Ma `lumot

Gram -musbat va gram -manfiy bakteriyalar o'rtasida gen uzatilishi?


Gram -musbat va gram -manfiy bakteriyalar o'rtasida genetik materialning uzatilishi qanday sodir bo'ladi?


Ushbu ikkita havolani ko'rib chiqing:

  • Genetik ma'lumot almashish va
  • Uzoq bog'liq bakteriyalar o'rtasida gen uzatilishi

Ayniqsa, ikkinchisi ko'plab savollarga javob berishi kerak.


Gram -musbat va gram -manfiy bakteriyalar o'rtasida gen uzatilishi? - Biologiya

Bakteriyalar populyatsiyasida eng ko'p ishlatiladigan farq - grammusbat va grammusbat bakteriyalar. Ularga ularni ajratish uchun ishlatiladigan usul nomi berilgan: Gram dog '(Xans Kristian Gram tomonidan ishlab chiqilgan). Gram-musbat bakteriyalarda peptidoglikan hujayralarining kattaroq devorlari bor, shuning uchun kristall binafsha rang dog 'saqlanib qoladi, Gram-manfiy bakteriyalar orasida ikkita peptidoglikanli devorli membrana bor, kristall binafsha dog' saqlanmaydi va safranin qarshi dog 'olinadi. Buning amaliy natijasi shundaki, siz mikroskop ostida mayda -chuyda shakllarda ko'zingizni qisib, pushti yoki binafsha rangga o'xshashligini aniqlashga harakat qilasiz:

Men ilgari hech qachon o'ylamagan narsam, ularning qaysi biri qaysi biridan paydo bo'lgan. Men juda ko'p taksonomiya qilmaganman va bakteriyalarni (laboratoriya ishiga aloqador bo'lmagan) o'z ichiga olgan yagona vaqt, mening patologiya kursim edi, bu har xil turdagi bakteriyalar qayerdan kelib chiqqanligi haqida juda xavotirlanmagan, faqat ular hozir qadar. Bir necha marta men bu haqda noaniq o'ylaganimda, men ijobiy va salbiy tomonga burilgan bo'lardim. Albatta, siz bitta hujayra membranasidan boshlaysiz va ikkitasiga o'tasiz.

Yaqinda men mutlaqo teskari xulosaga kelgan qog'ozni uchratdim va shuning uchun o'qimaslik juda qiziq edi. Bakterial taksonomiyaning muhim jihati shundaki, morfologiyada ko'plab katta o'zgarishlar "Deep Time" da sodir bo'lgan va bakteriyalar qimmatbaho qoldiqlarni qoldirgan. Bakteriyalar (va arxeyalar) eukaryotik narsalar haqida o'ylashdan oldin, bir milliard yildan ko'proq vaqt mobaynida mintaqada rivojlangan. Bu urinish va tartibga solish uchun juda ko'p vaqt. Buni kontekstga kiritish uchun, bundan bir milliard yil oldin, hamma narsa ko'p hujayrali bo'lishni o'ylay boshlagan edi. Dinozavrlar, o'simliklar yo'q, hatto hayotning eng murakkab shakli ham divan yostig'iga o'xshardi.

  • Paleontologik dalillar. Bakteriyalar juda ko'p miqdordagi toshqo'nmaslarni hosil qilmaydi, lekin ular vaqti -vaqti bilan ularning mavjudligini ko'rsatuvchi ba'zi dalillarni qoldirishi mumkin. Masalan, temirni iste'mol qiladigan bakteriyalar, tosh yeydiganlar, qolib ketadigan temir qutilarini qoldiradilar. Ular tuzilish va metabolizmning o'zgarishi uchun vaqtinchalik dalillar beradi.
  • O'tish tahlili. Bu katta o'zgarishlarni qutblashtirib, ularni oddiy savolga aylantirish orqali ishlatiladi va javoblarni aniqlash uchun qiyosiy, ishlab chiquvchi va tanlangan dalillardan foydalanadi. Masalan: birinchi navbatda oyoqlar yoki qanotlar rivojlanganmi? Yoki bakterial holatlarda: qaysi biri birinchi bo'lib, gramm manfiy yoki grammusbat?
  • Moslashuvchanlik testi. Bu evolyutsion daraxtlarning o'xshashligini qidiradi, bu evolyutsion qobiliyatlarni (qanotlari, tuklari, ikkinchi membranalari va boshqalarni) aniqlash va qutblash imkonini beradi. Bu ko'plab turlarning taqqoslanishi bo'lgani uchun, o'tish tahlilida keltirilgan dalillardan mumkin bo'lgan xatolarni topishga imkon beradi.
  • Daraxtlar navbati. Navbat daraxtlari. muammoli, lekin ayni paytda ajralmas foydali. Ular turli organizmlardan DNK ketma -ketligini olish, so'ngra algoritmlar yordamida ketma -ketliklar orasidagi "bog'liqlik" ni aytish va evolyutsion daraxtlarni yaratish uchun ushbu "bog'liqlik" darajalarini qo'llash orqali hosil bo'ladi. Ular sizning namunaviy taqsimotingizga moyil bo'ladilar, yo'nalishsiz, ishlab chiqarish vaqtini to'g'ri hisoblay olmaydilar va siz gorizontal gen uzatishni joriy qilmoqchi bo'lsangiz, biroz chalkashib ketishadi. Shunday bo'lsa-da, ular arxeeya va bakteriyalar-bu ikkita bir-biridan farq qiladigan super qirollik ekanligini ko'rsatadigan muhim ma'lumotlar edi (va men ularga ishonmasligimning aksariyatini men tan olaman, chunki men ularni la'natlagan narsalarni ishga sola olmayman).

Ammo, ko'pgina evolyutsion hikoyalar singari, agar u yaqinroq o'rganilsa, u biroz parchalanadi. Gram -musbat bakteriyalar oddiy "bitta hujayra membranasi" emasligi sababli, ularning atrofida katta hujayra devori ham bor. Buning ustiga ikkinchi hujayra membranasini ishlab chiqish bema'nilikka o'xshaydi. Va keyin nima uchun hujayra devori qisqaradi? Va qanday qilib bu to'satdan rivojlangan hujayra membranasidan qanday o'tish mumkin? Tashqi membrana uchun transport oqsillari odatda oqsil tuzilishini hosil qiladi, ichki membrana uchun esa alfa spirali hosil qiladi. Bu juda tez o'zgarishi kerak bo'lgan oqsillarni yig'ish tizimining mutlaqo yangi tizimi, chunki aks holda bakteriyalar och qoladilar, uning tashqi membranasidan hech narsa o'tolmaydi (bu ulkan hujayra devori tepasida muvozanatli).

Buni hisobga olgan holda, o'ngda ko'rilgan sxema biroz mantiqiy bo'la boshlaydi (rasm quyidagi havoladan olingan). "Murein" "peptidoglikan hujayra devori" degan ma'noni anglatadi va sitoplazma hujayraning ichki qismini bildiradi. Bu stsenariyda, ikki membranali protobakteriyalar (oxirgi yarim milliard yil davomida yoki yaxshi sozlangan er-xotin membranali tizimni rivojlantirgan) birdaniga tashqi membranani yo'qotadi. Juda oddiy genetik o'zgarish katta membranani o'stirib, tashqi membranani yirtib yuboradi. Hujayra o'zining barcha tashqi membranali teshiklari va signal tizimlarini yo'qotadi, lekin buning evaziga yuqori darajada himoyalangan hujayra devoriga ega bo'ladi, bu esa uning turli bo'shliqlarda omon qolishiga imkon beradi. Bu jihatlar qanday genetik tarzda yo'qoladi, bu boshqa masala va qog'oz ishlatilmaydigan genlar oxir-oqibat yo'qolib ketishini aytadi. Bu bakteriyalar uchun to'g'ri, ular shunday kichik genomga ega, ular uni keraksiz genlar bilan to'ldirishni xohlamaydilar, lekin menda genlar nimanidir qoldirishga moyilligini his qilaman. Shunday bo'lsa-da, endi kerak bo'lmagan genlar qaerga ketadi, degan savol, ehtimol, bu dalillarning zaif qismlaridan biri bo'lishi mumkin (hech bo'lmaganda o'qimagan o'quvchilarim nazarida).

