Adhesive Properties of YapV and Paralogous Autotransporter Proteins of Yersinia pestis

Nair, Manoj Kumar Mohan; Masi, Leon De; Yue, Min; Galván, Estela M.; Chen, Huaiqing; Wang, Fang; Schifferli, Dieter M.

doi:10.1128/iai.00094-15

Cited by 16 publications

(16 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Type Va Yersinia autotransporters have been mainly investigated in the context of Y. pestis infection. YapE, YapJ, YapK, and YapV promote development of bubonic and/or pneumonic plague in mice [38-40], likely by enhancing adherence to epithelial cells. YapC can induce aggregation when expressed in E. coli but no effects on Y. pestis biofilms following deletion of this gene were observed [41].…”

Section: Discussionmentioning

confidence: 99%

A trimeric autotransporter enhances biofilm cohesiveness inYersinia pseudotuberculosisbut not inYersinia pestis

Calder

Christman

Hawkins

et al. 2020

Preprint

View full text Add to dashboard Cite

15Cohesion of biofilms made by Yersinia pestis and Yersinia pseudotuberculosis (Yptb) has been 16 attributed solely to an extracellular polysaccharide matrix encoded by the hms genes (Hms-17 ECM). However, mutations in the Yptb BarA/UvrY/CsrB regulatory cascade enhance biofilm 18 stability without dramatically increasing Hms-ECM production. We found that treatment with 19 proteinase K enzyme effectively destabilized Yptb csrB mutant biofilms, suggesting that cell-cell 20 interactions might be mediated by protein adhesins or extracellular matrix proteins. We 21 identified an uncharacterized trimeric autotransporter lipoprotein (YPTB2394), repressed by 22 csrB, which has been referred to as YadE. Biofilms made by a yadE mutant strain were 23 extremely sensitive to mechanical disruption. Overexpression of yadE in wild-type Yptb 24 increased biofilm cohesion, similar to biofilms made by csrB or uvrY mutants. We found that the 25 Rcs signaling cascade, which represses Hms-ECM production, activated expression of yadE. The 26 yadE gene appears to be functional in Yptb but is a pseudogene in modern Y. pestis strains. 27 Expression of functional yadE in Y. pestis KIM6+ altered the production of Hms-ECM and 28 weakened biofilms made by these bacteria. This suggests that although the YadE autotransporter 29 protein increases Yptb biofilm stability, it may be incompatible with Hms-ECM production that 30 is essential for Y. pestis biofilm production in fleas. Inactivation of yadE in Y. pestis may be 31 another instance of selective gene loss in the evolution of flea-borne transmission by this species. 32 33 3 IMPORTANCE 34The evolution of Yersinia pestis from its Y. pseudotuberculosis (Yptb) ancestor involved gene 35 acquisition and gene losses, leading to differences in biofilm production. Characterizing the 36 unique biofilm features of both species may provide better understanding of how each adapts to 37 its specific niches. This study identifies a trimeric autotransporter YadE that promotes biofilm 38 stability of Yptb but which has been inactivated in Y. pestis, likely because it is not compatible 39 with Hms polysaccharide that is crucial for biofilms inside fleas. We also reveal that the Rcs 40 signaling cascade, which represses Hms expression in Y. pestis, activates YadE in Yptb. The 41 ability of Yptb to use polysaccharide or YadE protein for cell-cell adhesion may help it produce 42 biofilms in different environments. 44Environmental persistence, host interaction, and transmission of Yersinia depend on 45 biofilms, which are tightly regulated by both transcriptional and post-transcriptional control 46 mechanisms [1, 2]. Arguably, the best studied Yersinia biofilms are those made by Y. pestis 47 while in the flea digestive tract that block the proventriculus and increase transmission to new 48 hosts during flea feeding. These biofilms require the HmsHFRS proteins to produce and export a 49 polysaccharide extracellular matrix of poly-ß-1,6-N-acetylglucosamine that is crucial in forming 50 and maintaining ba...

show abstract

Section: Discussionmentioning

confidence: 99%

A trimeric autotransporter enhances biofilm cohesiveness inYersinia pseudotuberculosisbut not inYersinia pestis

Calder

Christman

Hawkins

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…ген yapM, по-видимому, входит в состав оперона из четырех генов, продукты трех из них уча-ствуют во взаимодействии с гликанами, входящими в состав экстраклеточного матрикса [26]. кроме того, в клетках Y. pestis в виде псевдогена присутствует ген yapX, который функционально активен у возбу-дителя пседотуберкулеза [38].…”

Section: Issueunclassified

“…аутотранспортный белок YapC является типичным ат-белком типа Va. он присутствует в штаммах KIM и CO92 и обладает высоким сходством с белками Yapа и YapL [38,49]. клонированный в штамме E. coli белок YapC имел размер 65 кд и ло-кализовался на поверхности бактериальной клетки [49].…”

