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Da li su mitohondriji živi?

Da li su mitohondriji živi?


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Radim na zadatku za svoj IB čas biologije i bila bi mi vrlo zahvalna neka pomoć. Pročitao sam nekoliko članaka i još uvijek nisam dobio odgovor koji tražim. Moram napisati sažetak na jednoj stranici o tome je li Mitohondrion živ ili nije.


Dobrodošli na Biology.SE

Polja interesovanja

Zadatak koji morate napisati ima malo veze s biologijom, a malo s filozofijom! Pitanje šta je živo, a šta nije, zavisi od same definicije šta je živo biće i ovo pitanje ne zanima biologe, već samo filozofe.

Kako riješiti ovaj zadatak

Stoga ćete za svoj zadatak morati razume šta je mitohondrija (dio biologije) i to razumjeti kako se različite definicije života primjenjuju na mitohondrije (Dio filozofije, iako će vam trebati određena znanja iz biologije da biste razumjeli važnost ovih definicija).

Šta je mitohondrija?

Ovo pitanje je preširoko i na njega se ovdje ne može odgovoriti. Obavezno pogledajte stranicu wikipedia. Ukratko:

  • mitohondrije sadrže DNK
  • mitohondrij je rezultat bakterije koja je nekako internalizirana u veću ćeliju (to je simbiont). Zbog toga danas mitohondriji sadrže DNK. Stoga nije baš organela poput drugih. Imajte na umu da biljke, osim što imaju mitohondrije, imaju i plazmide koji su također posljedica sličnog procesa internalizacije drugog oblika života.
  • evoluira DNK mitohondrija (naravno)
  • mitohondrije su u osnovi tvornica energije stanice.
  • mitohondriji nisu u stanju da žive sami izvan žive ćelije (prema mojim saznanjima).

Definicije života

Važno je shvatiti da definicija života nema apsolutno nikakav utjecaj na biologiju i nije ništa drugo nego pitanje nomenklature.

Postoji mnogo definicija i ne mogu ih ovdje obuhvatiti sve. Možda biste htjeli pogledati ovu wiki stranicu. Na prethodnom linku su navedena najčešća svojstva o kojima razmišljamo razmišljajući o definiciji života.

  • Homeostaza: Regulacija unutrašnjeg okruženja za održavanje konstantnog stanja; na primjer, znojenje radi smanjenja temperature. Organizacija: Strukturno se sastoji od jedne ili više ćelija – osnovnih životnih jedinica.
  • Metabolizam: Transformacija energije pretvaranjem kemikalija i energije u stanične komponente (anabolizam) i razgradnjom organske tvari (katabolizam). Živim bićima je potrebna energija za održavanje unutarnje organizacije (homeostaza) i za proizvodnju drugih pojava povezanih sa životom. [49] Rast: Održavanje veće stope anabolizma od katabolizma. Rastući organizam povećava veličinu u svim svojim dijelovima, umjesto da jednostavno nakuplja materiju.
  • Adaptacija: Sposobnost da se vremenom mijenja kao odgovor na okruženje. Ova sposobnost je fundamentalna za proces evolucije i određena je naslijeđem organizma, ishranom i vanjskim faktorima. Odgovor na podražaje: Odgovor može imati različite oblike, od kontrakcije jednostaničnog organizma do vanjskih kemikalija, do složenih reakcija koje uključuju sva osjetila višećelijskih organizama. Odgovor se često izražava pokretom; na primjer, listovi biljke okrenuti prema suncu (fototropizam) i kemotaksija.
  • Reprodukcija: Sposobnost stvaranja novih pojedinačnih organizama, ili aseksualno iz jednoroditeljskog organizma, ili seksualno iz dva roditeljska organizma, "sa stopom grešaka ispod praga održivosti".

