генетичен материал

Природата на генетичния материал

Definition:Thematerialthattransmitsgeneticinformationbetweenparentsandoffspring.

Chemicalnature:ExceptforsomeviruseswhosegeneticmaterialisRNAandprionswhosegeneticmaterialisprotein,thegeneticmaterialsofothervirusesandallorganismswithatypicalcellstructureareDNA.

Existencepart:Thissubstanceisthemaincomponentofthechromosome.Italsoexistsinorganellessuchasplastidsandmitochondriaoutsidethenucleus.

Basiccharacteristics:Relativestability,self-replication,continuitybetweenthepreviousgenerationsandgenerationsandcanproduceheritablemutations.

Заключение: Генетичният материал на повечето организми (организми с клетъчна структура и ДНК вируси) е ДНК, така че ДНК е основният генетичен материал.

Условия

1Canaccuratelyreplicateitselfduringcellgrowthandreproduction

2Може да съхранява огромна генетична информация

3canguideproteinsynthesis,therebycontrollingmetabolismandbiologicaltraits

4може да предава генетична информация между потомството

genetic material

5structureisstable,andcanproduceheritablemutations.

Проучвателен процес

Процес на трансформация

Thepurposeoftheexperiment:tostudywhoisthegeneticmaterialinDNAandprotein.Testprinciple:TypeSpneumococcuscancausepneumoniainhumansorsepsisinsmallanimals;TypeRpneumococcushasbasicallynoeffectonhumansandanimals.

Тест за трансформация

Inthetest,Averyetal.foundthatthehigherthepurityoftheDNA,themoreeffectivethetransformation.

Експериментирайте

provedthatT2bacteriophageisavirusthatspecificallyparasitizesE.coli,andDNAisthegeneticmaterial.

Тест за реконструкция

ProvethatinaviruswithonlyRNAbutnoDNA,RNAisthegeneticmaterial.

5) Приони

Thediscoveryofprionsconfirmsthatproteinscanexistasgeneticmaterialoforganismsundercertaincircumstances.

Опознай

Откриване на приони

Prionsareproteinviruses,theyareviruseswithonlyproteinsbutnonucleicacids.Thewinnerofthe1997NobelPrizeinMedicineorPhysiology,AmericanbiologistS.B.Prusiner(S.B.Prusiner)wasawardedthishonorforhisoutstandingcontributionstothestudyofprions.Prionsarenotonlycloselyrelatedtohumanhealthandlivestockbreeding,butalsoprovideimportantinformationforthestudyofotherdiseasesrelatedtodementia.

Asearlyasthreehundredyearsago,humansfirstdiscoveredprion-infectedanimalsinsheepandgoats.Becauseofthedifficultitchingofsickanimals,itoftenrubsonroughtreetrunksandstonesurfaces,sothatthehaironthebodyiswornoff,whichiscalled"sheeppruritus."ThediseasespreadswidelyinEuropeandAustralia,withanincubationperiodof18to26months.Thediseasedanimalsareexcited,itchy,paralyzeduntildeath.Later,infectiousminkencephalomalacia,chronicwastingdiseaseinreddeeranddeer,spongiformencephalopathyincats,etc.werediscoveredoneafteranother.Pathologicalstudieshaveshownthatthesediseasesallinvadethecentralnervoussystemofanimals.Asthediseaseprogresses,progressivevacuolizationoccursinneuronaldendritesandcellsthemselves,especiallyinastrocytesanddendriticcellsinthecerebellum.Glialhyperplasiaandspongylesionsappearingraymatter.Thesediseasesaremainlycharacterizedbyalongincubationperiod,aslowcourseofdisease,progressivebraindysfunction,recoverywithoutremission,anddeath.

Thedomesticanimalprionthathasbecomethefocusofhumanattentionwaswhenthe"madcowdisease"spreadintheUnitedKingdominthespringof1996.ItnotonlycausedanunprecedentedeconomicandpoliticalturmoilintheUnitedKingdom,butalsospreadtotheentireEurope.Reutzfeld-Jacob'sdisease(Crutzfeldt-Jakobsyndrome,apriondiseaseofhumans)hasincreased,andpeoplearenaturallyassociatedwitheatingimportedbeeffromtheUK,whichhascausedgreatpanic.AlthoughitwaslaterfoundthatthemaincauseofFrenchCreutzfeldt-Jakobsyndromewasiatrogenicinfection,otherexamplescouldnotruleouttheconnectionbetweenmadcowdiseaseandhumanpriondisease.

