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O'lik hujayralar doimo yadroga ega emasmi?

O'lik hujayralar doimo yadroga ega emasmi?



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Agar men o'lik hujayrani tekshirsam, uning yadrosi yo'qligiga ishonch hosil qila olamanmi?

Boshqa organellalar haqida nima deyish mumkin?


Agar siz standart apoptoz tufayli o'lim sababini qidirsangiz, jarayonni boshlash uchun sitoxrom c mitoxondriyadan ajralib chiqadi, apaf-1 bilan bog'lanadi va strukturaviy o'zgarishlarga uchraydi, natijada biokimyoviy ninja yulduziga o'xshaydi (4-rasm). ). Bu kaspaza-9 ni faollashtiradi, bu esa boshqa ijrochi kaspazalarni faollashtiradi va natijada oqsilni parchalovchi fermentlarning ko'chkisini hosil qiladi, bu hujayra tuzilishi va organellalarini qog'oz machega o'xshatadi. Yadroga kelsak, DNKning yaxlitligi va tuzilishini saqlab turish uchun mo'ljallangan fermentlar komplekslari buziladi, DNKning hujayraga tarmoq ta'siri asosan inert bo'ladi va DNK nukleazlar tomonidan kondensatsiyalanadi va parchalanadi. Yadro membranasi oqsillar va ribosomalar bilan to'la bo'lib, ular ham parchalanadi. Agar siz inert yadroni oddiygina skeleti bo‘yicha aniqlamoqchi bo‘lsangiz, siz ham unchalik muvaffaqiyatga erisha olmasligingiz mumkin – bu yerda yadroviy strukturaning bosqichma-bosqich yo‘q qilinishini ko‘rsatuvchi yaxshi tadqiqotdan bir nechta yaxshi suratlar.


Yo'q, haqiqatan ham, mRNK vaktsinalari DNKingizga ta'sir qilmaydi

Qisqa versiya: mRNK vaktsinalari sizning DNKingizni o'zgartirishining ishonchli usuli yo'q. Bu hujayra biologiyasi haqida biz bilgan hamma narsani buzadi.

Yaqinda men mRNK vaktsinalari DNKimizga ta'sir qilmasligiga qanday ishonch hosil qilishimiz mumkinligi haqida ko'plab savollar oldim. Mavzu bo'yicha oldingi postimda shunday yozgan edim:

Ko'tarilgan yana bir tashvish mRNK qandaydir tarzda uy egasining genomini o'zgartirishi mumkin degan fikr edi. Bu aslida juda zo'r bo'lardi va gen terapiyasi uchun juda katta bo'lar edi (va nihoyat o'zimga doimo xohlagan ulkan ko'rshapalak qanotlarini berishim mumkin edi), lekin bu unday emas. Bu, odatda, imkonsizdir, bundan tashqari, RNK shablonidan DNK ishlab chiqaradigan teskari transkriptaza fermenti mavjud bo'lsa, retroviruslar qanday ishlaydi. Har qanday mRNK vaktsina nomzodida bunday xavf yo'q. mRNK vaktsinalari to'liq hujayra sitozolida ishlaydi - ular barcha DNK joylashgan yadroga yaqinlashmaydi. Bu aslida RNKga asoslangan vaktsinalarning DNKga nisbatan katta afzalligi.

Men bu javobni katta qismda berdim, chunki men teskari transkripsiya, yadro savdosi, endotsitik yo'l va boshqa 11 yoki shunga o'xshash ilg'or hujayra biologiyasi mavzularini batafsil muhokama qilish juda murakkab ekanligini his qildim va bunga jiddiy javob berish uchun murojaat qilishim kerak edi. Buning mumkinmi yoki yo'qligini bilishni istagan oddiy odam uchun foydali bo'lishi. Biroq, menda retroviruslar yoki gepadnaviruslar (gepatit B) bilan bog'liq "agar bo'lsa, nima bo'ladi" degan ko'plab savollar bor edi va men bu javob bunga javob bermasligini tan olaman, shuning uchun bu erda men bunga aniq va minimal murakkablik bilan javob berishga harakat qilaman. men qodir ekanman.

Fosfolipid ikki qatlamlarining fazalarini va lipid nanopartikullarining molekulyar tarkibini barqarorlikka taalluqli (1, 2, 3, 4-bandlarda muhokama qilingan) tushuntirishga majbur bo'lmaslik uchun muhokamani soddalashtirish uchun men o'quvchilardan mRNKni tabiiy deb bilishlarini so'rayman. vaktsinalar endotsitozlanadi va hujayra sitoplazmasida chiqariladi (va bu).

Birinchidan, mRNK sizning DNKingizga ta'sir qilishi uchun, hech bo'lmaganda, u DNKga kirishi kerakligini aniqlashimiz kerak. Buni amalga oshirish mumkin bo'lgan ikkita subcellular bo'linma mavjud. Birinchisi - yadro, shuning uchun yadrodagi yuklarning savdosini muhokama qilishdan boshlaylik. Hujayra yadrosi erkin kirishi mumkin bo'lgan zarrachalarning o'lchamiga cheklovlar qo'yadigan gözenek komplekslari (NPC) bilan ajratilgan bo'linmadir. Transkripsiya yadroda sodir bo'lganligi sababli RNK osongina tashqariga chiqariladi, ammo oqsillarni ishlab chiqarish uchun zarur bo'lgan ribosomalar sitozolda yoki qo'pol endoplazmatik retikulumda bo'ladi. Bu jarayon chap tomonda ko'rishingiz mumkin bo'lgan bir nechta yordamchi oqsillar tomonidan amalga oshiriladi. Shuni yodda tutingki, sitozoldan RNKni yadroga qaytarish uchun zarur bo'lgan fiziologik holat yo'q. RNK yadroda sintezlanadi. Replikatsiya siklida yadro fazasiga ega bo'lgan viruslar RNK yukini kiritishiga imkon berish uchun turli xil fokuslarga ega bo'lishi kerak. RNK hujayralarga oson ko'chirilmasa ham, oqsillar bo'lishi mumkin. Bu importinlar deb ataladigan oqsillar tarmog'i orqali sodir bo'ladi (yuqoridagi 5-23C rasmga qarang). Yadro lokalizatsiyasi ketma-ketligi deb ataladigan aminokislotalar ketma-ketligini o'z ichiga olgan oqsillar (NLS ikkita keng tarqalgan) importinlarni bog'lashi mumkin, so'ngra ularni chapda ko'rsatilganidek, yadro gözenek kompleksi bo'ylab tashishi mumkin. RNK viruslari ko'pincha yadroga kirishni talab qilmaydigan replikatsiya davrlariga ega, ammo ba'zi istisnolar mavjud. Gripp viruslari, masalan, RNK viruslari bo'lib, ularning genomlari ribonukleoproteinlar bilan bog'liq va bu ribonukleoproteinlar o'zlarining genomik RNKlarining yadroga kirishini osonlashtiradigan yadro lokalizatsiya signallarini ifodalaydi. Boshqa tomondan, mRNK vaktsinalari hech qanday oqsil bilan bog'liq emas. Sitozolga kirgandan so'ng, mRNK yalang'och bo'lib, mRNKni bir necha soat ichida (ko'pi bilan) yo'q qiladigan ribosomalar va ekzonukleazlarning qattiq muhitiga duchor bo'ladi. mRNK o'z-o'zidan yadroga o'tishi mumkin bo'lgan hech qanday mexanizm mavjud emas. Nukleotidlardan tashkil topgan bo'lib, u yadroviy lokalizatsiya ketma-ketligini o'z ichiga olmaydi.