Srodna pitanja

Pitanje jesu li virusi živi vrlo je često. Evo dva postova Biology.SE na tu temu:


Među velikim, neriješenim evolucijskim misterijama, porijeklo eukariotskih ćelija - ćelija s jezgrama - visoko je rangirano. Nuklearne ćelije su gradivni blokovi svih višećelijskih organizama, uključujući i nas. Pokreću ih mitohondriji.1 Mitohondrije koriste kisik i niz enzima kako bi izvukle najveću moguću energiju iz šećera i zapakirale ga u upotrebljiv oblik. Odakle ćelije ove energetske fabrike?

Najpopularnija evolucijska priča koja objašnjava kako je posljednji eukariotski zajednički predak (LECA) dobio mitohondrije je da ih je pojeo. Ili bolje rečeno da je jeo male ćelije bez jezgre (prokariote, kao što su bakterije) - i da su tada ti prokarioti razvili simbiotski odnos sa ćelijom domaćinom, opskrbili je energijom i pretvorili se u mitohondrije. Ta priča, koju je 1970 -ih popularizirao pokojni dr. Lynn Margulis, naziva se "teorija serijske endosimbioze". Budući da su jednostanični organizmi i druge stanice poput naših bijelih krvnih zrnaca progutale krhotine i manje mikroorganizme-proces koji se može nazvati endosimbioza-evolucionistima se teorija serijske endosimbioze za podrijetlo eukariotskih stanica činila razumnom. Uostalom, zaključili su, mitohondrije i prokarioti imaju neke površne sličnosti. Oba su mala. I dok je većina DNK eukariotske ćelije u njenom jezgru, mitohondrije imaju nešto vlastite DNK, kao i ribozome za prevođenje njenih gena u proteine. Nuklearna DNK je u obliku dvostrukih spiralnih niti, ali mitohondrijska DNK nije. Iako je mitohondrijski genom mnogo manji od genoma bakterija, i mitohondriji i prokarioti imaju kružnu DNK.

Budući da su višećelijski organizmi napravljeni od eukariotskih ćelija, mnogi misle da je evolucija mitohondrija bila kamen temeljac koji je podstakao višećelijsku evoluciju. Međutim, postoji mnogo problema s pričom o evoluciji mitohondrija. Stoga, upravo kada su mitohondrije evoluirale, sudbina nestalih gena proto-mitohondrija i identitet njihovih predačkih bakterija ostali su kontroverzni.


Politika privatnosti

Datum stupanja na snagu: oktobar 2020

Sljedeća Pravila privatnosti uređuju praksu prikupljanja podataka na mreži Juniortine Productions, LLC d/b/a Holističkog psihologa („Kompanija“, “we ” ili “us ”). Konkretno, opisuje vrste informacija koje prikupljamo o vama dok koristite yourholisticpsychologist.com (“Site”) i načine na koje koristimo ove informacije. Ova Politika privatnosti prvenstveno se odnosi na podatke koje prikupljamo na mreži.

Stvorili smo ovu Politiku privatnosti kako bismo pokazali našu čvrstu posvećenost privatnosti i sigurnosti. Ova Pravila privatnosti opisuju kako naša kompanija prikuplja podatke od svih krajnjih korisnika naših internetskih usluga („Usluge“), uključujući one koji pristupaju nekim od naših usluga, ali nemaju račune („posjetitelji“) i one koji mogu kupiti proizvode i/ ili platite naknadu za uslugu da biste se pretplatili na Uslugu („Članovi“).

Molimo pažljivo pročitajte ovu Politiku privatnosti. Posjetom i korištenjem web stranice slažete se da je vaša upotreba naše web stranice i svaki spor oko privatnosti uređen ovom politikom privatnosti. U nastojanju da se pridržavamo tehnoloških promjena i usvajanja novih propisa i zakona, možda ćemo morati promijeniti našu Politiku u nekom trenutku u budućnosti, u tom slučaju ćemo objaviti izmjene ove Politike privatnosti na ovoj web stranici i ažurirajte Datum stupanja na snagu politike tako da odražava datum promjena. Nastavkom korištenja stranice nakon što objavimo takve promjene, prihvatate izmijenjenu Politiku privatnosti.