Thefollowingfourtypesofhumanprionshavebeenfound,namelyKurudisease,Creutzfeldt-Jakobsyndrome,Gerstmannsyndromeandfatalfamilyinsomnia.ThemaincharacteristicsoftheirsymptomsandpathologicalchangesareThesyndromeisverysimilartothesickanimal.Amongthem,theresearchonKurudiseaseistheearliest.Kurudisease(Kurudisease)isalocalepidemicinthePapua-NewGuinea-easternForehighlandresidentsintheAtlanticOceaninthefirsthalfofthe20thcentury.Itsmainsymptomsaretremor,ataxia,anddementia.Lossofexerciseability,anddeathduetoexhaustionwithin3to6months."Kuru"means"fear"or"chills"inthetribe,sothediseaseiscalledKurudisease.Thetotalnumberofpatientsisabout30,000,mostlywomenandunderagechildren.TheAmericanmedicalscientistGeDusekconductedresearchintheareafor20years,andfoundthattheoccurrenceofthediseasewascloselyrelatedtothesacrificeoflocalpeople'sconsumptionofhumanflesh,andproposedpreventivemeasures.Aftertheritualwasstoppedin1968,thediseasewasbroughtundercontrol,thussavingatribeofpeople.Forthis,Gedusekwonthe1976NobelPrizeinMedicine.

Thespecificactivitiesandreplicationmechanismsofprionsarenotveryclear,buttheyaregenerallyconsideredtocauseaseriesofpreviouslypoorlyunderstoodinfectiousspongiformencephalopathy,theseencephalopathyincludingscrapieWagyuspongiformencephalopathy(alsocalled"madcowdisease").Theeffectsofthesediseasesonthestructureofbraintissuearefatalandincurable.

Генетичният механизъм на прионите

Itisthemechanismofprionreplicationthatattractsthemostinterestandattentionoftoday'sscientists.Becauseprionsaremolecularorganismsthatonlycontainproteinbutnonucleicacid,theycanonlysurviveinparasitichostcells.Therefore,theinformationneededtosynthesizeprionsmaybepresentinthehostcells,andtheroleofprionsisonlytoactivatethegenesencodingtheprionsinthehostcellssothattheprionscanreplicateandreproduce.

Anothertheoryisthatprionproteinscanencodegeneticinformationforthemselves.Thishypothesisiscontrarytothe"centrallaw"intraditionalmolecularbiology,becauseprionshavenonucleicacid.Therefore,itisassumedthatthepossiblemethodofprionreplicationisthattheRNAorDNAencodingtheprionisproducedthroughtheprocessofreversetranslation(reversetranscriptionisrequiredinthelattercase).Theremustbeareversetranslationenzyme,andevenareversetranscriptase..Thesecondisproteinsynthesisundertheguidanceofprotein,thatis,proteinitselfcanbeusedasgeneticinformation.

In1982,Pruzinaproposedthe"proteinconformationaldiseasehypothesis"thatprionscausedisease,whichwasgraduallyimprovedbyWeismanetal.Themainpointsareasfollows:①Prionproteinhastwoconformations:celltype(normalPrPc)anditchytype(pathogenicPrPsc).Themaindifferencebetweenthetwoliesintheirspatialconformation.PrPconlyhasahelix,whilePrPschasmultipleβsheets,thelatterhaslowsolubilityandisresistanttoproteolysis;②PrpsccanforcePrPctotransformintoPrpsc,realizeself-replication,andproducepathologicaleffects;③GenemutationcanleadtocelltypePrPscTheα-helixstructureinthemediumisunstable,andspontaneoustransformationoccurswhenacertainamountisreached,andtheβ-sheetincreases,andfinallybecomesthePrpsctype,whichmultipliesthediseasethroughthedominoeffect.

Althoughthegeneticmechanismofprionsisnotyetfullyunderstood,asfarasbiologicaltheoryisconcerned,thereplicationofprionsdoesnotusenucleicacidsastemplates,butproteinsastemplates.ThisisboundtobeusefulfortheexplorationoflifeTheoriginandthenatureoflifephenomenahaveamajorimpact.

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