Bu gipotezani qo'llab-quvvatlaydigan narsa, gram-musbat bakteriyalar "mono-klad" hosil qilganini, ya'ni yagona universal umumiy ajdoddan chiqqanligini ko'rsatishdir. Afsuski, bu ma'lumotni aniqlash qiyin bo'lib turibdi, DNKni har xil va har xil narsalarni almashtirish bakterial hiylasi yordam bermadi. Yana bir chalg'ituvchi omil - bu bo'sh vaqt. Turli xil zamonaviy bakteriyalar bir necha million yil oldin bir xil blokdan chiqqanmi yoki yo'qligini aniqlash qiyin vazifadir. Siz monokladal gram-pozitivlarni qo'llab-quvvatlaydigan RNK ketma-ket daraxtlarini olishingiz mumkin, lekin agar siz bir ko'zingizni yumib, ko'zingizni qisib qo'ysangiz, bu umuman ilmiy amaliyot emas.

Men hech qachon taksonomiyaga, hatto bakteriyalarga ham kirmayman deb o'ylayman. lekin u dunyoni qanday o'zgarganini, qanday rivojlanganligini va nihoyat hozirgi holatga qanday aylanganini ko'rishning ajoyib usullarini ishlab chiqaradi. Orvell shunday mashhur deb yozgan edi: "O'tmishni boshqargan kelajakka buyruq beradi" va siz bakteriyalar qarshiligi qanday ishlashini va ularni qabul qilishni to'xtatish kerakligini aniqlamoqchi bo'lganingizda, bu ibora boshqa ma'noga ega bo'ladi. siyosiy

(Bu post uchun mukammal iqtibos emas. "O'tmishni tushunadi" yaxshiroq ishlagan bo'lardi. Ammo men yaxshiroq narsani topish uchun iqtibos arxivlarini aylanib o'tishga unchalik da'vogar emasman. Har qanday takliflar minnatdor bo'lardi: p)

9 ta sharh:

Juda qiziq gipoteza! Agar gram-manfiy bakteriyalarda ichki hujayra devorining to'satdan o'sishiga olib keladigan mutatsiyani sun'iy ravishda qayta yaratish mumkin bo'lganida (va kichkina odam ozgina tirik qola oladimi-yo'qmi), bu haqiqatan ham ishonchni qozonadi. bu fikr.
Men bakterial biokimyo haqida unchalik yaxshi bilmayman, lekin agar bu juda oddiy hodisa bo'lsa, Gram (+) va#39 ning taksonomik taqsimlanishini tushuntirib, "gramm pozitivizm" ning bir qancha kelib chiqishini ham ko'rib chiqish mumkin edi.

Ajoyib post, bu haqda prokaryotik mikrobiologdan eshitish juda yoqimli. Men har doim bakteriyalarga qiziqardim, lekin bizning bakteriologiya kurslarimizni Mikrobiologiya va IMMUNOLOGIYA kafedrasi o'rgatadi, shuning uchun, afsuski, bizda mikroblar nuqtai nazaridan hech qanday mikrobiologiya darslari yo'q. inson tanasi bilan o'zaro ta'sir, tbh). Men qaradim va hech narsa yo'q: hammasi tibbiy, hammasi MCAT-ga asoslangan. Grrr.

Aytgancha, TC-S hujayra biologining nazarida juda muhim va tez-tez o'tkazib yuboriladigan nuqta ekanligini ta'kidlaydi: genlar hujayra tuzilishi/tashkil etilishining yagona asosi emas. Yadro yadrosi merosi bor (va shunday qilib, evolyutsiya) va ehtimol u molekulyar biologlar o'ylagandan ko'ra katta rol o'ynaydi. Albatta, evolyutsiyani asosan ekologlar, populyatsion genetiklar va molekulyar biologlar o'rganadilar, shuning uchun bu jarayonda hujayralar e'tiborga olinmaydi. Va ha, men jiddiy mol go'shti oldim, chunki menimcha, sitoplazmatik va kortikal meros/evolyutsiya evolyutsiyada juda muhim omil bo'lishi mumkin va genlar kuchsiz bo'lgan muammolarni hal qilishga yordam beradi. Axir, yana bir bor, organizm faqat uning genomidan boshqa narsa emas.

Tom 2001 yilda "J Mol Evol" va "quotobcell" maqolasida shunday deb yozadi: "Nuklein kislotalari va oqsillar bilan solishtirganda, lipidlar molekulyar dunyoning uchinchi toifali fuqarolari bo'lib ko'rinishi kerak. ] & quot Va juda yaxshi fikr bor: albatta, siz RNK, DNK va oqsil evolyutsiyasi borasidagi cheksiz bahslar haqida eshitasiz, lipidlar tasodifan xuddi shunday sodir bo'lgan arzimas narsa sifatida tashlanadi. Membranlar genetiklar uchun zerikarli.

Shunday qilib, ba'zi membrana tuzilishining yo'qolishi, ortishi yoki o'zgarishi genetik o'zgarishlarning irsiy bo'lishini talab qilmaydi (va shu tariqa saqlanib qoladi). Aslida, bu butunlay o'z -o'zidan sodir bo'lishi mumkin va unga moslashuvchan ustunlik qo'shishi mumkin, va u xuddi gen kabi populyatsiyaga joylashadi. DNK haqida hech qanday "sehrli" hech narsa yo'q, bu uni evolyutsiyaga qodir yagona tuzilishga aylantiradi. Bu ajoyib substrat, ehtimol, eng yaxshisi, lekin yagona emas.

Albatta, membrananing ko'payishi yoki yo'qolishi genomning o'zgarishiga olib kelishi mumkin. Masalan, agar siz tashqi membranada biror narsaning o'tishiga ruxsat berish uchun maxsus teshikli tuzilmalarga muhtoj bo'lsangiz, agar siz membranani yo'qotib qo'ysangiz, sizga endi kerak bo'lmaydi, bu genlar boshqa joyda ishtirok etmaydi. Mening uyali molekulyar biologiya bilan ishlash bo'yicha cheklangan tajribam shuni ko'rsatadiki, oqsilning faqat bitta yo'lda ishlashi juda kam uchraydi. Uyali aloqa yo'llari - bu chalkashlik, siz menga ishonishingiz mumkin. & quot; Mening & quot; genim juda kulgili turli yo'llar va jarayonlar bilan uxlab yotganga o'xshaydi, shuning uchun agar siz bir nechtasini olib tashlasangiz, yo'qolishi dargumon.

Men Stoltzfus 1999 Mol Biol Evol va Lynch 2007 PNAS ni murakkablik va genetik tarmoqlarning neytral evolyutsiyasi haqida ma'lumot olish uchun tavsiya qilaman. Bu nima uchun genlarning o'zaro ta'siri MESS ekanligini tushuntirishga yordam beradi. *o'z tadqiqot yozuvlariga qaraydi**shivirlash*

Yaxshiyamki, siz, ehtimol, negibakteriyalarda tashqi membranada osilgan oqsillar bilan bog'liq bo'lgan genlarni yo'qotish hodisalari bo'lishi mumkin. Yoki, ehtimol, haddan tashqari tafovut. Siz haqsiz, bu prokaryotik evolyutsiya dunyosida uzoq davom etish, yuqori tezlik va qat'iy tanlov bilan bog'liq katta muammo - daraxtlarni gapirish qiyin va qiyin. Ammo bu erda faqat daraxtlarni emas, balki bir nechta omillarni o'lchash muhim bo'ladi va odatda molekulyar biologlar buni so'raydilar.