Uvod

Možemo prikupljati i pohranjivati ​​lične ili druge podatke koje nam dobrovoljno dostavite na mreži dok koristite Stranicu (npr. dok ste na Stranici ili kada odgovarate putem e-pošte na funkciju koja se nalazi na Stranici). Ova web stranica kontaktira samo pojedince koji to posebno zahtijevaju ili u slučaju da su se prijavili za primanje naše poruke ili su kupili neki od naših proizvoda ili usluga. Stranica prikuplja lične podatke od naših korisnika tokom online registracije i online kupovine. Općenito, ove informacije uključuju ime i adresu e-pošte za potrebe registracije ili prijave i ime, adresu e-pošte i podatke o kreditnoj kartici prilikom kupovine naših proizvoda ili usluga. Sve ove podatke nam pružate vi.

Također prikupljamo i pohranjujemo informacije koje se automatski generiraju dok se krećete online kroz web stranicu. Na primjer, možemo prikupljati podatke o vezi vašeg računara s internetom, što nam omogućava, između ostalog, da poboljšamo isporuku naših web stranica vama i da mjerimo promet na web stranici. Također možemo koristiti standardnu ​​funkciju koja se nalazi u softveru preglednika pod nazivom “cookie ” kako bismo poboljšali vaše iskustvo sa web lokacijom i web svjetionicima, za pristup kolačićima, brojanje korisnika koji posjećuju web lokaciju, datum i vrijeme posjeta, stranice pregledano, vrijeme provedeno na našoj web stranici, web stranice posjete prije i poslije naše web stranice, IP adrese ili otvorene e-poruke u HTML formatu.

Koristimo informacije koje prikupljamo od vas dok koristite stranicu na različite načine, uključujući korištenje informacija za prilagođavanje funkcija oglašavanja koje se pojavljuju na web stranici i stavljanje na raspolaganje drugih ponuda putem e-pošte, direktne pošte ili na drugi način.

Imajte na umu da kad god svoje lične podatke dobrovoljno učinite dostupnim trećim stranama na mreži –, na primjer na oglasnim pločama, web dnevnikima, putem e-pošte ili u područjima za ćaskanje –, te informacije se mogu vidjeti, prikupiti i koristiti od drugih osim nas. Ne možemo biti odgovorni za bilo kakvu neovlaštenu upotrebu takvih informacija od strane treće strane.

Neki od naših oglašivača i poslužitelja oglasa trećih strana koji postavljaju i predstavljaju oglašavanje na web stranici također mogu prikupljati vaše podatke putem kolačića, web svjetionika ili sličnih tehnologija. Ovi oglašivači i poslužitelji oglasa trećih strana mogu koristiti podatke koje prikupljaju kako bi pomogli u predstavljanju njihovih oglasa, za mjerenje i istraživanje efikasnosti oglasa ili u druge svrhe. Upotreba i prikupljanje vaših podataka od ovih oglašivača i poslužitelja oglasa trećih strana regulirana je odgovarajućom politikom privatnosti trećih strana i nije obuhvaćena našim Pravilima privatnosti. Zaista, pravila privatnosti ovih oglašivača trećih strana i oglasnih servera mogu se razlikovati od naših. Ako imate bilo kakvih nedoumica u vezi s upotrebom kolačića ili web svjetionika trećih strana ili korištenjem vaših podataka, trebali biste posjetiti web stranicu te strane i pregledati njenu politiku privatnosti.

Ova web stranica također sadrži poveznice na druge web stranice i pruža pristup proizvodima i uslugama koje nude treće strane, čije politike privatnosti ne kontroliramo. Kada pristupate drugoj web stranici ili kupujete proizvode ili usluge trećih strana putem web stranice, korištenje bilo kojih podataka koje pružate regulirano je politikom privatnosti operatera web stranice koju posjećujete ili davatelja takvih proizvoda ili usluga.

