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Niveau: Secondaire, Collège, Sixième
  0           INTERACADEMIES SYMPOSIUM Académie des sciences, German National Academy of Sciences Leopoldina and The Royal Society on “The New Microbiology” May 14, 15 and 16, 2012 Institut de France 23 quai de Conti Paris 6e POSTER BOOK Organizing Committee Pascale Cossart and Philippe Sansonetti, Académie des sciences, Joerg Hacker and Juergen Heesemann, German National Academy of Sciences Leopoldina David Holden and Richard Moxon,

•  and  norophthalmate


•  bacterial  l-??forms


• vacv   containing


• ??l-?? glutamyl-??l-??cysteinyl-??glycine


• n1  


•  rods  to


•  of  the

Sujets

• Sixième
• Institut de France
• National
• Holden
• collège

Informations

• Publié par: profil-onyi-2012
• Nombre de lectures: 37
• Langue: English

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INTERACADEMIES SYMPOSIUM
Académie des sciences, German National Academy of Sciences
Leopoldina and The Royal Society

on
“The New Microbiology”

May 14, 15 and 16, 2012

Institut de France
23 quai de Conti
eParis 6

POSTER
BOOK
Organizing Committee

Pascale Cossart and Philippe Sansonetti,
Académie des sciences,
Joerg Hacker and Juergen Heesemann,
German National Academy of Sciences Leopoldina
David Holden and Richard Moxon,
The Royal Society 1

InhibitionofapoptosisandNF-κBactivationbyvacciniavirusproteinN1occurvia
distinctbindingsurfacesandmakedifferentcontributionstovirulence

1 1 1CarlosMaluquerdeMotes ,SamanthaCooray ,HongweiRen ,GabrielMF.
1 1 2 2,3Almeida ,KeiranMcGourty ,MohammadWBahar ,DavidIStuart ,JonathanM
2 2 1Grimes ,StephenC.Graham ,GeoffreyL.Smith

1DepartmentofVirology,FacultyofMedicine,ImperialCollegeLondon,St.Mary’s
Campus,London,W21PG,UK
2TheDivisionofStructuralBiology,WellcomeTrustCentreforHumanGenetics,
UniversityofOxford,RooseveltDrive,Oxford,OX37BN,UK
3ScienceDivision,DiamondLightSourceLtd.,DiamondHouse,HarwellScienceand
InnovationCampus,DidcotOX110DE,UK

Vacciniavirus(VACV)proteinN1isanintracellularvirulencefactorthatbelongstoa
familyofVACVB-celllymphoma(Bcl)-2-likeproteins.Membersofthisfamilyinhibit
apoptosisoractivationofpro-inflammatorytranscriptionfactors,suchasinterferon
(IFN) regulatory factor-3 (IRF-3) and nuclear factor-κB (NF-κB). Remarkably, N1
inhibitsbothapoptosisandNF-κBactivation.

TounderstandhowN1exertsthesedifferentfunctions,wehavemutatedresiduesin
theBcl-2-likesurfacegrooveandattheinterfaceusedtoformN1homodimers.
IntroductionofbulkyresiduesintheBcl-2-likegrooveabolishedonlytheN1anti-
apoptoticactivity,anditsinteractionwithcellularpro-apoptoticBcl-2proteinssuch
asBadorBid.Proteincrystallographyshowedthesemutantsdifferedfromwild-type
N1onlyatthesiteofmutation.Conversely,mutagenesisofthedimerinterface
converted N1 to a monomer and affected only inhibition of NF-κB activation.
Collectively,thesedatashowthatN1inhibitspro-inflammatoryandpro-apoptotic
signallingusingindependentsurfacesoftheprotein.