Linch bo'lishimdan oldin, ba'zilar buni yaxshi bilishadi, shu jumladan bizning bo'limimizda ham. * asabiylik bilan atrofga qaraydi* Aslida men o'ylaganlar ko'p morfologik ishlarni o'z ichiga oladi, shuning uchun ular xavfsiz. * puf* Ammo, shunga qaramay, maydonning ko'p qismi izchil ibodat bilan o'tadi. shuning uchun Tom o'zining "giperbolik tasdiqlari" bilan chiqadi va ularni o'z gipotezalari ustida ishlashga majbur qiladi. Juda samarali strategiya, menimcha = P

Oh, va muhim tafsilot: Tomning fikricha, dastlabki prokuror ikki membranali birinchi hujayrani (2001 JME) hosil qilish uchun ikkita ' hujayralari birlashishi natijasida ikki qavatli membranali bo'lgan. Haqiqatan ham, agar men topa oladigan bo'lsam, Nature Review -da birovga yoqdi. Oh, bu erda (bepul kirish), shuning uchun Tom bu jinnilikda yolg'iz emas.

Agar posibakteriyalar polifiletik bo'lsa, qiziq bo'lardi. Men Tom bu haqda nima deb o'ylayotganini unutaman, lekin u ba'zilarini mustaqil ravishda tashqi membranasiz deb bilishi mumkin.

Bu erda yillik yillik sharhni yozganingiz uchun uzr. (lekin men bu narsalarni juda yaxshi ko'raman!)

PS: & quot; Agar siz bir ko'zingizni yumib, ko'zingizni qisib qo'ysangiz, bu umuman ilmiy amaliyot emas. & quot

Oh, keling, bu erda halol bo'lishingiz mumkin = P

Xo'sh, biz elektron pochta orqali buni qanday amalga oshiramiz? Mening blogimda/profilimda menikilar.

Menimcha, Orvellning taklifi ishlagan. 1984 hamma narsani, shu jumladan bakteriyalar merosini ham tushuntiradi. Men hech qachon birinchi yoki salbiy bo'lganini o'ylamaganman, lekin ular birlashtirgan nazariya o'z -o'zidan paydo bo'ladigan ikkinchi membrana va kichikroq devor nazariyasidan ko'ra mantiqiyroqdir.

Menimcha, biz bir guruh bakteriyalarni olib, ular paydo bo'lgan sharoitlarni qayta tiklashga harakat qilishimiz kerak, la Miller tajribasi. Bu qiyin bo'lishi mumkin emas, to'g'rimi?

Hamma sharhlar uchun katta rahmat bolalar!

@Lucas: Bu sof spekülasyonlar sohasida, lekin men his qilamanki, bu oddiy hodisa * genetik jihatdan * organizmning omon qolishi juda qiyin bo'lardi. bu juda ixtisoslashgan joy bo'lishi kerak edi.

Bu juda ajoyib tajriba bo'lardi, lekin Gram -v ' lar o'shandan beri juda ko'p rivojlanishni boshdan kechirishdi va endi tashqi membrana avvalgisidan ko'ra hayotiyroq bo'lishi mumkin (men bu erda ayniqsa flagella haqida o'ylayman) ). ehtimol urinishga arziydi.

@Psi: & quotgenlar hujayra tuzilishi/tashkil etilishining yagona asosi emas & quot; Men bu erda umuman siz bilanman! Afsuski, (asosan tarixiy) sabablarga ko'ra, irsiyat genetiklar tomonidan o'rganiladi, demak, epigenetika endigina qadrlanmoqda. Men hech qachon bu haqda o'ylamaganman, lekin bakteriyalar uchun hujayra devori/membrana komponentining merosxo'rligi juda muhim bo'lardi va hujayra ikkiga bo'linib ketganda, ikkala qiz hujayra ham har xil bitlarga ega bo'ladi (vaqti-vaqti bilan aytilgan "nanobren" bilan nima sodir bo'ladi) bu nuqta!)

Men "Stoltzfus" gazetasini ko'rib chiqaman va tabiatni ko'zdan kechirish ajoyib eshitiladi :)

@Skellet: Menimcha, bu tajribani o'tkazishda asosiy muammolardan biri a) bizga milliard yillik mablag 'bilan tadqiqotchi kerak va b) hech kim bu shartlar nima ekanini aniq bilmaydi! Butun tartibsizlik paytida kislorod portlashi sodir bo'ldi, bu hammasini biroz chalkashtirib yuborgan bo'lsa kerak :)

Voy-buy! Bu ajoyib. Sizning qimmatli ma'lumotlaringizni baham ko'rganingiz uchun tashakkur. Biz zararkunandalarga qarshi kurashda ishlaymiz. Biz zararkunandalarga qarshi kurashga ham ishonamiz. Qo'shimcha ma'lumot olish uchun bizga tashrif buyurishingiz mumkin.
Zararkunandalarga qarshi kurash xizmatlari NJ

UCLA shtatidan Jeyms Leykning tabiat haqidagi qiziqarli maqolasi bor edi, gramm negativlar aktinobakteriyalar va klostridiylarning endosimbiyozidan kelib chiqqan bo'lishi mumkin. Bu faqat bitta qog'oz, lekin juda qiziqarli va jozibali. Bilamizki, eukaryotlar uchun simbioz ularning evolyutsiyasi uchun juda muhim edi (ya'ni mitoxondriyalar va xloroplastlarning prokaryotik homologlari), nega prokaryotlar emas? Hech bo'lmaganda, biz bu imkoniyatni e'tiborsiz qoldiramiz deb o'ylamayman.

Leyk, JA. 2009. Erta prokaryotik endosimbiyozga dalillar. Tabiat 460: 20 p.967-71.

Genetika ma'lumotlari va tahlillari buni tasdiqlashi mumkin yoki ijobiydan salbiyga. Qalin peptidoglikan bu bakteriyalar million yillar oldin yashashi kerak bo'lgan hash muhitining natijasi bo'lishi mumkin. Shunda bakteriya boshqa membrananing mavjudligi natijasida boshqasini yutib yuborishi va peptidoglikan qatlamini kamaytirishi mumkin edi. Faqat nazariya. Qanday bo'lmasin, yaxshi narsalar

@Charles: Qog'oz uchun rahmat! Xo'sh, albatta ko'rib chiqing :)

@anon: Men bakterial membrananing evolyutsiyasi haqidagi turli nazariyalarni uchratdim, bu men eshitgan birinchi salbiy manfiy va ijobiy tomonni taklif qilgan, shuning uchun men uni juda qiziq deb topdim.


Xulosa

IV tipli sekretsiya tizimlari (T4SSs) gram-manfiy va grammusbatli bakteriyalarda butun hujayra konvertini qamrab oladigan ko'p qirrali ko'p proteinli nanomaxinalardir. Ular efektor molekulalarining kontaktga bog'liq holda eukaryotik xo'jayinlarga sekretsiyasi va DNKning ko'chma elementlarining konjugativ o'tkazilishi, shuningdek hujayradan tashqari muhit bilan DNKning kontaktga bog'liq bo'lmagan almashinuvi orqali muhim rol o'ynaydi. So'nggi bir necha yil ichida T4SS ning molekulyar mexanizmlari haqida ko'plab tafsilotlar aniqlandi. Dan T4SS komplekslarining hayajonli tuzilmalari Escherichia coli plazmidlar R388 va pKM101, Helicobacter pylori va Legionella pneumophila hal qilindi. F-pilusning tuzilishi haqida ham xabar berildi va hayratlanarli tarzda fosfolipid molekulalari bilan 1: 1 stoxiometriyadagi pilin bo'linmalaridan tashkil topgan filament aniqlandi. Ko'plab yangi T4SSlar aniqlandi va tavsiflandi, bu superfamilyaning tarkibiy va funktsional xilma -xilligini ta'kidlaydi. Murakkab tartibga soluvchi sxemalar, shuningdek, hujayraning fiziologik holatiga yoki yaqin atrofdagi bakterial qabul qiluvchi hujayralar kvorumiga javoban, T4SS mashinasini ishlab chiqarishni boshqarishi ko'rsatilgan. Bu erda biz "paradigmatik" va rivojlanayotgan tizimlar haqidagi bilimlarimizdagi so'nggi yutuqlarni sarhisob qilamiz va bakterial infektsiyalarda T4SS funktsiyalarini bostirishga va mikroblarga qarshi qarshilikning tarqalishiga qaratilgan strategiyalarni ishlab chiqishda yangi asosiy tushunchalar qanday yordam berishini o'rganamiz.