Boshqa tegishli bo'linma mitoxondriya bo'ladi. Mitoxondriyalar aslida o'z genomlariga ega bo'lgan vestigial bakteriyalar bo'lib, milliardlab yillar oldin qadimiy bakteriyalar mitoxondriyalarning ajdodini iste'mol qilishga uringan, ammo hazm qilish uchun mexanizm yo'q edi va ikkalasi simbiotik munosabatlar o'rnatdilar. O'sha paytdan beri mitoxondriya bizning hujayra biologiyasining muhim xususiyati bo'lib kelgan. Bu mitoxondriyaga atigi 37 genni o'z ichiga olgan juda kamaytirilgan genomni ishlab chiqishga imkon berdi (mitoxondriyal funktsiyaga tegishli genlarning aksariyati hali ham yadroda). Mitoxondriyalarning o'z ribosomalari va hatto o'zlarining genetik kodlari (turi). Shuningdek, kasal mitoxondriyalarni tozalash uchun maxsus jarayon mavjud mitofagiya, bu ko'plab ajoyib sharhlar mavzusidir, masalan. bu, bu va bu.

Ushbu biologik jarayonni tushunishimizdan kelib chiqadigan umumiy xulosa shundan iboratki, sitozoldagi yalang'och mRNK o'z DNKimizni o'z ichiga olgan hujayra bo'linmasida tugaydi, degani, boshqa omillar mavjudligi yoki yo'qligidan qat'i nazar, hech qanday imkoniyat yo'q. mRNK vaktsinasining DNKga zarari. Ammo baribir odamlar mendan teskari transkriptazalar haqida so'rashni xohlashdi, shuning uchun ularni muhokama qilaylik.

RNK dan DNK ga o'tish jarayoni (molekulyar biologiyaning markaziy aqidasi belgilaydigan narsaga mutlaqo zid) deb nomlanadi. teskari transkripsiya, va u a deb ataladigan ferment bilan amalga oshiriladi teskari transkriptaza (bu haqiqatan ham qiziqarli fermentlar guruhidir). Umuman olganda, teskari transkripsiya bir necha xil genetik shaxslar tomonidan amalga oshiriladi: retroviruslar, gepadnaviruslar, telomerlarva retrotranspozonlar. Bularni aniqlashga arziydi.

  • Retroviruslar - bu RNK genomiga ega bo'lgan viruslar bo'lib, ular teskari transkripsiya orqali DNK nusxasini yaratadilar, so'ngra xostning hujayrasiga integratsiyalashadi (bu orqali o'zini xost hujayra genomiga kiritib, uning doimiy qismiga aylanadi). a deb ataladigan ketma-ketlik shaklida provirus). Keyin proviral ketma-ketlikning o'zi keyingi hujayraga tarqalishi mumkin bo'lgan virusli oqsillar va zarrachalarni ishlab chiqarish uchun xost hujayrasida transkripsiya qilinishi mumkin. Eng mashhur retrovirus OIV-1 hisoblanadi.
  • Gepadnaviruslar DNK viruslari bo'lib, genomlari bo'shliqqa ega (bir to'liq DNK zanjiri va pregenomik RNK bilan bog'langan boshqa qisman DNK zanjiri mavjud) va retroviruslardan farqli o'laroq, ular yuqtirgan xost hujayralarining genomiga qo'shilmaydi. Eng mashhur misol Gepatit B virusi bo'lib, unga qarshi ko'plab samarali vaktsinalar mavjud.
  • Telomerlar inson xromosomalarining uchlarida joylashgan tuzilmalar bo'lib, ularni saqlash uchun TERT deb ataladigan teskari transkriptazadan foydalanadigan telomeraza deb ataladigan protein kompleksi tomonidan saqlanadi. Buning zarurligi sabablari chapdagi 9-12-rasmda muhokama qilinadi. Ular odatda 5-15 kilobaza uzunlikda bo'lib, ularning qisqarishi hujayra o'sishi va replikatsiyasining to'xtatilishiga olib keladi (qariylik) yoki hatto apoptoz orqali hujayra o'limiga olib kelishi mumkin.
  • Retrotranspozonlar aslida bizning genomimizning eng keng tarqalgan tarkibiy qismidir. Inson genomida 21 000 dan 27 000 gacha genlar mavjud (siz olingan son genni qanchalik aniq aniqlaganingizga va qaysi manbaga murojaat qilishingizga bog'liq), ular 40-48 million tayanch juftni o'z ichiga oladi, ammo bu 3,2 milliarddan atigi 1,5% ni tashkil qiladi. umumiy tayanch juftliklari. Retrotranspozonlar taxminan 2 milliard tayanch juftlikni tashkil qiladi. Retroelementlarning bir nechta turlari mavjud, ular batafsilroq muhokama qilishga arziydi:

  1. SINElar (qisqa kesilgan yadroviy elementlar) tRNK kabi qisqa transkriptlarni kodlaydi va LINE kodlangan oqsilsiz ishlay olmaydi.
  2. Chiziqlar (uzoq kesishgan yadroviy elementlar) ORF1 va pol genlaridan hosil bo'lgan teskari transkriptazani kodlaydi, ular o'zini va boshqa LINE va SINE elementlarini genomning boshqa hududlariga nusxalashi mumkin.
  3. Inson genomining taxminan 5-8% ni ham tashkil qiladi insonning endogen retroviruslari, HERV, bu ham retrotranspozonlar toifasiga kiradi, aniqrog'i LTR (uzoq terminal takrorlanadi) retrotranspozonlar (bu haqda birozdan keyin). HERVlar 3 ta genni o'z ichiga oladi: gag (natijadagi retrovirusning tarkibiy oqsillariga bo'linadigan poliproteinni kodlaydigan guruh antijenlari), pol (virusning ko'payishi uchun zarur bo'lgan teskari transkriptaza) va env (konvert, virusni kodlaydigan konvert). Virusli zarrachalarga shaklini beradigan protein).
  4. Kengroq aytganda, atama retroelement teskari transkripsiya orqali genomning bir hududidan boshqasiga o'tgan genetik ketma-ketliklarga ishora qiladi va bularga retrotranspozonlar va qayta ishlangan psevdogenlar kiradi. Qayta ishlangan psevdogenlar teskari transkripsiya orqali kiritilgan intronlarga ega bo'lmagan qayta ishlangan mRNK ketma-ketligiga murojaat qiling (biz bilamizki, ular genomga teskari transkripsiya orqali kiritilishi kerak edi, chunki ularda intronlar yo'q). Ular hech qanday gen mahsulotini ishlab chiqarishga qodir emas.
  5. Genom bo'ylab harakatlanishi mumkin bo'lgan yagona retrotranspozonlar (o'z DNKlarini dastlab mavjud bo'lmagan yangi joylarga ko'chiradi) LINE va SINElardir va ulardan faqat bir nechtasi buni amalga oshirishga qodir. HERVlar o'zlari turgan joyda, qayta ishlangan psevdogenlar ham tiqilib qoladi.

Telomerazalarning yechimi sifatida rivojlangan replikatsiya muammosini tugatish. Yangi paydo bo'lgan (yangi) DNK zanjirlari etakchi va orqada qolgan zanjir bilan sintezlanadi, chunki DNK polimerazalari juda cheklangan yo'nalishga ega, chunki ular shablon zanjiriga nisbatan 3' dan 5' gacha bo'lishi kerak. Bu muammoni keltirib chiqaradi, chunki DNK antiparallel yo'naltirilgan (iplar parallel, lekin bir ip ikkinchisiga qarama-qarshi yo'nalishda yo'naltirilgan), shuning uchun ikkala ipni bir vaqtning o'zida qilish uchun bitta DNK polimeraza bir vaqtning o'zida harakatlanishi kerak bo'ladi. qarama-qarshi yo'nalishlarda (tasvir bir vaqtning o'zida sharqqa va g'arbga 10 milya masofani bosib o'tishga harakat qilish) uchun Sizif uzunligi qanday bo'ladi. Ushbu dilemma bilan shug'ullanish uchun iplardan biri ko'plab nukleotidlar uchun uzluksiz ravishda ip bo'ylab harakatlanadigan polimeraza bilan etakchi ip sifatida sintezlanadi (rasmiy atama "jarayonli ravishda”) va DNK parchalari joylashgan orqada qolgan ip (deb ataladi Okazaki qismlari) bir-biriga bog'langan (biriktirilgan) boshqa ipni to'ldiruvchi doimiy ravishda hosil bo'ladi. Dilemma shundaki, bizning xromosomalarimiz aylana bo'lmaganligi sababli, xromosomaning 3'-uchiga yetganimizdan so'ng, har doim etishmayotgan bo'lak bo'ladi va shuning uchun DNKning har bir replikatsiya sikli genom hajmining kichrayishiga olib keladi, oxir-oqibatda xromosoma hajmi kamayadi. biologik funktsiya uchun muhim genlarni urish potentsiali. Bu oxirgi replikatsiya muammosi sifatida tanilgan.