Section: Issueunclassified

“…при из-учении адгезивных свойств этих белков показано, что клетки E. coli, экспрессирующие белки YapV и YapK, эффективно связывались с альвеолярными (линия а549) и эпителиальными (линия W126VA4) клетками, а также компонентами экстраклеточного матрикса, что позволило предположить участие этих ат-белков в развитии легочной чумы и обеспечении контакта бактерий с эпителиальными клетками ре-спираторного тракта [38]. YapG не имеет значения для вирулентности ни при бубонной, ни при легоч-ной видах чумы, его функцию еще предстоит рас-шифровать [23].…”

Section: Issueunclassified

“…в то же время, все штаммы возбуди-теля чумы, в отличие от Y. pseudotuberculosis, несут ген yapJ [38].…”

Section: Issueunclassified

See 2 more Smart Citations

Adhesines of the Plague Agent

Куклева¹

2018

Problemy Osobo Opasnykh Infektsii

View full text Add to dashboard Cite

удк 616.98:579.842.23 л.м.куклева адгеЗинЫ воЗБудителя чумЫ ФКУЗ «Российский научно-исследовательский противочумный институт «Микроб», Саратов, Российская Федерация возбудитель чумы обладает комплексом адгезинов, обеспечивающих прикрепление возбудителя к клеткам-мишеням в организме хозяина и во многом определяющих начало, характер и течение болезни. наличие адгези-нов обеспечивает транслокацию эффекторных белков в клетки-мишени млекопитающих. в обзоре представлены литературные данные как о наиболее изученных адгезинах Yersinia pestis (белках Ail и pH6 антиген), так и о недавно выявленных аутотранспортных белках различных классов, участвующих в процессах адгезии (YadBC, Yaps, Ilp). описано их значение для патогенеза чумы, генетическая детерминированность, структура и локализа-ция в клетке. отмечено, что адгезины возбудителя чумы действуют на разных стадиях инфекционного процесса, выполняют множественные функции, участвуют не только в процессах прикрепления к клеткам хозяина, но так-же обеспечивают устойчивость к действию иммунных механизмов хозяина.Ключевые слова: возбудитель чумы, адгезины, патогенность.

show abstract

Alternative lifestyles: A plague persistence hypothesis

Wimsatt,

Eads,

Matchett

et al. 2023

Ecosphere

View full text Add to dashboard Cite

Several explanations have been posited for how the plague bacterium (Yersinia pestis) reemerges during sylvatic cycles within the same foci over many years, and often without direct evidence of host die‐offs. One prevalent view is that transmission‐optimized Y. pestis bacteria, exhibiting epizootic/enzootic behavior, almost continually replicate and survive through repeated, linked, host‐centered propagation events. These bacteria, we will refer to as “r‐pestis” type ecotype(s), represent a limited number of phenotypic lineages exhibiting optimal transmissibility and high rates of reproduction. These attributes, it is thought, assure their durability through time. For continuous r‐pestis type expansions to be successful, adequate numbers of fleas and hosts must become infected to produce massive numbers of bacteria. In the process, host and flea numbers decline as they succumb to plague. Here we hypothesize that r‐pestis population expansions seed the environment and confront a unique, highly competitive local milieu, where natural selection favors new ecotypes that incorporate a range of emergent adaptive survival strategies. These newly adapted survivors we recognize as a range of “K‐pestis” ecotypes with greater durability and lower reproduction rates. These emergent K‐pestis forms may arise in succession or coexist for varying periods of time with r‐pestis ecotypes, and with other K‐pestis ecotypes. Among K‐pestis ecotypes, we hypothesize that through adaptive radiations, some persist within flea life stages, soil, organic waste, amoebae, plants, carcasses, hosts, or within niches yet to be characterized. In some settings, after a long quiet period, when favorable, K‐pestis bacteria may trigger a singular event where an r‐pestis transmission stream emerges precipitating another enzootic/epizootic progression. If this hypothesis withstands rigorous testing, then Y. pestis might represent an even more formidable, enduring, and adaptable foe, where unforeseen local events could trigger new epidemic and epizootic/enzootic events threatening humans and populations of other mammals, including those of conservation concern.

show abstract

Adhesive Properties of YapV and Paralogous Autotransporter Proteins of Yersinia pestis

Cited by 16 publications

References 59 publications

A trimeric autotransporter enhances biofilm cohesiveness inYersinia pseudotuberculosisbut not inYersinia pestis

A trimeric autotransporter enhances biofilm cohesiveness inYersinia pseudotuberculosisbut not inYersinia pestis

Adhesines of the Plague Agent

Alternative lifestyles: A plague persistence hypothesis

Contact Info

Product

Resources

About