Takođe imajte na umu da kako naše poslovanje raste, možemo kupovati ili prodavati različitu imovinu. U malo vjerovatnom slučaju da prodamo dio ili cijelu svoju imovinu, ili jednu ili više naših web stranica kupi druga kompanija, informacije o našim korisnicima mogu biti među prenesenim sredstvima.

Osobni podaci koje naša kompanija prikuplja i kako se koriste

Uvod

Od članova se može zatražiti da daju određene lične podatke prilikom registracije za naše proizvode ili usluge, uključujući ime, adresu e -pošte i podatke za naplatu (poput broja kreditne kartice). Osobni podaci prikupljeni od članova tijekom procesa registracije (ili u bilo koje drugo vrijeme) koriste se prvenstveno za pružanje prilagođenog iskustva prilikom korištenja naših proizvoda i usluga. Vaši podaci nikada neće biti otkriveni, trgovani, licencirani ili prodani trećim stranama. Međutim, možemo otkriti otkrivanje ličnih podataka pod posebnim okolnostima opisanim u nastavku.

Vrste informacija koje prikupljamo i čuvamo

Neke od informacija koje možemo prikupiti o vama i pohraniti u vezi s pružanjem i ispunjavanjem naših usluga za vas mogu uključivati:

  • Ime
  • Dob
  • E-mail adresa
  • Poštanska adresa
  • Broj telefona
  • Maskirane informacije o kreditnoj kartici u obliku tokena
  • Izvor prometa
  • Sve bilješke ili izjave koje date

Kako koristimo Vaše lične podatke

Gore navedeni lični podaci mogu se koristiti u sljedeće svrhe:

  • Za rad, poboljšanje ili promicanje naše usluge
  • Za pružanje korisničke usluge ili podrške
  • Za obradu plaćanja
  • Da vas kontaktiram
    • Kada ste se uključili u primanje poruka e -pošte
    • Da odgovorite na vaše upite putem e -pošte. Konkretno, kada nam Posjetioci ili Članovi pošalju upite putem e-pošte, povratna e-mail adresa se koristi za odgovor na upit e-pošte koji primimo. Povratnu adresu e -pošte ne koristimo u bilo koje druge svrhe niti je dijelimo s trećim stranama.
    • Istorija kupovine
    • Izvještaji o prodaji
    • Ponašanje na stranici
    • E-pošta klikne i otvori se
    • Marketing putem e -pošte
    • Oglašavanje, uključujući ponovno ciljanje putem Googlea i Facebooka
    • Obavještenja

    Ko ima pristup vašim podacima unutar naše organizacije

    Unutar naše organizacije, pristup vašim podacima je ograničen na one osobe kojima je potreban pristup kako bi vam pružili proizvode i usluge koje kupujete od nas, kako bi vas kontaktirali i odgovorili na vaše upite, uključujući zahtjeve za povrat novca. Zaposleni imaju pristup podacima samo na osnovu „potrebe da znaju“.

    S kim dijelimo vaše podatke izvan naše organizacije i zašto

    Nepovezane treće strane.
    Bez vašeg pristanka nećemo dijeliti ili prenositi vaše podatke nepovezanim trećim stranama. Možemo koristiti pružatelje usluga u vezi s upravljanjem i poboljšanjem web stranice, za pomoć u određenim funkcijama, poput obrade plaćanja, prijenosa e -pošte, hostinga podataka, upravljanja oglasima, ispunjavanja prodaje proizvoda i nekih aspekata naše tehničke i korisničke podrške. Poduzet ćemo mjere kako bismo osigurali da ti pružatelji usluga pristupaju, obrađuju i pohranjuju informacije o vama samo u svrhe koje ovlastimo, podložno obvezama povjerljivosti, uključujući i izvršavanjem Ugovora o zaštiti podataka o usklađenosti s podacima GDPR-a i CCPA-e ili Dodataka, prema potrebi.