Chap tomonda siz o'zining sevimli telomeraza RNKiga ega telomeraza kompleksini ko'rasiz. Xromosomaning uchlari telomerlar deb ataladigan tuzilmalarni o'z ichiga oladi, ular takrorlanuvchi, qisqa, palindromik ketma-ketliklar bo'lib, iplar orasidagi bo'shliqlar taxminan 5000 dan 15000 nukleotidlar uzunligiga to'lguncha ko'p marta nusxalanadi. Telomerik DNK ishlab chiqarilishi telomeraza deb ataladigan katta protein kompleksi orqali sodir bo'ladi, bu esa undan foydalanadi TERT (telomeraza teskari transkriptaza), palindromik DNK ketma-ketliklarini yaratish uchun RNK shablonini oladigan teskari transkriptaza. Muhimi shundaki, hujayralar oxir-oqibat telomeraza funktsiyasini yo'qotadi, bu saraton kasalligiga qarshi himoya hisoblanadi (telomerazani yuqori darajada ifodalovchi hujayralar bo'linishda davom etishi va shuning uchun mutatsiyalarni to'plashi mumkin, ularning ba'zilari zararli bo'lishi mumkin - abadiy va shuning uchun aksariyat hujayralarda. 50 ga yaqin bo'linishdan keyin hujayralar bo'linishni to'xtatadi telomeraza ildiz hujayralarida yuqori darajada namoyon bo'ladi). Amalda, funktsional telomerazaga ega bo'lmagan sichqonlar 3 avlod ichida sezilarli xromosoma qisqarishiga ega bo'ladi va to'rtinchi avlodga kelib ko'paya olmaydi. Bu erda men RNK qanday ishlashi haqidagi barcha oldindan o'ylangan g'oyalaringizni buzishim kerak. DNK va RNK haqida gapirganda, biz ipning tasvirini keltirib chiqaradigan "ip" atamasini ishlatishga moyilmiz. Ip nisbatan chiziqli, u egri bo'lishi mumkin, ammo tuzilishi nisbatan zerikarli. Bu ko'pchilik DNKning oqilona taxminidir, chunki DNK asosan A, B va Z deb ataladigan 3 ta tuzilishdan biriga ega bo'lishi mumkin (kamroqlari bor, masalan, i-motiflar va DNKzimlar g'alati narsalarni qilishi mumkin). Boshqa tomondan, RNK tuzilishga kelganda ancha erkin ruhdir. RNK oqsillarga o'xshamaydigan tarzda har xil strukturaviy motivlarga ega bo'lgan murakkab shakllarga aylanadi, chunki oqsilning tuzilishi bevosita uning funktsiyasiga bog'liq. Buning ma'nosi: o'ziga xos RNKlar qanday katlanishlariga qarab, ularning ketma-ketligiga bog'liq bo'lgan muayyan ishlarni bajaradi. O'ng tomonda telomeraza kompleksiga bog'langan telomeraza RNKning batafsil diagrammasini ko'rishingiz mumkin. Narvon va pufakchalar kabi panjaralari bo'lgan egri chiziqli narsa telomeraza RNKidir. TERT, telomerazaning teskari transkriptazasi, telomeraza RNKni yadro domenida va CR4/CR5 deb ataladigan mintaqada bog'laydi. Men kompleksning boshqa tarkibiy qismlariga kirmayman, lekin bu erda va bu erda qanday ishlashi haqida batafsil o'qishingiz mumkin. Darhol o'ng tomoningizdagi diagramma ostida siz telomerazaning takrorlanuvchi palindromik RNK ketma-ketligi yordamida xromosomaning 3' qopqog'ini kengaytirish uchun qanday ishlashini ko'rishingiz mumkin: CAAUCCCAAUC, bu DNKda telomerni hosil qilish uchun takroriy "GGGTTA" ni ko'paytiradi. uzunligi taxminan 5000-15000 nukleotid. Buning ishlashi uchun ko'p narsalar to'g'ri borishi kerak, ammo TERT telomeraza RNKni taniy olishi uchun bu erda bo'lishi kerak: teskari transkripsiya uchun shablon (CCCAAU palindromik ketma-ketligi), psevdoknot domeni (asosiy domen). diagramma), TERT (CR4/CR5) bilan o'zaro ta'sir qiluvchi stend-loop va RNK barqarorligi uchun zarur bo'lgan 3' element (CR7). Bu juda o'ziga xos cheklovlar to'plami va mRNK vaktsinalari ularga ega bo'lishi uchun ishlab chiqilishi kerak (mRNK vaktsinasini standart tashkil qilish uchun yuqoridagi rasmga qarang). Ribosomalar shuningdek, oqsil sintezi uchun o'qilishi va qayta ishlanishi uchun bunday tuzilmalarni yo'q qiladigan ichki mRNK helikaz faolligiga ega. Bundan tashqari, etuk inson telomeraza RNKsi uzunligi 451 nukleotidni tashkil qiladi. Ushbu vaktsinalarning mRNK uzunligi taxminan 1200-1300 nukleotidni tashkil qiladi. U odamlarda telomeraza RNK vazifasini bajarish uchun juda katta (ba'zi hayvonlarda shunday o'lchamdagi telomeraza RNKlari bor, lekin biz ulardan emasmiz) va telomeraza RNK qanchalik aniq katlanishi kerakligini hisobga olsak, u kerakli tuzilmalarni egallashi dargumon. telomerazani tanib olish va bog'lash uchun.