Todeterminetherelativecontributionofeachactivitytovirusvirulence,mutantN1
alleleswereintroducedintoaVACVstrainlackingN1andthevirulenceofthese
viruseswasanalysedafterintradermalandintranasalinoculationinmice.Inboth
models, VACV containing a mutant N1 unable to inhibit apoptosis had similar
virulencetowild-typevirus,whereasVACVcontainingamutantN1impairedforNF-
κBinhibitioninducedanattenuatedinfectionsimilartothatoftheN1-deletedvirus.
Thisindicatesthatanti-apoptoticactivityofN1doesnotdrivevirulenceinthesein
vivomodels,andhighlightstheimportanceofpro-inflammatorysignallinginthe
immuneresponseagainstviralinfections. 2
Ergothioneinandtheglutathioneanalogsophthalmateandnorophthalmate:from
mammalstocyanobacteria

NarainsamyK.(1),FarciS.(1),BraunE.(1),JunotC.(2),Cassier-ChauvatC.(1)and
ChauvatF.(1)
CEA,iBiTec-S(1)UMR8221,LBBCand(2)SPI,LEMM,CEASaclay91191GifsurYvette

Cyanobacteria,theonlyknownprokaryotesthatperformoxygenicphotosynthesis,
areregardedasbeing(i)amongsttheoldestlifeformsonearth;(ii)theproducersof
theEarth’soxygenicatmosphere;and(iii)theprogenitoroftheplantchloroplast.
Overtime,cyanobacteriahaveevolvedasthemostdiversegroupofbacteriathat
colonizemostbiotopes(fresh,brackishandmarinewaters,andsoils).Thehardiness
ofcyanobacteriaisduetotheirefficientphotosynthesisthatusesnature'smost
abundantresources,solarenergy,water,CO2andmineralnutrients,toproducea
largepartoftheatmosphericoxygenandorganicassimilatesforthefoodchain.
Cyanobacteriafixannuallyabout25GigatonsofcarbonfromCO2intoenergydense
biomass.Forthis,cyanobacteriauseabout0.3%ofthesolarenergy,178,000TW,
reachingtheEarthsurface,avalueexceedingbymorethan25timestheenergy
demand of the human society (about 15 TW). Furthermore, the availability of
moleculartoolsforgenemanipulationmakecyanobacteriapromising“low-cost”
microbialcellfactoriesforthecarbon-neutralproductionofbiofuels,whilesaving
arablesoilsforcrops.
Inproducingtheoxygenicatmosphere,cyanobacteriawerethefirstorganismsto
faceoxidativestressandironlimitation(duetoironoxydation),whichisespecially
detrimental to the iron-requiring photosynthesis pathway. Consequently,
cyanobacteria have developed powerful strategies to cope with the oxidant
byproductsgeneratedbytheiractivephotosynthesisandrespiration.Manyofthese
strategieswereconservedbyevolutionsuchastheproductionofglutathione(γ-L-
glutamyl-L-cysteinyl-glycine),whichwasregardedmerelyasaredoxbufferuntilwe
andothergroupsshowedthatitalsooperatesintheassemblyoftheiron-sulfur
clusterofanti-oxidantglutaredoxinenzymes.
Using a systems biology approach* (functional genomics, transcriptomics,
metabolomicsetc;..)wethoroughlyanalyzedoftheroleofglutathionesynthesis
(GshAandGshBenzymes)anddegradation(Ggt)inthephysiologyandtoleranceto
metalandoxidativestressesintwomodelcyanobacteria.
Amongotherresultswereport,forthefirsttime,thatGshAandGshBalsosynthesize
thetwoGSHanalogs,ophthalmate(γ-L-glutamyl-L-α-amino-n-butyryl-glycine)and
norophthalmate(γ-L-glutamyl-L-alanyl-glycine),whichwehadbeendescribedonlyin
mammalssofar.Wewilldiscusstheroleophthalmateandnorophthalmateinstress
signalling (ie; sulfur status or starvation) and in both amino-acid and sugars
metabolisms.
Wealsoreport,forthefirsttimethatsomecyanobacteriaareabletosynthesize
anothersulfur-containingantioxidant:ergothionein(EGT),whichwasalsodescribed
onlyinmammals,whichacquireEGTsolelythroughtheirdiet.Wewilldiscussthe
reciprocalroleofGSHinthesynthesisEGTanditsinterplayinthetoleranceto
oxidativeandmetalstresses.
*http://www.researcherid.com/rid/E-7505-2010andhttp://www.researcherid.com/rid/E-7394-2010 3
MechanismsunderlyingtheswitchfromrodstoL-formsinBacillussubtilis

PatriciaDomínguez-Cuevas,RomainMercierandJeffErrington.