    Vlasti.
    Možemo pristupiti, sačuvati i otkriti informacije o vama trećim stranama, uključujući sadržaj poruka, ako smatramo da je otkrivanje u skladu s važećim zakonom, propisom, pravnim postupkom ili revizijama ili to zahtijeva. Također možemo otkriti informacije o vama ako vjerujemo da vaše radnje nisu u skladu s našim Uvjetima pružanja usluge ili povezanim smjernicama i politikama, ili ako je potrebno da zaštitimo prava, imovinu ili sigurnost ili spriječimo prijevaru ili zloupotrebu Kompanije ili drugih .

    Zašto pohranjujemo informacije koje prikupljamo od vas

    Zadržavamo određene podatke koje prikupljamo od vas dok ste član stranice, a u određenim slučajevima kada ste izbrisali svoj račun, iz sljedećih razloga:

    • Tako da možete koristiti našu stranicu
    • Kako biste bili sigurni da nećemo komunicirati s vama ako ste to od nas zatražili
    • Da vam obezbijedimo povrat novca, ako imate pravo
    • Kako bismo bolje razumjeli promet na našoj stranici kako bismo svim članovima mogli pružiti najbolje moguće iskustvo
    • Za otkrivanje i sprječavanje zloupotrebe naše web stranice, nezakonitih aktivnosti i kršenja naših Uslova usluge i
    • U skladu sa važećim zakonskim, poreskim ili računovodstvenim zahtjevima.

    Kada nemamo stalnu legitimnu poslovnu potrebu za obradom vaših podataka, izbrisat ćemo ih ili anonimizirati.

    Kolačići i alati za praćenje

    Koristimo kolačiće kako bismo vam olakšali korištenje naše web stranice, kao što su:

    • Da zapamtite svoju državu i jezičke preferencije
    • Za isporuku informacija koje odgovaraju vašim interesovanjima
    • Da nam pomogne da razumijemo našu publiku i obrasce prometa
    • Da bismo vam omogućili automatsko prijavljivanje u programe i dijelove naše web stranice za koje je potrebno članstvo
    • Za upravljanje i predstavljanje informacija o web stranici prikazanih na našoj web stranici koje će biti specifične za vas

    Web Beacons koristimo i za prikupljanje neosobnih podataka o tome kako koristite našu web stranicu, na primjer koliko ste dugo posjetili našu stranicu, koji web preglednik koristite, koji je vaš operativni sistem i ko je vaš davatelj internetskih usluga. Osim toga, također koristimo podatke Google Analyticsa i DoubleClick kolačić za posluživanje oglasa na temelju prethodnih posjeta korisnika našoj web stranici. Ovi podaci se prikupljaju od hiljada posjeta web lokaciji i analiziraju se u cjelini. Ovo nam pomaže da izgradimo bolju web stranicu koja odgovara potrebama naših posjetitelja.

    Također koristimo Web Beacons za prikupljanje neličnih podataka o tome kako koristite našu stranicu, kao što su koliko dugo ste posjećivali našu stranicu, koji web pretraživač koristite, koji je vaš operativni sistem i ko je vaš dobavljač internetskih usluga. Osim toga, također koristimo podatke Google Analytics i DoubleClick kolačić za posluživanje oglasa na osnovu prethodnih posjeta korisnika našoj web stranici. Ovi podaci se prikupljaju iz hiljada poseta sajtu i analiziraju u celini. To nam pomaže da izgradimo bolju web stranicu koja će odgovarati potrebama naših posjetitelja.