Men dastlab gepadnaviruslarning (ya'ni, gepatit B) va retroviruslarning (ya'ni, OIV va HERV) teskari transkriptazalarini batafsil muhokama qilishni ko'rib chiqdim, lekin tezda muhokama qilish imkonsiz bo'lib qoldi. Shuni aytish kifoya, teskari transkriptazalar har qanday tasodifiy RNKni yig'ishga va undan DNK hosil qilishga qodir emas. Reaksiyani boshlash uchun ular RNK ketma-ketligini talab qiladi. Retroviruslar uchun mezbon hujayradan o'g'irlangan va virionga qadoqlangan tRNK mavjud. Bundan tashqari, retroviruslarda teskari transkripsiya nukleokapsid ichida sodir bo'ladi, bu dNTP (DNKning qurilish bloklari) ga kirishga imkon beradi, lekin taxminan 1200 asosni qamrab olgan butunlay alohida RNK molekulasi kabi katta narsaga ruxsat bermaydi. Gepadnaviruslar tomonidan teskari transkripsiya printsipial jihatdan o'xshash bo'lib, gepadnavirusning DNKsi bilan kimyoviy bog'langan pregenomik RNK segmentini talab qiladi. Har qanday RNK bilan teskari transkripsiya o'z-o'zidan sodir bo'lmaydi. Hatto RT-PCR reaktsiyalari uchun ham reaktsiya oligodeoksitimidin ketma-ketligini ko'rib chiqilayotgan mRNKning poliA dumiga bog'lashni talab qiladi. Bundan tashqari, bu erda uy egasining DNKsini "o'zgartirish" imkoniyatiga ega bo'lish uchun ikkinchi darajali talab mavjud: uni qandaydir tarzda manipulyatsiya qilish. Gepadnaviruslar bo'lsa, bu haqiqatan ham sodir bo'lmaydi. Gepadnavirus genomi yadroga kirib, o'ziga xos gistonlarga ega bo'lgan kovalent yopiq dumaloq DNKni, asosan kichik, alohida xromosomani hosil qiladi. U uy egasining DNKsiga tegmaydi. Retroviruslar holatida DNK xost xromosomasiga integratsiya qilinadi va ta'sir uning integratsiyalashuviga bog'liq. Masalan, OIV o'zini genlarga kiritishda kuchli moyillikka ega, masalan, gen genom yaxlitligini saqlash uchun muhim bo'lgan protein ishlab chiqarsa, bu muammoli bo'lishi mumkin (agar tekshirilmasa, saratonga olib kelishi mumkin). Biroq, bunday jarayondan saraton rivojlanishi boshqa ko'p narsalar noto'g'ri bo'lmasdan sodir bo'lishi mumkin emas, masalan, immunitet tizimining hujayralarni xavfli o'sish va o'ldirishni tekshirish qobiliyatini jiddiy ravishda buzadigan yordamchi T hujayralarining katta o'limi. ular OIVda bo'lgani kabi. Endi biz hujayra biologiyasi qanday ishlashi haqida hozirgacha aniqlangan hamma narsani, shu jumladan teskari transkriptaza reaktsiyasini boshlash uchun primerga bo'lgan ehtiyojni e'tiborsiz qoldirishni tanlasak va retrovirus natijada paydo bo'lgan spike protein RBD yoki butun boshoq oqsili genini osongina integratsiya qilishiga imkon beradi. mezbonga, bu shunchaki spike oqsilini yoki faqat RBD ni yaratishi mumkin bo'lgan genning kiritilishiga olib keladi (u qaerga kiritilganiga va transkripsiya mexanizmini jalb qilishi mumkinligiga qarab), bu faqat immunitetga taqdim etish uchun xizmat qiladi. tizimga qarshi javob berish uchun tayyorlangan begona proteinni yo'q qiladi va keyinchalik hujayrani o'ldiradi. Bundan tashqari, ular mushak ichiga in'ektsiya yo'li bilan yuborilganligi sababli, ko'rib chiqilayotgan hujayralar, ehtimol, mushak hujayrasi (hech qanday ma'noli funktsiyani yo'qotmasdan yo'qotishingiz mumkin) yoki dendritik hujayra (siz uni sezilarli darajada yo'qotmasdan ham yo'qotishingiz mumkin) bo'lishi mumkin. immunologik funktsiya).

Xulosa qilish uchun va umid qilamanki, bu nihoyasiga etadi:


Hujayra yadrosining tuzilishi

Hujayra yadrosi qo'sh membrana bilan o'ralgan bo'lib, bu membrana deb ataladi yadroviy konvert. Bu membrana DNKni fizik va kimyoviy shikastlanishdan qoplaydi va himoya qiladi. Bunda membrana DNK ni qayta ishlash uchun alohida muhit yaratadi. Tashqi membrana sitoplazma bilan aloqada bo'lib, ba'zi joylarda u bilan bog'lanadi. endoplazmatik retikulum. Ichki membrana bilan bog'lanadi yadro qatlami. Hujayra yadrosi ichidagi bu yadroviy ramka uning shaklini saqlab qolishga yordam beradi. Proteinlarning bu iskala yadro ichida va tashqarisida mahsulotlarni tashish va tarqatish uchun matritsani shakllantirishga yordam beradigan dalillar ham mavjud. Yadro teshiklari yadro membranasi orqali o'tishlarni hosil qiladi va hujayra yadrosi mahsulotlarini sitoplazma yoki endoplazmatik retikulumga kirishiga imkon beradi. Teshiklar, shuningdek, sitoplazmadagi ba'zi o'ziga xos makromolekulalar va kimyoviy moddalarning hujayra yadrosiga qaytishiga imkon beradi. Ushbu makromolekulalar DNK va RNKni sintez qilish uchun zarur va hujayra yadrosida yangi oqsillar va makromolekulalar yaratish uchun kerak. Bo'yalgan yadroda qorong'u nuqta ko'rinishi mumkin. Bu joy yadro. Yadrochaning ichida bir nechta turli qismlar mavjud ribosomalar ishlab chiqariladi va eksport qilinadi. Ushbu tuzilmalarni quyidagi rasmda ko'rish mumkin.

O'simliklar va hayvonlarning hujayra yadrolari nozik jihatlari bilan farq qilsa-da, ularning asosiy maqsadi va umumiy faoliyati bir xil bo'lib qoladi. Hujayra yadrosi har bir hujayraning harakatlarini qo'llab-quvvatlash uchun ikkita asosiy mahsulot ishlab chiqarish uchun javobgardir. Birinchi, xabarchi RNK, yoki mRNK, DNK tuzilishidan RNK tuzilishiga ma'lum bir oqsilni kodlovchi genni ko'chirish mahsulidir. Ushbu qisqaroq mRNK zanjiri yadrodan chiqib, sitoplazmaga kirishi mumkin. Ribosoma ushbu mRNKni olganida, u bu mRNKni oqsillar tiliga tarjima qiladi va aminokislotalarning uzun zanjirini hosil qiladi. Keyin bu ip minglab turli rollardan biriga xizmat qilishi mumkin bo'lgan funktsional oqsilga aylanadi. O'simlik va hayvon hujayralari yadrolari o'rtasidagi farqlarga misollarni quyida ko'rish mumkin.


Genetik material: xususiyatlar va dalillar | Hujayra biologiyasi

Tirik hujayra bir nechta noorganik va organik komponentlardan iborat. Ular orasida, shubhasiz, irsiy belgilarni boshqarish uchun javob beradigan genetik material rolini o'ynaydi. Ushbu genetik materialni aniqlash va shitifikatsiya qilish uzoq vaqt davomida ziddiyatli va ziddiyatli bo'lib qoldi.

Endi har qanday komponent genetik juft va shirial bo'lishi uchun u bir qator asosiy xususiyatlarga javob berishi kerak:

i. Genotipik funksiya yoki replikatsiya yoki avtosintez.

ii. Fenotip funksiyasi yoki ifodasi yoki geterokataliz.

Birinchi xususiyat shuni ko'rsatadiki, genetik material irsiy ma'lumotni saqlashga qodir bo'lishi va u boshqaradigan irsiy xususiyatlarni uzatish uchun asos bo'lgan ketma-ket hujayra avlodlarida yuqori samaradorlik bilan takrorlanishi kerak.

Ikkinchi xususiyat gen ta'sirida ishtirok etadigan asosiy xususiyat bo'lib, u bir qator kimyoviy reaktsiyalar natijasida organizm ichidagi xususiyatlarning yakuniy ifodalanishiga olib keladi. Uchinchi xususiyat shuni ko'rsatadiki, genetik material mutatsiya deb ataladigan vaqti-vaqti bilan irsiy o'zgarishlarga uchraydi.

U rekombinatsiyadan tashqari organizmlar o'rtasida o'zgarishlarni keltirib chiqaradi. Variatsiyalar esa evolyutsiya uchun muhim xom ashyo manbai hisoblanadi.

Genetik materialning yuqorida qayd etilgan muhim xususiyatlaridan tashqari, gen moddasi quyidagi qo'shimcha xususiyatlarni ham ko'rsatadi:

a. Tabiatda mavjud bo'lgan organizm xususiyatlarining son-sanoqsiz xilma-xilligini nazorat qilish uchun genetik material shakl jihatidan juda keng xilma-xillikni ko'rsatishi kerak.

b. Fenotip xarakteri gen darajasida boshlangan reaktsiyalar zanjirining yakuniy ifodasi bo'lganligi sababli, genetik sherik va shirial kimyoviy jihatdan noyob shaxs bo'lishi kerak.