2. Gram-manfiy bakteriyalarga chidamli

2.1. Enterobakteriyalar

Enterobakteriyalar kabi oila Escherichia coli, Klebsiell spp., va Enterobakteriya spp. siydik yo'llari infektsiyalari (UTI), qon oqimi infektsiyalari, kasalxona va sog'liqni saqlash bilan bog'liq pnevmoniyaning asosiy sababidir. Qarshilik asosan ESBL ishlab chiqarish bilan bog'liq, lekin boshqa qarshilik mexanizmlari ham vujudga kelmoqda, bu esa ko'p dori-darmonli qarshilikka (MDR) olib keladi [10].

2.1.1. Enterobakteriyalar- 3-avlod sefalosporinlarga chidamli

Enterobakteriyalar uchinchi avlod sefalosporinlariga qarshilik β-laktamazalar ishlab chiqarish natijasidir. Masalan, ESBLlar keng spektrli sefalosporinlar, monobaktam va penitsillinlarni gidroliz qila oladi. A va#x003b2-laktamazalar fermentlari, masalan, TEM-1, TEM-2 va SHV-1 ampitsillin, amoksitsillin va erta avlod sefalosporinlariga qarshilik uchun javobgardir. Uchinchi avlod sefalosporinlariga qarshilik TEM-1, TEM-2 yoki SHV-1 kodlovchi genlarning mutatsiyasi ularni gidroliz qila oladigan yangi β-laktamazalarni keltirib chiqarganda paydo bo'ladi.

ESBLning boshqa turlari bilan ifodalanishi mumkin Enterobakteriyalar asosan, seftazidim va karbapenem gidroliz qiluvchi oksatsillinazalarga (OXA) qaraganda sefotaksimni yanada samarali gidrolizlaydigan CTX-M (CTX-Myunxen, ESBL fermenti) P. aeruginosa va kamdan -kam hollarda Enterobakteriyalar. ESBLlardan tashqari, AmpC β-laktamazalar ham uchinchi avlod sefalosporinlarini gidrolizlashga qodir va klavulanat va boshqa β-laktamaz inhibitörleri tomonidan inhibisyonga chidamli [10].

2.1.2. Enterobakteriyalar- karbapenemga chidamli

Karbapenemga chidamli Enterobakteriyalar (CRE) - bu Enterobakteriyalar ertapenem, imipenem, meropenem yoki mikroblarga qarshi har qanday karbapenemga chidamli izolyatsiya. Birinchi izolatlar 1990-yillarda xabar berilgan va qarshilik AmpC β-laktamazalar ishlab chiqarilishi va tashqi membrana oqsilining yo'qolishi bilan bog'liq. CREning ikki turi mavjud: karbapenemaza ishlab chiqaruvchi CRE (CP-CRE), ularning genlari mobil genetik elementlarda mavjud va hech qanday karbapenemaza ishlab chiqaruvchi CRE (CP-CRE bo'lmagan) [11].

Beshta yirik karbapenemaza mavjud, ular: (1) Klebsiella pnevmoniyasi karbapenemazasi(KPC), A sinfli serin asosli β-laktamazalar, (2) B sinf, Nyu-Dehli Metallo-va#x003b2-laktamazalar (NDM), (3) Verona integrin kodlangan Metallo-β-laktamaz (VIM), (4) sinf D, OXA yoki OXA-48 ga o'xshash karbapenemazalar va (5) IMP, imipenemda faol. Enterobakteriyalar o'ziga xos imipenem qarshilikka ega bo'lgan turlar kiradi Morganella morganii, Proteus spp. Va Providensiya spp. [12]

2.2. Acumanetobacter baumannii

Acumanetobacter baumannii Bu aerob gram-manfiy bakteriyalar va eng jiddiylaridan biridir Enterococcus faecium, Staphylococcus aureus, Klebsiella pnevmoniyasi, A. baumannii, Pseudomonas aeruginosa, va Enterobakteriya JSST tomonidan e'lon qilingan bakteriyalarga qarshi dorilar ta'siridan qochib qutuladigan turlar (ESKAPE). A. baumannii butun dunyo bo'ylab kasalxonadan yuqadigan infektsiyalar bilan bog'liq va mikroblarga qarshi qarshilikni tez rivojlantiradi, masalan:

(1) β-laktamalarni β-laktamazalar tomonidan inaktivatsiyasi, bu MDRning asosiy mexanizmi hisoblanadi. A. baumannii. A, B, C va D β-laktamazalarning barcha to'rtta sinflari aniqlangan A. baumannii, u o'z genomiga ekzogen DNKni kiritishi va ko'p sonli β-laktamazalarni aniqlashi mumkin. Bu fermentlarning ba'zilari TEM-1, SCO-1 va CARB-4 kabi tor spektrli va#x003b2-laktamazalardir, boshqalari esa ESBL GES-11 va CTX-M gidroliziga javobgardir, bu esa karbapenemlarga sezuvchanlikni pasaytiradi. . B toifasi-bu metallo-β-laktamazalar (MBL), ular keng diapazonga ega, kuchli karbapenemaza faolligi va barcha & x003b2-laktamli antibiotiklarga qarshilik ko'rsatadi, lekin monobaktamlarga emas. C va#x003b2 sinfidagi laktamazalar sefamitsinlarga (sefoksitin va sefotetan), penitsillinlarga va sefalosporinlarga chidamli. A. baumannii ichki AmpC sefalosporinazaga ega. Oksatsilindan afzal D yoki OXA sinflari va#x003b2-laktamazalar kengaytirilgan spektrli sefalosporinlar va karbapenemlarni gidroliz qila oladi.

(2) Qarshilikning yana bir usuli - bu turli xil antibiotiklar sinflariga, shu jumladan tigetsiklin yoki imipenem qarshiligiga qarshi ko'p dorivor nasoslar. A. baumannii. Oqim nasoslarining to'rt toifasi mavjud: qarshilik nodulyatsiyasi bo'linmasi (RND) superfamily, asosiy yordamchi superfamily (MFS), ko'p dori va toksik birikmalar ekstruziyasi (MATE) oilasi va kichik dorilarga qarshilik (SMR) oilaviy tashuvchilar. Rde tipidagi AdeABC oqimi nasosining haddan tashqari ko'payishi tigetsiklinga sezuvchanlikni pasayishiga olib keladi.

(3) ning qarshiligi A. baumannii aminoglikozidga fermentlarning uchta klassi vositachilik qiladi, ular orasida asetiltransferazalar, adeniltransferazalar va fosfotransferazalar bor. Bu fermentlar aminoglikozidlarni kimyoviy jihatdan o'zgartiradi. Kodlash genlari plazmidlar, transpozonlar va integrallar orqali o'tkazilishi mumkin.

(4) konvertning o'tkazuvchanligini o'zgartirish orqali o'tkazuvchanlik nuqsonlari. Porinlar molekulalarni tashqi membrana orqali tashish uchun kanallar hosil qiluvchi va qarshilik mexanizmida muhim rol o'ynaydigan oqsillardir. Caro, Omp22-33 kabi ba'zi porinlarning ifodasini kamaytirish karbapenem qarshiligi bilan bog'liq A. baumannii. Tashqi membrana oqsillaridan tashqari, LPSning yo'qolishi kolistin qarshiligini oshiradi A. baumannii membrana yaxlitligining pasayishi tufayli.

(5) Penitsillinni bog'laydigan oqsillar (DBP), DNK-giraza mutatsiyalari va boshqalar kabi maqsadli joylarning o'zgarishi antibiotiklar uchun mo'ljallangan joylarni o'zgartiradi. Ayrim PBPlarning haddan tashqari oshishi, xinolon va tetratsiklin qarshiligida bo'lgani kabi, DNK girazasida imipenem qarshiligiga va mutatsiyaga olib keladi. A. baumannii.

(6) Integronlar bakterial xromosomalarda yoki plazmidlarda joylashgan va to'rtta sinfga ega. Integronlar giyohvandlikka chidamli genlarni to'plash va ifodalashning yagona qobiliyatiga ega va epidemik shtammlar uchun foydali belgidir. A. Baumanniy [13,14].