    Objavljivanja oglašivača

    Google Analytics

    Koristimo funkcije Google Analytics oglašivača za optimizaciju našeg poslovanja. Karakteristike oglašivača uključuju:

    • Remarketing s Google Analyticsom
    • Izvještavanje o impresijama na Google prikazivačkoj mreži
    • Integracije DoubleClick platforme
    • Izvještavanje o demografskim i interesnim podacima Google Analytics

    Omogućavanjem ovih značajki prikaza Google Analytics, od nas se traži da obavijestimo naše posjetitelje otkrivajući upotrebu ovih značajki i da mi i dobavljači trećih strana koristimo kolačiće prve strane (poput kolačića Google Analytics) ili druge identifikatore prve strane, i kolačići trećih strana (poput DoubleClick kolačića) ili drugi identifikatori trećih strana zajedno za prikupljanje podataka o vašim aktivnostima na našoj web stranici. Između ostalih upotreba, ovo nam omogućava da vas kontaktiramo ako počnete ispunjavati naš obrazac za odjavu, ali ga napustite prije dovršetka s porukom e-pošte koja vas podsjeća da dovršite svoju narudžbu. Funkcija “Remarketing” omogućuje nam da dopremo do ljudi koji su prethodno posjetili našu web stranicu i da odgovarajuću publiku uporedimo s pravom oglasnom porukom.

    Možete isključiti Googleovu upotrebu kolačića tako što ćete posjetiti Googleove postavke oglasa i/ili možete isključiti upotrebu kolačića dobavljača trećih strana posjetom stranici za odjavu Inicijative za mrežno oglašavanje.

    Kao oglašivači na Facebooku i putem naše Facebook stranice, mi (ne Facebook) možemo prikupljati sadržaj ili informacije od korisnika Facebooka i takve informacije se mogu koristiti na isti način naveden u ovoj Politici privatnosti. Pristajete na naše prikupljanje takvih informacija.

    Poštujemo Facebook -ova ograničenja upotrebe podataka.

    – Svi podaci o oglasima prikupljeni, primljeni ili izvedeni iz našeg Facebook oglasa ("Facebook podaci o oglašavanju") dijele se samo s nekim ko djeluje u naše ime, poput našeg davatelja usluga. Odgovorni smo za to da naši pružatelji usluga zaštite sve podatke o oglašavanju na Facebooku ili bilo koje druge podatke dobivene od nas, ograniče našu upotrebu svih tih podataka i drže ih povjerljivima i sigurnima.

    – Ne koristimo podatke o oglašavanju na Facebooku ni u koju svrhu (uključujući ponovno ciljanje, miješanje podataka u kampanjama više oglašivača ili omogućavanje povezivanja ili preusmjeravanja s oznakama), osim na zbirnoj i anonimnoj osnovi (osim ako to nije ovlašteno od strane Facebooka) i samo za procijeniti performanse i efikasnost naših Facebook reklamnih kampanja.

    – Ne koristimo Facebook podatke o oglašavanju, uključujući kriterije ciljanja za Facebook oglas, za izradu, dodavanje, uređivanje, utjecaj ili povećanje korisničkih profila, uključujući profile povezane s bilo kojim identifikatorom mobilnog uređaja ili drugim jedinstvenim identifikatorom koji identificira bilo koji određenog korisnika, pretraživača, računara ili uređaja.

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      Promjene u načinu života koje mogu poboljšati mitohondrijalnu funkciju

      1) Povremeni post

      Ograničenje unosa kalorija i post s prekidima, na primjer u fiksne sate dana, smanjuje nivo energije u tijelu. Za kompenzaciju se povećava nivo NAD+, što povećava sposobnost mitohondrija da proizvode ATP. To dovodi do kasnijeg povećanja razine ATP -a zbog poboljšane funkcije mitohondrija. Ovo je ipak samo naučna hipoteza [2].

      2) Vježbe

      Na sličan način kao ograničenje kalorija i post, vježbanje troši energiju iz tijela. To pak poboljšava mitohondrijsku funkciju povećanjem dostupnosti molekula NAD+ potrebnih za stvaranje ATP -a, prema nekim znanstvenicima [2].