1900 yilgacha bir qancha biologlar irsiy material hujayra yadrosi xromosomasida bo'lishi kerakligini taklif qilishdi. 1903 yilda Sutton va Boveri genlar xro va shimosomada joylashganligini taxmin qilishdi. Eukaryotik tizimda xromosomalar asosan oqsil va nuklein kislotadan (DNK va RNK) iborat bo'lib, ulardan biri genetik materialni tashkil etishi aniq.

Ammo qaysi biri genetik materialning pozitsiyasi uchun eng munosib nomzod bo'lishi uzoq vaqt davomida munozarali va tortinchoq bo'lib qoldi.

Dastlabki molekulyar biologlar va shyogistlar genetik materialning xususiyatlarini xromosoma oqsillariga bog'lashdi, chunki ular nuklein kislotani genetik ma'lumotni tashish uchun juda oddiy deb topdilar. Bundan tashqari, nuklein kislota shakar, fosfat va asos kabi monoton kimyoviy tarkibiy qismlardan iborat.

Boshqa tomondan, oqsil turli xil aminokislotalardan tashkil topgan juda murakkab tuzilishga ega edi. Demak, organizmning xarakteristikasidagi son-sanoqsiz xilma-xillikni nazorat qilish uchun genetik materialda zarur bo'lgan xilma-xillikni bajarish uchun oqsil tuzilishida xilma-xillikning keng doirasi mumkin.

Gen moddasining xromosoma oqsiliga yoki nuklein kislotaga biriktirilishi haqidagi munozaralar 1950 yilgacha mavjud bo'lib, oxir-oqibat genetik ma'lumotlar oqsillarda emas, balki nuklein kislotalarda joylashganligi bir ovozdan qabul qilindi.

Aniqroq aytganda, bir nechta nafis tajribalar DNK ko'pchilik mikroorganizmlar va yuqori organizmlarning genetik materiali ekanligini ko'rsatdi. Keyinchalik, RNK DNK bo'lmagan ba'zi viruslarning genetik materiali ekanligi aniqlandi.

Genetik materialning dalillari:

DNK yoki RNK ko'pchilik organizmlarning genetik materiali ekanligi haqidagi kontseptsiya quyidagi dalillar bilan ishlab chiqilgan va tasdiqlangan:

I. To'g'ridan-to'g'ri dalillar:

(a) Pnevmokokkdagi transformatsiya:

Genetik material oqsil yoki RNK emas, balki DNK ekanligini ko'rsatadigan birinchi to'g'ridan-to'g'ri dalillar OT Avery, CM Macleod va M. McCarthy tomonidan 1944 yilda nashr etilgan. Ular hujayra moddasi Diplococcus pneumoniae bakteriyasida transformatsiya hodisasiga javob berishini va uyatchan ekanligini aniqladilar. DNK hisoblanadi.

Transformatsiya - bu bakteriyaning bir shtammidan boshqa bakteriya shtammiga ular o'rtasida to'g'ridan-to'g'ri aloqa qilmasdan genetik ma'lumotni almashish yoki o'tkazish usuli (rekombinatsiya). Transformatsiya va harakatlanish jarayoni birinchi marta 1928 yilda Frederik Griffit tomonidan kashf etilgan.

Bu Griffithning ef­fect deb nomlangan. Griffitning tajribasi transformatsiyani ko'rsatdi, ammo u transformatsiya printsipini taniy olmadi.

Pnevmokokklarning turli shtammlari turli xil fenotiplarning mavjudligi bilan tan olinishi mumkin bo'lgan genetik o'zgaruvchanlikni ko'rsatadi. Griffit o'z tajribasini pnevmokokklarning fenotipik jihatdan bir-biriga zid bo'lgan ikkita shtammi ustida o'tkazdi.

Ular ozuqaviy agar muhitida sun'iy ravishda o'stirilganda, ular ikki turdagi koloniyalarni hosil qiladi:

Silliq (S) koloniyalarni hosil qiluvchi shtammlar hujayralari shtammga xos polisaxaridlar (glyukoza va glyukuron kislotasi polimeri) kapsulasi mavjudligi sababli silliq yaltiroq ko'rinishga ega. Bunday shtammlar pnevmoniyani keltirib chiqarishi mumkin va ular virulent deb ataladi.

Polisaxarid kapsulasi virulentlik uchun zarur, chunki u bakterial hujayrani leykotsitlar tomonidan fagotsitozdan himoya qiladi. Ammo dog 'hujayralari bu kapsuladan mahrum va ular zerikarli qo'pol (R) koloniyalarni hosil qiladi. Bunday dog'lar avirulent deb ataladi, chunki ular pnevmoniyani keltirib chiqara olmaydi.

Shuning uchun silliq (S) va qo'pol (R) fenotipik xarakteristikalar kapsulaning mavjudligi yoki yo'qligi bilan bevosita bog'liq va bu xususiyat genetik jihatdan aniqlanganligi ma'lum.

Ikkala S va R shakllari bir nechta kichik tiplarda uchraydi va ularning kapsulasidagi polisaxa va shiridlarning antigen xususiyatlariga ko'ra, mos ravishda SI, S II, S III va boshqalar va RI, R II, R III va boshqalar sifatida belgilanadi. . Bu xususiyat oxir-oqibat hujayraning genotipiga bog'liq.

Griffitning tajribalari (12.1-rasm) quyida uning kuzatishlari asosida bosqichma-bosqich qisqacha tavsiflanadi:

Griffit sichqonlarga virus va shilen III S tipidagi jonli hujayralarni kiritdi, barcha sichqonlar pnevmoniya tufayli nobud bo'ldi va sichqonlarning o'lik tanalari qon zardobidan III S tipdagi tirik hujayralar topildi.

Avirulent II R turining tirik hujayralari sichqonlarning alohida guruhiga kiritilganda, sichqonlarning hech biri o'lmadi va II R turi barcha sichqonlarning qon zardobidan ajratildi.

Sichqonlarga faqat issiqlik bilan o'ldirilgan III S tipdagi virusli pnevmokokklar kiritilganda, yana sichqonlarning hech biri nobud bo'lmadi, bu issiqlik bilan o'ldirilgandan keyin virulentlik yo'qolishini ko'rsatdi.

Sichqonlarga issiqlik bilan o'ldirilgan III S tipidagi pnevmokokklar (tirikda virusli) va jonli II R pnevmokokklar (virulent bo'lmagan) yuborilganda, sichqonlarning bir qismi pnevmoniya tufayli nobud bo'lgan o'lik sichqonlardan ajratilgan pnevmokokk hujayralari III S tipiga tegishli edi.

Ma'lumki, kapsulali bo'lmagan R tipidagi hujayralar virulent kapsullangan S tipidagi hujayralarga qayta mutatsiyaga uchraganligi sababli, hosil bo'lgan hujayra III S turiga emas, II S tipiga ega bo'ladi. S hujayralarini mutatsiya bilan izohlab bo'lmaydi, aksincha, III tipdagi o'lik S hujayralarining ba'zi komponentlari ("o'zgartirish printsipi") II turdagi tirik R hujayralarini III S turiga aylantirishi kerak.

Bu hujayralar xususiyatining o'zgarishiga olib keladi va o'zgartirilgan hujayrada ba'zi yangi belgilarni olib kelishiga yordam beradi. Demak, transformatsiya printsipi ba'zi genetik materiallarni o'z ichiga olishi kerak.

(b) Transformatsiya printsipi DNK:

Averi, Makleod va Makkarti eksperimental ravishda o'zgartirish printsipi DNK ekanligini isbotladilar. Ular ko'rsatdiki, agar IIS tipidagi pnevmokokklarning DNK ekstrakti IIR tipidagi pnevmokokklar bilan in vitro aralashtirilsa, pnevmokokklarning bir qismi III S turiga aylanadi.

Ammo III S tipidagi DNK ekstrakti bir nechta oqsil molekulalari, RNK bilan ifloslangan bo'lishi mumkin va bu ifloslantiruvchi oqsil va RNK II R turidan III S turiga o'tish uchun javobgar bo'lishi mumkin. bakterial madaniyat tizimi va DNK, RNK va oqsillarni parchalovchi maxsus fermentlar.