Imipenem, meropenem va doripenem kabi karbapenemlar davolash uchun eng yaxshi vositalar ediA. baumannii, lekin sezuvchanligi pasayganligi sababli A. baumannii Minotsiklin/tigetsiklin va polimiksinlar eng samarali hisoblanadi va ularga qarshi sinergik ta'sir ko'rsatadi. A. baumannii infektsiyalar. Biroq, tigetsiklin va kolistinga chidamli A. baumannii paydo bo'ldi. Sulfaktam va ampitsillin + sulbaktam + karbapenem kombinatsiyasi bilan ampitsillinning kombinatsiyalangan terapiyasi MDRni davolashda samarali bo'ladi. A. baumannii bakteremiya. Minotsiklin terapiyasi, shuningdek, davolanishning yuqori muvaffaqiyat darajasi va yaxshi bardoshliligiga ega, ammo minotsiklinning kiritilishi tufayli uning 20% ​​ga yaqini. A. baumannii qarshilikni rivojlantirdilar. Minosiklin kolistin bilan birgalikda minotsiklinga chidamli bo'lganlarni davolashda samarali A. baumannii infektsiyalar va kolistin/rifampin-kolistinga chidamli bo'lganlar uchun eng samarali davo A. Baumanniy. Shuningdek, trimetoprim-sulfametoksazol kolistin bilan birgalikda karbapenemga chidamlilarni tezda yo'q qiladi. A. baumannii infektsiyalar. Boshqa antibiotik bo'lmagan terapiya-bu bakteriyofaglar, bu bakteriyalarni parchalaydigan viruslardir. Amerikalik alligator plazma peptidi va antimikrobiyal peptid dendrimer G3KL MDRga qarshi in vitro mikroblarga qarshi faollikka ega. A. baumannii lekin ular qisqa yarim umr va yuqori ishlab chiqarish xarajatlariga ega. Shuning uchun, nazorat qilish uchun antibiotiklarning yangi sinflarini kashf qilishning yangi strategiyalarini chaqirish uchun harakat qilish kerak A. baumannii infektsiyalar muvaffaqiyatli o'tdi [13,14].

2.3. Pseudomonas aeruginosa

Pseudomonas aeruginosa Oddiy ichak florasining bir qismi sifatida topilgan gram-manfiy aerob bakteriya va o'ta og'ir bemorlarda ICU-dan olingan infektsiyalar uchun mas'ul bo'lgan ESKAPE organizm sifatida tasniflangan kuchli patogen. Ko'p mexanizmlar uning antibiotiklarga chidamliligiga hissa qo'shishi mumkin: tug'ma qarshilik P. aeruginosa Chiqib ketadigan nasoslarning haddan tashqari ifodalanishi va tashqi membrana o'tkazuvchanligining pasayishi, shuningdek, qarshilik genlarini sotib olish yoki porinlar va boshqa oqsillarni kodlaydigan genlarda mutatsiya kabi qarshilik mexanizmlari, bularning barchasi bu mikroorganizmni davolashni qiyinlashtirishi mumkin.

P. aeruginosa birinchi marta 1882 yilda yashil yiringdan ajratilgan va nafas olish uskunalari va dializ naychalari kabi shifoxona muhitining quruq yuzasida omon qolishi mumkin bo'lgan immuniteti zaif bemorlarda opportunistik patogen deb topilgan. Bu to'rtinchi eng ko'p ajratilgan nozokomial patogen, ventilyator bilan bog'liq bo'lgan pnevmoniyaning ikkinchi va qon oqimidagi infektsiyalarning gram-manfiy sabablari orasida uchinchi o'rinda turadi.

β-Penitsillin, sefalosporin va karbapenem kabi laktamli antibiotiklar bakterial peptidoglikan hujayra devorlarining sintezini inhibe qiladi. Tsefazidim va sefepim kabi sefalosporinlarning uchinchi va to'rtinchi avlodi, davolashda ishlatiladigan eng samarali β-laktamdir. P. aeruginosa. Bu antibiotiklarga qarshilik β-laktam halqasining amid bog'lanishini buzadigan va antibiotiklarni samarasiz qiladigan & x003b2-laktamazalar vositachiligida bo'ladi. β-laktamazalarning to'rtta asosiy klassi aniqlangan P. aeruginosaA, C va D sinflari serin qoldig'ining katalitik faolligi orqali β-laktamlarni inaktivatsiya qiladi, B yoki MBL sinflari o'z faoliyati uchun sink kationiga muhtoj.

AmpC β-laktamaz kabi endogen β-laktamazalar, benzilpenitsillin va imipenem kabi bir qancha β-laktamlarni qo'zg'atishi mumkin. P. aeruginosa gen mutatsiyasi orqali qarshilikka ega bo'lishi mumkin, bu esa AmpC β-laktamazaning haddan tashqari oshishiga olib keladi. AmpC genining indüksiyasida bir nechta genlar ishtirok etadi, bu ampRni o'z ichiga oladigan transkripsiyali regulyatorni kodlaydigan ampR va ampC induktsiya qiladigan 1,6-anhidromurapeptidlar uchun o'tkazuvchi transmembranli oqsilni kodlovchi ampG. va sitozolik N-asetil-angidromuramil-L-alanin amidazani kodlaydigan va ampC ifodasini repressor vazifasini bajaruvchi ampD. AmpE-bu sitoplazmatik membrana oqsilini kodlaydigan to'rtinchi gen, u induktsiya uchun zarur bo'lgan sensorli transduser molekulasi vazifasini bajaradi.

Pseudomonas Aminoglikozidlarga qarshilik aminoglikozid fosforil transferazalar (APH), aminoglikozid adenilil transferazalar (AADlar) va aminoglikozid atsetiltransferaza aminoglikatsidlarni (AACs) saqlaydigan aminoglikozidlarni o'zgartiruvchi fermentlar (AME) vositachiligida amalga oshiriladi. yoki antibiotik molekulasiga atsetil, va bakterial hujayradagi nishonga bog'lanish afinitesini kamaytiradi.

FQ ga qarshilik DNK girazasi yoki topoizomerazasini 1 V kodlovchi bakterial xromosoma genining mutatsiyasi yoki preparatni hujayradan faol tashish orqali rivojlanadi.

Kolistin MDRni davolashda samarali ekanligi aniqlandi Pseudomonas boshqa β-laktamli dorilarga qaraganda va imipenem, piperatsillin, aztreonam, seftazidim yoki siprofloksatsin kabi psevdomonazaga qarshi vosita bilan birgalikda ishlatilganda samaraliroq bo'ladi. Bundan tashqari, fosfomitsin terapiyasi, aminoglikozidlar, sefalosporinlar va penitsillinlar bilan, dorilarga chidamliligini davolashda yaxshi natija beradi. P. aeruginosa [15].

2.4. Helicobacter pylori- klaritromitsinga chidamli

Helicobacter pylorus (HP)-odamlarda gastrit, oshqozon yarasi va oshqozon saratoni kabi infektsiyalar uchun mas'ul bo'lgan eng muhim patogen sifatida tan olingan grammusbat bakteriya. Antibiotik qarshiligining tez rivojlanishi tufayli HPni davolash samaradorligi pasaygan [16,17]. Klaritromitsin birinchi darajali uch tomonlama terapiyaning bir qismi bo'lib, 23S rRNA genining V sohasidagi turli mutatsiyalar tufayli rivojlanishi mumkin. A2142G, A2142C yoki A2143G bakteriyalarda, bu preparatga yaqinlikni pasayishiga olib keladi. IF-2 tarjimasini boshlash faktori, L22 ribosomal oqsil va oqimli nasoslarning haddan tashqari ko'payishi bilan bog'liq bo'lgan boshqa qarshiliklar ham qayd etilgan. JSST ma'lumotlariga ko'ra, klaritromitsinning HPga chidamliligi antibiotiklarni tadqiq qilish va ishlab chiqish uchun birinchi o'rinda turadi.

