthermore, MAF L5 a...

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“…A further increase in detection of surface-exposed EspC was achieved by treatment with 10 fold-dilutions of the previously used Genapol X-080 solution (0.025%), which partially removed the capsule but left the association of EspC filaments with the cell envelope intact. The finding that EspC was present in the capsule of M. tuberculosis only when cultured without Tween-80, in combination with the fact that detection of EspC was improved by treatment with GenapolX-080 highlights the fact that the mycobacterial capsule consists of not one homogenous, but multiple layers of protein-, sugar-and/or lipidcontaining moieties (Sani et al, 2010;Daffe et al, 2014;Ates et al, 2016b).…”

Section: Featured Opinionmentioning

confidence: 99%

Discovery of the type VII ESX‐1 secretion needle?

Ates

Brosch

2016

Molecular Microbiology

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Summary Mycobacterium tuberculosis, the etiological agent of human tuberculosis, harbours five ESAT‐6/type VII secretion (ESX/T7S) systems. The first esx gene clusters were identified during the genome‐sequencing project of M. tuberculosis H37Rv. Follow‐up studies revealed additional genes playing important roles in ESX/T7S systems. Among the latter genes, one can find those that encode Pro‐Glu (PE) and Pro‐Pro‐Glu (PPE) proteins as well as a gene cluster that is encoded >260 kb upstream of the esx‐1 locus and encodes ESX‐1 secretion‐associated proteins EspA (Rv3616c), EspC (Rv3615c) and EspD (Rv3614c). The espACD cluster has been suggested to have an important function in ESX‐1 secretion since EspA‐EspC and EsxA–EsxB are mutually co‐dependent on each other for secretion. However, the molecular mechanism of this co‐dependence and interaction between the substrates remained unknown. In this issue of Molecular Microbiology, Lou and colleagues show that EspC forms high‐molecular weight polymerization complexes that resemble selected components of type II, III and/or IV secretion systems of Gram‐negative bacteria. Indeed, EspC‐multimeric complexes form filamentous structures that could well represent a secretion needle of ESX‐1 type VII secretion systems. This exciting observation opens new avenues for research to discover and characterize ESX/T7S components and elucidates the co‐dependence of EsxA/B secretion with EspA/C.

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Genetics of Capsular Polysaccharides and Cell Envelope (Glyco)lipids

Cited by 19 publications

References 346 publications

Mycobacterium tuberculosis Sulfolipid-1 Activates Nociceptive Neurons and Induces Cough

Mycobacterium tuberculosis Sulfolipid-1 Activates Nociceptive Neurons and Induces Cough

Comparative Genomics Shows Differences in the Electron Transport and Carbon Metabolic Pathways ofMycobacterium africanumrelative toMycobacterium tuberculosisand suggests an adaptation to low oxygen tension

Discovery of the type VII ESX‐1 secretion needle?

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