Alohida tajribalarda (12.2-rasm) III S tipidagi hujayralardan DNK ekstrakti bilan ishlov berildi:

i. DNKni buzadigan DNKaz.

ii. RNKni buzadigan RNKaz.

iii. tripsin, oqsilni parchalaydigan proteaz va keyin qayta ishlangan DNK ekstraktining II R tipidagi pnevmatik va shimokokklarni III S turiga aylantirish qobiliyatini sinab ko'rdi.

iv. Ular RNKaz yoki tripsin bilan davolash DNK ekstraktining II R turini III S turiga aylantirish qobiliyatiga ta'sir qilmasligini kuzatishdi. Ammo DNK bilan ishlov berish DNK preparatining transformatsion faolligini yo'q qildi va II R hujayralari III S ga aylantirilmadi. hujayralar. Bu hech qanday shubhasiz DNKni o'zgartiruvchi printsip ekanligini tasdiqladi.

Ammo Avery va hamkasblarining bu topilmalari transformatsiyaning molekulyar mexanizmini tushuntirib bera olmadi. Shunday qilib, ba'zi biologlar bu topilmalarning ahamiyatini tushuna olmadilar va ularni DNKning genetik material ekanligiga shubhasiz dalil sifatida qabul qilishda ikkilanishdi.

(c) Hershey-Cheyz tajribasi:

DNK genetik material ekanligini ko'rsatuvchi yana bir to'g'ridan-to'g'ri dalil 1952 yilda A. D. Xershi va M. Cheyz tomonidan ko'rsatildi. Ular birinchi marta T ning hayot aylanishini o'rganishdi.2 Escherichia coli bakteriofaglari. T2 bakteriofaglar oqsildan yasalgan olti burchakli qutiga o'xshash bosh ko'ylagi va dumidan iborat. DNK oqsilli bosh po'stlog'ining ichida joylashgan.

Bakteriofaglar hujayrali bo'lib, sitoplazma, organellalar va yadrolarni o'z ichiga olmaydi. DNK yuqori sof shaklda mavjud va RNK va oqsil bilan bog'liq emas. Bakteriofaglar majburiy parazitdir, chunki ular faqat bakteriya ichida xost hujayra sifatida ko'payishi mumkin.

Xershi va Cheyz bakteriofaglarning ko'payishi jarayonida fagning DNKsi mezbon hujayraga kirib borishini ko'rsatdi, oqsilning boshi va quyruq qismi esa hujayraning tashqi tomonida so'rilgan holda qoladi. Demak, virusning ko'payishi uchun zarur bo'lgan genetik ma'lumotlar DNKda mavjudligini qat'iy nazarda tutadi.

DNK tarkibida fosfor (P) bor, lekin oltingugurt (S) yo'q, bosh va quyruq oqsillarida esa oltingugurt (S) mavjud, ammo fosfor yo'q.

Hershey va Chase fag DNKsini fosforning radioaktiv izotopi, ya'ni oddiy fosfor o'rniga 32 P bo'lgan muhitda o'sishi bilan aniq belgilashga muvaffaq bo'ldi. Xuddi shunday, faglarning boshqa guruhida oqsil qatlamlari oddiy oltingugurt o'rniga 35 S radioaktiv oltingugurt bo'lgan muhitda o'sishi bilan belgilandi.

E. coli cells were then infected with 32 P labelled T2 bacteriophage and, after being allowed 10 minutes for infection, they were agitated in a blender which sheared off the phase coats. The phase coats and the infected cells were then separated by centrifugation (Fig. 12.3).

Radioactivity was then measured of the sed­iment and in phage coat suspension. Most of the radioactivity was found in the cells. When the same experiment was done using phage with 35 S-labelled protein coat, most of the radioactivity was found in the suspension of phage coats very little entered the host cells.

Since phage reproduction (both DNA synthesis) occurs inside the infected cells, and, since only the phage DNA enters the host cell, the DNA—not the protein—must carry the genetic information. As a result of the findings of Hershey and Chase led to the universal acceptance of DNA as the genetic material.

(d) Bacterial Conjugation:

Another direct evidence for DNA as the genetic material comes from the phenomenon of conju­gation of bacteria. Conjugation was discovered by J. Lederberg and E. I.

Tatum in 1946. During conjugation DNA is transferred from a donor bacterial cell to a recipient bacterial cell through conjugation tube that forms between them. The donor cell—also called male—contains a F factor or fertility factor whereas recipient cells—or fe­male cells, lack F factor, i.e., F – cell (Fig. 12.4).

In male, the F factor can exist in two dif­ferent states:

(2) Integrated state (Fig. 12.4) where the F factor is inserted with main DNA and thus the male become Hfr male (Fig. 12.5).

The F factor is a mini-circular DNA molecule. Beadle and Tatum observed that when a F + male E. coli cell conjugated with a F – female E. coli cell, an unidirectional transfer of F + factor of male cell to F – or female cell took place, so that the latter was covered into a F + or male strain.

The F factor is actually a fragment of DNA molecule that replicates during transfer. Thus mixing a population of F + or Hfr cells with a population of F + cells results in virtually all the cells in the new population becoming F + or Hfr (Fig. 12.6).

Ii. Indirect Evidence:

The fact that DNA is the genetic material of higher organisms has also been supported by some indirect evidences:

The genetic substance should have a fixed location within the cell. If it has no fixed location, then the genes are not able to function properly. It is known that the DNA, as a gene sub­stance, is always located primarily within the chromosome in the nucleus of the eukaryotic cell.

The specific location of DNA can be stud­ied in situ by the Feulgen reaction—which is re­garded as the most specific one for DNA. Feul­gen staining stains chromosome magenta colour against the clear cytoplasmic background. This technique has shown that DNA entirely remains restricted to the chromosome and it forms the major component of chromosomes.

Various macromolecules present within the cell are continuously being anabolised and catabolized. But this is not desirable for a genetic substance containing valuable hereditary information. If it happens, the genetic function will be lost. Of all the macro- molecules in the cell, DNA is the metabolically stable.

(c) Sensitivity to Mutagens:

Mutation is an important characteristic feature of the genetic material. The agents capable of inducing mutation are called mutagens. Different types of radiation (UV-ray, X-ray, y-ray) and a variety of chemical compounds acts as mutagens. When the cells of an organism are treated with mutagens, they cause a change in the structure of gene.

Since genes are DNA segments, the gene mutation include changes in the number and arrangement of nucleotide. Sometimes muta­tion causes the breaks in the DNA molecule. The changes in the DNA structure ultimately reflect the changes of the organism’s hereditary character. Therefore sensitivity of DNA to mutagens is an indirect evidence for DNA being the genetical materials.

One of the striking features of the genetic ma­terial is the correlation between DNA content and the number of chromosome sets. Various quantitative assay methods have shown that diploid cells contain twice as much DNA as do haploid cells of the same species (Table 12.1).

Similarly, tetraploid and octaploid cells con­tains four times and eight times DNA as com­pared with DNA content of the haploid cells. Even the DNA content of sperm cells shows a correlation with the same or different tissues of different organisms (Table 12.2).

Thus the parallelism of behaviour in DNA and chromosome indirectly indicates that DNA is the genetic material.

(e) RNA as Genetic Material:

The genome of viruses may be DNA or RNA. Most of the plant viruses have RNA as their hereditary material. Fraenkel-Conrat (1957) conducted experiments on tobacco mosaic virus (TMV) to demonstrate that in some viruses RNA acts as genetic material.

TMV is a small virus composed of a single molecule of spring-like RNA encapsulated in a cylindrical protein coat. Different strains of TMV can be identified on the basis of differences in the chemical composition of their protein coats. By using the appropriate chemical treatments, proteins and RNA of RNV can be separated.