2.5. Kampilobakteriyalar- ftorxinolonlarga chidamli

Kampilobakteriya Gram-manfiy bakteriyalar, odatda, ifloslangan yoki pishmagan ovqatni iste'mol qilgandan so'ng, odam va hayvonlarga gastroenterit kabi infektsiyani keltirib chiqaradi. Kampilobakteriyalar va Kampilobakteriyalar bir nechta hayvonlarning parranda go'shti kabi kolonizatsiyalanadigan keng tarqalgan patogen turlari. Davolash uchun antibiotiklar kerak emas, chunki u odatda o'z-o'zidan o'tib ketadi, lekin og'ir holatlarda siprofloksatsin kabi FQ ishlatiladi. 1980 -yillarda FQ qarshiligi Kampilobakteriya xabar qilingan va tez tarqaldi, bu mustaqil mutatsiya va qarshilik DNKning shtammlar orasidagi gorizontal o'tkazilishi, C257T ning bir nuqtali mutatsiyasi. gyrA Gen siprofloksatsinga chidamli shtammlarda qayd etilgan, natijada giraza A bo'linmasida aminokislotalar almashtiriladi. FQ ga qarshilikni haddan tashqari ifodalash orqali oshirish mumkin CmeABC efflux nasosi, 16 bp teskari takroriy (IQ) mutatsiya cmeR –cmeABC genlararo mintaqasi va agar mutant chastotali gen kamaysa o'zgarishi (mfd) [19,20].

2.6. Salmonella spp.- Ftorxinolonga chidamli

Salmonellalar gram-manfiy bakteriyalar bo'lib, ular ikki guruhga bo'linadi: tifoidal Salmonella va tifoid bo'lmagan Salmonella (NTS) odamlar uchun patogen hisoblanadi. MDR kirish Salmonella Ampitsillin, xloramfenikol va trimetoprim/sulfametoksazol FQ siprofloksatsin va uchinchi avlod sefalosporin seftriaksonni intensiv ishlatilishiga olib keldi, bu esa bu dorilarga qarshilikning tez rivojlanishiga olib keldi. Bu FQ-ga chidamli reytingining sababi edi Salmonella 2017 yilda JSST tomonidan yangi antibiotiklarni tadqiq qilish va ishlab chiqish uchun ustuvor patogen sifatida.

Xinolonlarga qarshilik xromosomaning xinolon qarshiligini aniqlaydigan hududlaridagi (QRDR) mutatsiyalar kabi ko'plab mexanizmlarning natijasidir. gyr va par xinolonning topoizomeraza fermentlariga past bog'lanishiga olib keladigan genlar. Boshqa mexanizm-plazmid vositachiligidagi xinolon qarshiligi (PMQR) Qnr genes which provide physical protection from quinolones, the aac(6′)-lb-crgene decreases FQ activity, and oqxAB va qepA encodes quinolone efflux pumps [21].

2.6.1. Typhoidal Salmonella Resistance

In the seventies, chloramphenicol was the treatment of choice for enteric fever caused by Salmonella Typhi, but chloramphenicol-resistant strain starts to appear due to determinant located on a self-transmissible plasmid of the HI1 incompatibility type (IncHI). This led to an increase in the use of ampicillin and trimethoprim-sulfamethoxazole to the 1980s when their resistance was reported from multiple countries. Ciprofloxacin was used as an alternative treatment after the spread of MDR Salmonella Typhi in 1992 [22].

2.6.2. Non-typhoidal Salmonella Resistance

In the eighties, MDR Salmonella Typhimurium began to appear and was associated with a phage-type called definitive type 104 (DT104). The isolates are resistant to ampicillin, chloramphenicol, streptomycin, sulfonamides, and tetracycline. FQ resistance was developed among non-typhoidal Salmonella after the introduction of FQs as an alternative treatment [22].

2.7. Neisseria gonorrhoeae

Neisseria gonorrhoeae is a Gram-negative diplococcus and an obligatory human pathogen responsible for the sexually transmitted disease gonorrhea. The gonococcus can infect different mucosal surfaces such as urethra, endo-cervix, pharynx, conjunctiva and the rectum [23]. The spread of gonococcal infections is due to the ability of N. gonorrhea to acquire resistance to antibiotics like penicillin, tetracycline, and quinolones. In 1936 sulfonamides were the best treatment for gonococcal but resistance developed shortly thereafter. In 1940s penicillin was introduced and penicillinase-producing N. gonorrhoeae (PPNG) was spread, which led to a switch to alternative therapy. Tetracyclines were widely used in some developing countries and the first reports of tetracycline resistant N. gonorrhea e(TRNG) appeared in 1985 [24].

2.7.1. Neisseria gonorrhoeae- 3rd Generation Cephalosporin-Resistant

Third-generation cephalosporins have broader activity against Gram-negative bacteria and are used frequently to treat N. gonorrhoeae. Resistance to cephalosporins started to develop and spread in Asia and the United States in the 1990s then to Australia and Europe in the 2000s.There are several mechanisms for cephalosporins resistance: (1) altered PBPs N. gonorrhoeae has three penicillin-binding proteins (PBPs), alteration in PBP2 by the penA gene results in decreasing the binding of penicillin through a single amino acid insertion (Asp-345a). This alteration is mostly related to cephalosporin resistance, (2) changes in penA transpeptidase domain to form mosaic penA responsible for most observed reduced susceptibility to cephalosporins such as cefixime. (3) A reduction of intracellular antimicrobial concentration by preventing its entry or actively pumping by efflux pumps like the MtrC-D-E system, a mutation in the mtrR gene which results in increasing efflux and resistance to antibiotics. Finally, (4) mutations in the penB porin gene reduce permeability to antimicrobial agents [25].

2.7.2. Neisseria gonorrhoeae- Fluoroquinolone-Resistant

Quinolones affect the activity of DNA gyrase and topoisomerase IV, resistance to ciprofloxacin is mediated by mutations in quinolone resistance determining region (QRDR), single or more mutation in amino acids in gyrA positions 91, 95 and 102, and point mutation in parC genes which code for the DNA gyrase and topoisomerase IV proteins led to increasing resistance to ciprofloxacin and prevented it from binding to their target enzymes. Other mechanisms of FQ resistance include overexpression of efflux pumps like NorM pumps and decrease the permeability of antimicrobial agents by a reduction in the outer membrane porin protein expression [26,27].

2.8. Haemophilus influenza- Ampicillin-resistant

Haemophilus influenza are Gram-negative, coccobacilli, facultatively anaerobic bacteria that have two types based on its polysaccharide: (1) capsulated with six serotypes from a ga f or (2) non-capsulated [28]. Pneumonia, meningitis, and bacteremia are the major diseases caused by type b strain H. influenza while community-acquired pneumonia, acute otitis media, and sinusitis are commonly caused by a non-capsulated form [29].

Ampicillin, which inhibits the synthesis of the cell wall, is the main treatment against H. influenza. The mechanism of resistance is either by acquired β- lactamases or by PBP target modifications or efflux mechanisms [28]. Resistance to ampicillin is mediated by the production of the β-lactamase TEM-1 or ROB-1 (TEM-1 and ROB-1 are two β-lactamases identified in Haemophilus influenza), which causes a decrease in the affinity of penicillin-binding proteins. H. Influenza isolates are classified according to their ampicillin resistance mechanism into a β-lactamase negative, ampicillin-sensitive (BLNAS) strains, β-lactamase positive, ampicillin-resistant (BLPAR) strains, BLNAR strains, and BLPACR strains.

Resistance in BLNAR strains are due to PBP 3 amino acid substitutions (as a result of an acquisition of point mutations in the ftsI gene by antibiotic pressure) and are classified into three groups (I, II, and III) according to Ubukata et al. and Dabernat et al., however, BLPACR are more resistance to amoxicillin-clavulanate, chloramphenicol, and cefuroxime than BLNAS strains and all strains of BLPACR had TEM-1 type β-lactamase and multiple mutations within the ftsI gene [30]. High levels of resistance among H. Influenza encouraged the WHO to recognize it in the list of medium-priority antimicrobial-resistant pathogens.

2.9. Shigella spp.- Fluoroquinolone-Resistant

Shigella seps is a Gram-negative bacterium including four types: Shigella flexneri (the most predominant), Shigella sonnei, Shigella boydiiva Shigella dysenteriae. Shigella infection causes acute dysentery or chronic diarrhea.