CentreforBacterialCellBiology,InstituteforCellandMolecularBiosciences.
NewcastleUniversity.RichardsonRoad,NE24AX.NewcastleuponTyne.UK

The cell wall is a crucial protective layer that surrounds virtually all bacteria.
However,somebacteriahavedevelopedmechanismstoswitchbetweenwalledand
wall-deficientstates.Thesecellwall-deficientbacteria,knownasL-forms,havebeen
isolatedfrommanydifferentspecies1.Theyrepresentaninterestingmodelofstudy
considering their potential involvement in antibiotic resistance and persistent
infections2.Butdespitedecadesofstudythemechanismsunderlyingcelldivisionin
theabsenceofthecellwallarepoorlyunderstood..Wehaveisolatedastrainof
BacillussubtilisthatcanquicklyandquantitativelyconvertfromthewalledtotheL-
formstate.MutationsintwodifferentgenescontributetothehighfrequencyofL-
formtransition:walR,atranscriptionalregulatorinvolvedincellwallhomeostasis;
andsepF,requiredforaccurateandefficientcelldivision.Time-lapseimagingshows
thatthemutationsactbyfacilitatingthereleaseoftheL-formfromitswalledparent
cellbutthattheyactindifferentways3.
Inapreviouswork,weshowedthatL-formdivisiondoesnotrequireFtsZorany
residualpeptidoglycansynthesis4.Infact,manyessentialproteinsforthecellwalled
form have turned out to be dispensable for L-form survival and proliferation.
Therefore,weconductedageneticscreenusingrandomtransposonmutagenesisto
identifygenesexclusivelyessentialforL-formdivision.Ourresultshaveshownthe
crucialroleofmembranelipidcompositionanditsbiophysicalpropertiesduringL-
formdivision5.
1.AllanEJ,HoischenC,GumpertJ.BacterialL-forms.AdvApplMicrobiol.2009.68:1-
39.
2. Domingue and Woody. Bacterial persistence and expression of disease. Clin
MicrobiolRev.1997Apr;10(2):320-44.

3.Domínguez-Cuevas,P.,Mercier,R.,Leaver,M.,Kawai,Y.,Errington,J.Molecular
Microbiology.2012Jan;83(1):52-66.TherodtoL-formtransitionofBacillussubtilis
islimitedbyarequirementfortheprotoplasttoescapefromthecellwallsacculus.

4.LeaverM,Domínguez-CuevasP,CoxheadJM,DanielRA,ErringtonJ.Lifewithouta
wallordivisionmachineinBacillussubtilis.Nature.2009Feb12;457(7231):849-53.
5.Mercier,R.,Domínguez-Cuevas,P.,Errington,J.Crucialroleofmembranefluidity
inproliferationofprimitivecells.CellReports.Inpress.
4
TheYvcKproteinisrequiredformorphogenesisvialocalizationofPBP1under
gluconeogenicgrowthconditionsandisregulatedbySer/Thrphosphorylationin
Bacillussubtilis.

1 1 2 1ElodieFoulquier ,FrédériquePompeo ,AlainBernadac ,CélineFreton ,Christophe
3 1 1Grangeasse ,LeonEspinosa andAnneGalinier
1 2LaboratoiredeChimieBactérienne,UMR7283and Serviced'ImagerieCellulaire,
FR3479-IMM,CNRS,Aix-MarseilleUniversité,31cheminJosephAiguier,13402
3MarseilleCedex20,France. InstitutdeBiologieetChimiedesProtéines,UMR5086,
CNRS,UniversitédeLyon,7,passageduVercors,69367Lyoncedex07,France

TheYvcKproteinwaspreviouslyshowntobedispensablewhenB.subtiliscellsare
grownonglycolyticcarbonsourcesbutessentialforgrowthandnormalshapeon
gluconeogeniccarbonsources.YvcKislocalizedasahelical-likepatterninthecell.
This localization seems independent of the actin-like protein, MreB. A YvcK
overproduction restores a normal morphology in an mreB mutant strain when
bacteria are grown