Moreover, these processes are reversible by missing the protein and RNA under appropriate conditions—reconstitution will occur yielding complete infective TMV particles. Fraenkel-Conrat and Singer took two differ­ent strains of TMV and separated the RNAs from protein coats, reconstituted hybrid viruses by mixing the proteins of one strain with the RNA of the second strain, and vice versa.

When the hybrid or reconstituted viruses were rubbed into live tobacco leaves, the progeny viruses produced were always found to be phenotypically and genotypically identical to the parental type from where the RNA had been isolated (Fig. 12.7). Thus the genetic information of TMV is stored in the RNA and not in the protein.


Cell size and numbers

An adult human body contains about 60 trillion (60 x 10 12 ) cells. Most of these cells are so small that a microscope is necessary to see them. The small size of cells fulfills a distinct purpose in the functioning of the body. If cells were larger, many of the processes that cells perform could not occur efficiently. Such a large cell has a large volume, which is much larger than surface area. Since nutrients enter the cell via the surface, only a relatively small amount of nutrients could enter the cell. Put another way, a cell would likely starve, since the nutrient supply could not keep pace with the nutrient demand of the cell. In a small cell, the correspondingly smaller volume means that the available nutrient level is usually sufficient to support cell survivial and growth.

Another reason for the small size of cells is that control of cellular processes is easier in a small cell than in a large cell. Cells are dynamic, living things. Cells transport substances from one place to another, reproduce themselves, and produce various enzymes and chemicals for export to the extracellular environment. All of these activities are accomplished under the direction of the nucleus, the control center of the cell. If the nucleus had to control a large cell, then this direction might break down. Substances transported from one place to another would have to traverse great distances to reach their destinations reproduction of a large cell would be an extremely complicated endeavor and products for export would not be as efficiently produced. Smaller cells, because of their more manageable size, are much more efficiently controlled than larger cells.


Neural Stem Cells

There has long been a consensus in the scientific community that once neurons have died, there is no way to replace them. Other cells of the body, like skin cells and blood cells are replaced when their stem cells divide to give new skin and blood cells respectively. Neurons, it was thought, did not have its special pool of stem cells.

In the 1980s, Fernando Nottebohm at Rockefeller University questioned this notion, and found stem cells in the adult brain of songbirds. These stem cells are called neural stem cells. Since then, we&rsquove found neural stem cells in rats, mice, monkeys, and even humans.

Neural stem cells aren&rsquot everywhere in the brain. They are only found in two nooks &ndash the anterior sub-ventricular zone (SVZ) in the forebrain, and the subgranular zone in the hippocampus. These stem cells cannot form long distance connection, so major regeneration after a severe injury is not possible.

This is seen as a partial explanation for the occasional recovery in patients with serious brain injuries. This process takes time, and is not a constant part of brain maintenance, so it is still important to avoid any damage to the brain and spinal cord at all costs.

These neural stem cells or NSCs are primarily active while the brain is initially developing as an infant, but many of them cease to function as we age. Some of the cells remain active throughout our lives, differentiating into different types of cells, including astrocytes, oligodendrocytes and neurons.

Neural stem cells are very intriguing for researchers, who are now isolating these cells and trying to determine their mechanism for turning their replication functions on and off. Researchers could potentially apply their findings to healing or treating the brain, especially when it comes to neurodegenerative diseases like Alzheimer&rsquos or dementia, in ways we thought were impossible.

The nervous system is the seat of consciousness and control in the human body understanding how it works, and what makes nerve cells different from other cells, provides yet another glimpse into the incredible complexity of our existence!


80 Comparing Meiosis and Mitosis

Mitosis and meiosis, which are both forms of division of the nucleus in eukaryotic cells, share some similarities, but also exhibit distinct differences that lead to their very different outcomes. Mitosis is a single nuclear division that results in two nuclei, usually partitioned into two new cells. The nuclei resulting from a mitotic division are genetically identical to the original. They have the same number of sets of chromosomes: one in the case of haploid cells, and two in the case of diploid cells. On the other hand, meiosis is two nuclear divisions that result in four nuclei, usually partitioned into four new cells. The nuclei resulting from meiosis are never genetically identical, and they contain one chromosome set only—this is half the number of the original cell, which was diploid.

The differences in the outcomes of meiosis and mitosis occur because of differences in the behavior of the chromosomes during each process. Most of these differences in the processes occur in meiosis I, which is a very different nuclear division than mitosis. In meiosis I, the homologous chromosome pairs become associated with each other, are bound together, experience crossover between homologous chromosomes, and line up in the center of the cell with spindle fibers from opposite spindle poles attached to each centromere. All of these events occur only in meiosis I, never in mitosis.

Homologous chromosomes move to opposite poles during meiosis I so the number of sets of chromosomes in each nucleus-to-be is reduced from two to one. For this reason, meiosis I is referred to as a reduction division. There is no such reduction in mitosis.

Meiosis II mitotik bo'linishga ko'proq o'xshaydi. In this case, duplicated chromosomes line up at the center of the cell. One sister chromatid is pulled to one pole and the other sister chromatid is pulled to the other pole. Agar o'zaro bog'liqliklar bo'lmaganida, har bir meioz II bo'linishining ikkita mahsuloti mitozdagi kabi bir xil bo'lar edi, ular bir-biridan farq qiladi, chunki har doim har bir xromosomada kamida bitta krossover bo'lgan. Meiosis II is not a reduction division because, although there are fewer copies of the genome in the resulting cells, there is still one set of chromosomes, as there was at the end of meiosis I.

Cells produced by mitosis will function in different parts of the body as a part of growth or replacing dead or damaged cells. Mitosis typically occurs in somatic cells, but they may be involved in asexual reproduction in some organisms. Cells produced by meiosis will only participate in sexual reproduction.

Figure 1 Meiosis and mitosis are both preceded by one round of DNA replication however, meiosis includes two nuclear divisions. The four daughter cells resulting from meiosis are haploid and genetically distinct. The daughter cells resulting from mitosis are diploid and identical to the parent cell.


How does foreign DNA affect or utilize a cells nucleus?

Biology With the DNA based J&J vaccine coming out for COVID-19, it got me thinking how foreign DNA affects or utilizes the cells nucleus?

What goes on in a cell nucleus and how does it affect our own DNA, when there is a foreign invader?

How do cells protect itself from foreign DNA? Or can it even protect itself? In the case of the vaccine, the DNA is a good guy, but in other cases, it can be a bad guy?

So how does this whole cell nucleus work with foreign DNA?

First of all, DNA can't enter a cell or nucleus on its own. In many cases (e.g. vaccines), a virus is used that injects a strand of DNA into a cell.

As far as I know, once a strand of DNA is inside a nucleus, what happens next depends on what it codes for. If it codes for a virus, this virus can be produced within the cell. This happens when a person is infected by a virus. In the case of the J&J vaccine, the DNA only codes for one protein of Covid19. Then, this one protein is synthesised, but the person won't get sick. Then, if the strand of DNA is not integrated into the genome of the cell, the strand is eventually degraded.

Lastly, the immune system can recognise cells infected by viruses and can kill these cells.

So let me see if I understand this correctly.

Assuming DNA gets inside the nucleus, any set of DNA can hijack the nucleus of a cell and generate whatever structures it needs to create. In the case of our own DNA, stuff for our own cells, but in the case COVID-19, the spike protein.

What happens to virus DNA after it makes more viruses?

What happens to the vaccine DNA after it makes the spike protein?

Can foreign DNA live in the nucleus forever?

Okay, let me try to answer your question, but bear with me a moment, because I need to tell you about a lot of cell biology first.

First, let's talk about DNA, RNA, and Protein.

You probably already know of DNA. DNA, deoxyribonucleic acid, is a long, double helix-shaped string of A's, T's, C's and G's. On an atomic and molecular level, DNA is just a long string of bits. But from an informational perspective, when we study how the DNA gets used by a cell, it becomes obvious that the information it contains is organized into many discrete blocks, where each block is read together as a single unit to make a single product or a limited number of variants. We call these blocks of information Genes.