FQs are the best treatment for Shigella infection but antimicrobial resistance reduces the effectiveness of this antibiotic. FQ resistance is associated with multiple mutations in the quinolone resistance determining region (QRDR) that encodes DNA gyrase (gyrA and gyrB) and topoisomerase IV (parC and parE). This is in addition to plasmid-mediated quinolone resistance due toQnr genes and efflux pump mediators like mdfA, tolC, ydhE and marA [31,32].


GRAM STAIN:

The Gram stain is the most important and universally used staining technique in the bacteriology laboratory. It is used to distinguish between gram (+) and gram (-) bacteria. The difference between gram (+) and gram (-) bacteria lies in the ability of the cell wall of the organism to retain the crystal violet.

18. Use the slides that you already prepared (1) S. epidermidis (2) P. aeruginosa (3) S. epidermidis and P. aeruginosa mixed together.

19. Stain with crystal violet for 1 minute, then rinse gently with water.

20. Treat with iodine mixture for 1 minute, then rinse gently with water.


3. Pseudomonas aeruginosa: CPO

Pseudomonas infection is caused by strains of Gram-negative bacteria found widely in the environment. It is an opportunistic infection that causes disease in plants and animals, and humans.

Severe Pseudomonas infections usually occur in people in the hospital and/or with weakened immune systems e.g. cancer patients, on chemotherapy, suffering from HIV/AIDS, etc. Cystic fibrosis patients are especially at risk. Patients in hospitals, especially those on respirators, those with devices such as catheters, and patients with wounds from surgery or from burns are potentially at risk for serious, life-threatening infections.


Biologiya 171

Ushbu bo'lim oxirida siz quyidagilarni qila olasiz:

  • Describe the basic structure of a typical prokaryote
  • Describe important differences in structure between Archaea and Bacteria

There are many differences between prokaryotic and eukaryotic cells. The name “prokaryote” suggests that prokaryotes are defined by exclusion—they are not eukaryotes, or organisms whose cells contain a nucleus and other internal membrane-bound organelles. However, all cells have four common structures: the plasma membrane, which functions as a barrier for the cell and separates the cell from its environment the cytoplasm, a complex solution of organic molecules and salts inside the cell a double-stranded DNA genome, the informational archive of the cell and ribosomes, where protein synthesis takes place. Prokaryotes come in various shapes, but many fall into three categories: cocci (spherical), bacilli (rod-shaped), and spirilli (spiral-shaped) ((Figure)).


The Prokaryotic Cell

Recall that prokaryotes are unicellular organisms that lack membrane-bound organelles or other internal membrane-bound structures ((Figure)). Their chromosome—usually single—consists of a piece of circular, double-stranded DNA located in an area of the cell called the nucleoid . Most prokaryotes have a cell wall outside the plasma membrane. The cell wall functions as a protective layer, and it is responsible for the organism’s shape. Some bacterial species have a capsule outside the cell wall. The capsule enables the organism to attach to surfaces, protects it from dehydration and attack by phagocytic cells, and makes pathogens more resistant to our immune responses. Some species also have flagella (singular, flagellum) used for locomotion, and pili (singular, pilus) used for attachment to surfaces including the surfaces of other cells. Plasmids, which consist of extra-chromosomal DNA, are also present in many species of bacteria and archaea.


Recall that prokaryotes are divided into two different domains, Bacteria and Archaea, which together with Eukarya, comprise the three domains of life ((Figure)).


Characteristics of bacterial phyla are described in (Figure) and (Figure). Major bacterial phyla include the Proteobacteria, the Chlamydias, the Spirochaetes, the photosynthetic Cyanobacteria, and the Gram-positive bacteria. The Proteobacteria are in turn subdivided into several classes, from the Alpha- to the Epsilon proteobacteria. Eukaryotic mitochondria are thought to be the descendants of alphaproteobacteria, while eukaryotic chloroplasts are derived from cyanobacteria. Archaeal phyla are described in (Figure).




The Plasma Membrane of Prokaryotes

The prokaryotic plasma membrane is a thin lipid bilayer (6 to 8 nanometers) that completely surrounds the cell and separates the inside from the outside. Its selectively permeable nature keeps ions, proteins, and other molecules within the cell and prevents them from diffusing into the extracellular environment, while other molecules may move through the membrane. Recall that the general structure of a cell membrane is a phospholipid bilayer composed of two layers of lipid molecules. In archaeal cell membranes, isoprene (phytanyl) chains linked to glycerol replace the fatty acids linked to glycerol in bacterial membranes. Some archaeal membranes are lipid monolayers instead of bilayers ((Figure)).


The Cell Wall of Prokaryotes

The cytoplasm of prokaryotic cells has a high concentration of dissolved solutes. Therefore, the osmotic pressure within the cell is relatively high. The cell wall is a protective layer that surrounds some cells and gives them shape and rigidity. It is located outside the cell membrane and prevents osmotic lysis (bursting due to increasing volume). The chemical composition of the cell wall varies between Archaea and Bacteria, and also varies between bacterial species.

Bacterial cell walls contain peptidoglycan , composed of polysaccharide chains that are cross-linked by unusual peptides containing both L- and D-amino acids including D-glutamic acid and D-alanine. (Proteins normally have only L-amino acids as a consequence, many of our antibiotics work by mimicking D-amino acids and therefore have specific effects on bacterial cell-wall development.) There are more than 100 different forms of peptidoglycan. S-layer (surface layer) proteins are also present on the outside of cell walls of both Archaea and Bacteria.

Bacteria are divided into two major groups: Gram -musbat va Gram -manfiy , based on their reaction to Gram staining. Note that all Gram-positive bacteria belong to one phylum bacteria in the other phyla (Proteobacteria, Chlamydias, Spirochetes, Cyanobacteria, and others) are Gram-negative. The Gram staining method is named after its inventor, Danish scientist Hans Christian Gram (1853–1938). The different bacterial responses to the staining procedure are ultimately due to cell wall structure. Gram-positive organisms typically lack the outer membrane found in Gram-negative organisms ((Rasm)). Up to 90 percent of the cell-wall in Gram-positive bacteria is composed of peptidoglycan, and most of the rest is composed of acidic substances called teichoic acids. Teichoic acids may be covalently linked to lipids in the plasma membrane to form lipoteichoic acids. Lipoteichoic acids anchor the cell wall to the cell membrane. Gram-negative bacteria have a relatively thin cell wall composed of a few layers of peptidoglycan (only 10 percent of the total cell wall), surrounded by an outer envelope containing lipopolysaccharides (LPS) and lipoproteins. This outer envelope is sometimes referred to as a second lipid bilayer. The chemistry of this outer envelope is very different, however, from that of the typical lipid bilayer that forms plasma membranes.


Quyidagi gaplarning qaysi biri to'g'ri?

  1. Gram-positive bacteria have a single cell wall anchored to the cell membrane by lipoteichoic acid.
  2. Porins allow entry of substances into both Gram-positive and Gram-negative bacteria.
  3. The cell wall of Gram-negative bacteria is thick, and the cell wall of Gram-positive bacteria is thin.
  4. Gram-negative bacteria have a cell wall made of peptidoglycan, whereas Gram-positive bacteria have a cell wall made of lipoteichoic acid.

Archaean cell walls do not have peptidoglycan. There are four different types of archaean cell walls. One type is composed of pseudopeptidoglycan , which is similar to peptidoglycan in morphology but contains different sugars in the polysaccharide chain. The other three types of cell walls are composed of polysaccharides, glycoproteins, or pure protein. Other differences between Bacteria and Archaea are seen in (Figure). Note that features related to DNA replication, transcription and translation in Archaea are similar to those seen in eukaryotes.