The product of these Genes are Proteins. Proteins are long strings of amino acids, and unlike strings of DNA which are made of 4 different letters, there are 20 different amino acid letters possible for each spot on a protein string. These strings of proteins spontaneously fold into a specific shape based on the amino acids along the chain, like a rope studded with magnets snarling up onto itself. The shape of the protein carries out a specific function, playing its part in the complex biochemical ballet of life. Proteins are made by molecular ticker-tape reader machines called Ribosomes. In order for the DNA of a gene to be made into protein, DNA gets read and transcribed into Messenger RNA (mRNA), a different format which uses A, U, C, G instead of DNA's ATCG. mRNA is a transient messenger molecule, a short-lived copy which feeds into the Ribosomes that create the amino acid chains that turn into proteins, but the mRNA itself naturally gets destroyed and recycled by the cell eventually.

DNA makes RNA, RNA makes Protein. This rule is what biologists call the Central Dogma, coined in 1958 by Francis Crick, one of the co-discoverers of the structure of DNA. It turned out to be a regrettably bad name for many reasons, one of which is that exceptions to this turned out to be plentiful, but it is broadly true almost all of the time.

So, that's enough about DNA, let's talk about how your immune system works.

When an unpleasant microbe gets into your body, intent on feasting upon your cells and reproducing inside you, your body has two lines of defense. The first line of defense is your innate immune system: it doesn't care what's attacking, it reacts to anything foreign, any signs of damage, and to alarm signals produced by cells that are under attack. Your innate immune system does a lot of things: it ramps up inflammation (fever), raising the temperature to stress the attacker, produces noxious and destructive compounds, and rallies an army of carnivorous defenders to clean up dead & dying cells, eat the attacking microbes, and harvest pieces of their proteins for analysis.

Your innate immune system buys time for your adaptive immune system. Specialized immune cells take the harvested protein pieces and get to work making antibodies: little Y-shaped proteins that circulate in your blood and specifically identify and stick to those attacker's proteins, tagging the microbes en-masse and flagging them for extermination. Antibodies often stick in a way that gums up the proteins critical for the microbe's life cycle, too. Once the active infection of microbes is wiped out, our immune system keeps those antibodies on file, so that production of those antibodies can ramp up right away if the microbe's ever encountered again and future attacks will get squished before they can do any noticeable damage at all.

Vaccination is our way of hijacking this process to grant us immunity while skipping the potentially deadly or disabling active infection necessary to get there naturally. The first vaccines, for smallpox, polio, and so on, were what we call live-attenuated vaccines. For vaccinating people against smallpox, we infected people with cowpox, a much more benign cousin of the smallpox virus which was close enough that immunity to cowpox gets smallpox squished at the front gates. For others, we used weakened or crippled but otherwise still infectious microbes: they wouldn't cause severe sickness or death, but they would do enough damage and trigger our immune system enough to establish antibodies, which protects us against the fully deadly virus in the wild.

Today, we've mostly forgotten how much vaccination changed the world and our relationship with disease. For the first time, we had the ability to give ourselves permanent protection from entire classes of terrifying diseases that have been killing and crippling people for longer than history remembers. And many of these were viral diseases for which the previous generation's miracle wonderdrug, antibiotics, could do nothing against.

Even though they revolutionized the world, these first-generation vaccines had obvious downsides. The two most glaring were that, first, taking a live, deadly microbe and weakening it is an inherently inconsistent process, and second, even a weakened virus could sporadically cause a bad case of the disease, especially in people whose immune systems were already weak.

So we developed vaccines where we deliver completely inactive and dead microbes, and then after that we made vaccines which only deliver the specific critical protein or protein fragment of the microbe that the microbe needs to attack us.

The newly approved Johnson and Johnson vaccine is part of a new generation of vaccines that include the mRNA-based Pfizer and Moderna vaccines. The new idea is this: instead of delivering the microbe's critical protein itself, we deliver the DNA or RNA blueprint for how to make one, your own cells make a bunch of it, your innate and adaptive immune systems react to it, and your adaptive immune system eventually learns to kill it on sight.

The J&J vaccine uses a DNA fragment that contains the gene for the covid spike protein, encased inside an adenovirus-like particle. Like a real live adenovirus, these virions are able to attach to cells and inject their DNA contents into a cell. Unlike a real live adenovirus, they don't contain genes for making more viral DNA molecules and virus particles, they instead contain the gene for the covid spike protein.

Once the DNA's inside your cell, it gets read just like any other piece of DNA, and mRNA messenger transcripts are created. Those mRNAs go into ribosomes, and spike proteins get made.

If the invading genes were actually a real foreign invader, like, for example, the SARS-Cov-2 virus itself, what would happen would be much the same. The covid virus's shell fuses with the receptor on the surface of our cell like a key opening a lock, and the viral RNA genome gets dumped into the cell. It gets read and the cell starts manufacturing viral spikes, capsids, and more viral RNA genomes, and these parts self-assemble into viral particles until the cell exhausts all its energy and resources and dies, blowing apart as all the new viral particles inside get scattered into the rest of your body.


  • Personal protective equipment (sterile gloves, laboratory coat, safety visor)
  • Waterbath set to appropriate temperature
  • Microbiological safety cabinet at appropriate containment level
  • Santrifuga
  • CO2 inkubator
  • Hemocytometer
  • Inverted phase contrast microscope
  • Pre-labelled flasks
  1. Bring adherent and semi-adherent cells into suspension using trypsin/EDTA as described previously and resuspend in a volume of fresh medium at least equivalent to the volume of trypsin. For cells that grow in clumps centrifuge and resuspend in a small volume and gently pipette to break up clumps.
  2. Under sterile conditions remove 100-200 μL of cell suspension.
  3. Add an equal volume of Trypan Blue (dilution factor =2) and mix by gentle pipetting.
  4. Clean the hemocytometer.
  5. Moisten the coverslip with water or exhaled breath. Slide the coverslip over the chamber back and forth using slight pressure until Newton’s refraction rings appear (Newton’s refraction rings are seen as rainbow-like rings under the coverslip).
  6. Fill both sides of the chamber with cell suspension (approximately 5-10 μL) and view under an inverted phase contrast microscope using x20 magnification.
  7. Count the number of viable (seen as bright cells) and non-viable cells (stained blue). Ideally >100 cells should be counted in order to increase the accuracy of the cell count (see notes below). Note the number of squares counted to obtain your count of >100.
  8. Calculate the concentration of viable and non-viable cells and the percentage of viable cells using the equations below.

Do dead cells always contain no nucleus? - Biologiya

All cells, whether they are prokaryotic or eukaryotic, have some common features. These common features are:

DNK, the genetic material contained in one or more chromosomes and located in a nonmembrane bound nucleoid region in prokaryotes and a membrane-bound nucleus in eukaryotes

Plazma membranasi, a phospholipid bilayer with proteins that separates the cell from the surrounding environment and functions as a selective barrier for the import and export of materials

Sitoplazma, the rest of the material of the cell within the plasma membrane, excluding the nucleoid region or nucleus, that consists of a fluid portion called the cytosol and the organelles and other particulates suspended in it

1. The genetic material (DNA) is localized to a region called the nucleoid which has no surrounding membrane.

2. The cell contains large numbers of ribosomes that are used for protein synthesis.

3. At the periphery of the cell is the plasma membrane. In some prokaryotes the plasma membrane folds in to form structures called mesosomes, the function of which is not clearly understood.

4. Outside the plasma membrane of most prokaryotes is a fairly rigid wall which gives the organism its shape. The walls of bacteria consist of peptidoglycans. Sometimes there is also an outer capsule. Note that the cell wall of prokaryotes differs chemically from the eukaryotic cell wall of plant cells and of protists.


Videoni tomosha qiling: Prokariot va eukariot hujayralar. Hujayra strukturasi. Biologiya (Avgust 2022).