Differences and Similarities between Bacteria and Archaea
Structural Characteristic Bakteriyalar Arxeya
Cell type Prokaryotic Prokaryotic
Cell morphology O'zgaruvchan O'zgaruvchan
Cell wall Contains peptidoglycan Does not contain peptidoglycan
Cell membrane type Lipid bilayer Lipid bilayer or lipid monolayer
Plasma membrane lipids Fatty acids-glycerol ester Phytanyl-glycerol ethers
Chromosome Typically circular Typically circular
Replication origins Yagona Ko'p
RNK polimeraza Yagona Ko'p
Initiator tRNA Formyl-methionine Metionin
Streptomycin inhibition Sensitive Resistant
Calvin cycle Ha Yo'q

Qayta ishlab chiqarish

Reproduction in prokaryotes is jinssiz and usually takes place by binary fission. (Recall that the DNA of a prokaryote is a single, circular chromosome.) Prokaryotes do not undergo mitosis instead, the chromosome is replicated and the two resulting copies separate from one another, due to the growth of the cell. The prokaryote, now enlarged, is pinched inward at its equator and the two resulting cells, which are klonlar, separate. Binary fission does not provide an opportunity for genetic recombination or genetic diversity, but prokaryotes can share genes by three other mechanisms.

In transformation , the prokaryote takes in DNA shed by other prokaryotes into its environment. If a nonpathogenic bacterium takes up DNA for a toxin gene from a pathogen and incorporates the new DNA into its own chromosome, it too may become pathogenic. In transduction , bacteriophages, the viruses that infect bacteria, may move short pieces of chromosomal DNA from one bacterium to another. Transduction results in a recombinant organism. Archaea also have viruses that may translocate genetic material from one individual to another. In conjugation , DNA is transferred from one prokaryote to another by means of a pilus, which brings the organisms into contact with one another, and provides a channel for transfer of DNA. The DNA transferred can be in the form of a plasmid or as a composite molecule, containing both plasmid and chromosomal DNA. These three processes of DNA exchange are shown in (Figure).

Reproduction can be very rapid: a few minutes for some species. This short generation time coupled with mechanisms of genetic recombination and high rates of mutation result in the rapid evolution of prokaryotes, allowing them to respond to environmental changes (such as the introduction of an antibiotic) very quickly.


The Evolution of Prokaryotes How do scientists answer questions about the evolution of prokaryotes? Unlike with animals, artifacts in the fossil record of prokaryotes offer very little information. Fossils of ancient prokaryotes look like tiny bubbles in rock. Some scientists turn to genetics and to the principle of the molecular clock, which holds that the more recently two species have diverged, the more similar their genes (and thus proteins) will be. Conversely, species that diverged long ago will have more genes that are dissimilar.

Scientists at the NASA Astrobiology Institute and at the European Molecular Biology Laboratory collaborated to analyze the molecular evolution of 32 specific proteins common to 72 species of prokaryotes. 1 The model they derived from their data indicates that three important groups of bacteria—Actinobacteria, Deinokok, and Cyanobacteria (collectively called Terrabacteria by the authors)—were the first to colonize land. Actinobacteria are a group of very common Gram-positive bacteria that produce branched structures like fungal mycelia, and include species important in decomposition of organic wastes. You will recall that Deinokok is a genus of bacterium that is highly resistant to ionizing radiation. It has a thick peptidoglycan layer in addition to a second external membrane, so it has features of both Gram-positive and Gram-negative bacteria.

Cyanobacteria are photosynthesizers, and were probably responsible for the production of oxygen on the ancient earth. The timelines of divergence suggest that bacteria (members of the domain Bacteria) diverged from common ancestral species between 2.5 and 3.2 billion years ago, whereas the Archaea diverged earlier: between 3.1 and 4.1 billion years ago. Eukarya later diverged from the archaean line. The work further suggests that stromatolites that formed prior to the advent of cyanobacteria (about 2.6 billion years ago) photosynthesized in an anoxic environment and that because of the modifications of the Terrabacteria for land (resistance to drying and the possession of compounds that protect the organism from excess light), photosynthesis using oxygen may be closely linked to adaptations to survive on land.

Bo'lim haqida qisqacha ma'lumot

Prokaryotes (domains Archaea and Bacteria) are single-celled organisms that lack a nucleus. They have a single piece of circular DNA in the nucleoid area of the cell. Most prokaryotes have a cell wall that lies outside the boundary of the plasma membrane. Some prokaryotes may have additional structures such as a capsule, flagella, and pili. Bacteria and Archaea differ in the lipid composition of their cell membranes and the characteristics of the cell wall. In archaeal membranes, phytanyl units, rather than fatty acids, are linked to glycerol. Some archaeal membranes are lipid monolayers instead of bilayers.

The cell wall is located outside the cell membrane and prevents osmotic lysis. The chemical composition of cell walls varies between species. Bacterial cell walls contain peptidoglycan. Archaean cell walls do not have peptidoglycan, but they may have pseudopeptidoglycan, polysaccharides, glycoproteins, or protein-based cell walls. Bacteria can be divided into two major groups: Gram positive and Gram negative, based on the Gram stain reaction. Gram-positive organisms have a thick peptidoglycan layer fortified with teichoic acids. Gram-negative organisms have a thin cell wall and an outer envelope containing lipopolysaccharides and lipoproteins.

Prokaryotes can transfer DNA from one cell to another by three mechanisms: transformation (uptake of environmental DNA), transduction (transfer of genomic DNA via viruses), and conjugation (transfer of DNA by direct cell contact).


Types of Eubacteria

Bacteria commonly take on one of three shapes: bacilli, cocci, and spirilla. Bacilli have a rod shape, cocci have a spherical shape, and spirilla have a spiral or wave shape. Their shape was often used as a classification system until recent DNA studies cast doubt on these classifications. Bacteria may stay linked after division, forming other shapes such as clusters, filaments, and tight coils.

Eubacteria are typically classified into Gram-positive, Gram-negative, and Miscellaneous. While there are many phyla of eubacteria under the Domain Bacteria, these relationships are often changing and are still being defined based on new DNA experiments.

Some bacteria have an additional layer enclosing the cell wall referred to as the bacterial outer membrane. This extra layer cannot be dyed with a Gram stain that is often used to classify bacteria by researchers. Thus, they are referred to as “Gram-negative” bacteria or Bacteria that can be seen with a Gram stain are referred to as Gram-positive. Typically, Gram-negative bacteria contain more species that are pathogenic to humans, whereas Gram-positive bacteria are either beneficial or not harmful to human health.


Hemolysis

Hemolysis serves to differentiate streptococci based on the various types of hemoglobin degradation

  • Alpha hemolysis
    • Hemoglobin present in the agar is partially oxidized → methemoglobin, a substance with a characteristic biliverdin-green color ( green hemolysis ).
    • Characteristic of gram‑positivecocci (e.g., S. pneumoniae , viridans streptococci)
    • Complete degradation of hemoglobin with a translucent halo around the bacterial colony.
    • Characteristic of gram‑positivecocci (e.g., S. aureus , S. pyogenes , S. agalactiae )
    • Lancefield groups : further classify β-hemolyticstreptococci according to the specific bacterial cell wallcarbohydrate composition

    Bo'lim haqida qisqacha ma'lumot

    Prokaryotes (domains Archaea and Bacteria) are single-celled organisms that lack a nucleus. They have a single piece of circular DNA in the nucleoid area of the cell. Most prokaryotes have a cell wall that lies outside the boundary of the plasma membrane. Some prokaryotes may have additional structures such as a capsule, flagella, and pili. Bacteria and Archaea differ in the lipid composition of their cell membranes and the characteristics of the cell wall. In archaeal membranes, phytanyl units, rather than fatty acids, are linked to glycerol. Some archaeal membranes are lipid monolayers instead of bilayers.

    The cell wall is located outside the cell membrane and prevents osmotic lysis. The chemical composition of cell walls varies between species. Bacterial cell walls contain peptidoglycan. Archaean cell walls do not have peptidoglycan, but they may have pseudopeptidoglycan, polysaccharides, glycoproteins, or protein-based cell walls. Bacteria can be divided into two major groups: Gram positive and Gram negative, based on the Gram stain reaction. Gram-positive organisms have a thick peptidoglycan layer fortified with teichoic acids. Gram-negative organisms have a thin cell wall and an outer envelope containing lipopolysaccharides and lipoproteins.

    Prokaryotes can transfer DNA from one cell to another by three mechanisms: transformation (uptake of environmental DNA), transduction (transfer of genomic DNA via viruses), and conjugation (transfer of DNA by direct cell contact).