      Osim toga, vježbanju je potrebna energija mišića za snabdijevanje i opskrbljuje tijelo kisikom. Kontinuirano vježbanje povećava broj mitohondrija u mišićnim stanicama tako da se adekvatni nivoi ATP-a mogu obezbijediti za korištenje tokom vježbanja [3].

      U stvari, jedno istraživanje na 8 zdravih starijih dobrovoljaca pokazalo je da je samo 2 sedmice intervalnog treninga visokog intenziteta (HIIT) značajno povećalo mitohondrijsku funkciju u mišićima. Treba poticati dodatne studije [4].

      3) Hladna izloženost

      Niske temperature imaju dubok utjecaj na mitohondrijski broj životinja. Izlaganje štakora plivanju na niskim temperaturama (23 & degC) povećalo je stvaranje mitohondrija povećavajući protein odgovoran za pokretanje mitohondrijske sinteze (PGC-1alfa) [5].

      Slični rezultati uočeni su kod pacova&rsquo ćelija jetre i skeletnih mišića nakon izlaganja hladnoći tokom 15 dana. Ovi nalazi nisu potvrđeni kod ljudi [6].

      4) Ketogena dijeta

      Ketogena dijeta je dijeta s visokim udjelom masti i niskim udjelom ugljikohidrata za koju se tvrdi da će vaše tijelo prebaciti s trčanja na ugljikohidratima na rad na masti [7].

      Kada se masti razgrađuju radi dobivanja malih molekula koji se nazivaju ketonska tijela. Ovi molekuli se koriste za proizvodnju ATP-a umjesto glukoze. Neki istraživači vjeruju da to rezultira poboljšanom mitohondrijskom funkcijom (PGC-1alpha, SIRT1/3, aktivacija AMPK), većim nivoima ATP-a iz lanca transporta elektrona i ukupnim staničnim zdravljem [7].

      Jedno je istraživanje pokazalo da je ketogena dijeta usporila mitohondrijsku miopatiju (mišićnu bolest) djelomično povećavajući broj novih mitohondrija (mitohondrijska biogeneza). Nedostaju ljudske studije [8].


      U gotovo svakoj ćeliji našeg tijela žive male elektrane poznate kao mitohondrije. Ovi sićušni organeli, sa svojim genomom, prvenstveno proizvode adenozin trifosfat (ATP), gorivo o kojem ovise vaše ćelije kako bi funkcionirale. Ako nešto pođe po zlu u lancu komponenti transporta elektrona mitohondrija koje na kraju proizvode ATP, dolazi do bolesti.

      „Proizvodnja ATP -a je jedini sistem u tijelu koji je pod dvostrukom genetskom kontrolom“, kaže Joeva J. Barrow, Nutricion Sciences. “Vaši nuklearni geni i vaši mitohondrijski geni rade zajedno kako bi sistem učinili funkcionalnim. Svaki nedostatak bilo kojeg genoma dovodi do bolesti, jer ako ne možete proizvesti dovoljno ATP -a, tada nemate dovoljno energije u tijelu, a vaše ćelije počinju odumirati. Obično su tkiva koja su vrlo energična i zahtijevaju puno ATP -a, poput mozga, srca i mišića, najosjetljivija. "

      Mitohondrijski poremećaji, šta su to

      Ne postoji lijek za mitohondrijalne poremećaje, koje je teško dijagnosticirati i koje je nemoguće liječiti. One dovode do složenih bolesti koje se teško nazivaju domaćim imenom, kao što su mitohondrijalna encefalomiopatija, laktacidoza i epizode slične moždanom udaru (MELAS) i Leberova nasljedna optička neuropatija (LHON), ali su češće nego što većina ljudi misli. Jedan od 4.500 ljudi pati od mitohondrijske bolesti, a jedan od 200 nema simptome, ali nosi mitohondrijsku mutaciju koja potencijalno može izazvati bolest kasnije u životu ili kada se prenese na sljedeću generaciju. Sve te asimptomatske nositeljice su žene, budući da su mitohondrije naslijeđene od majke.

      Da bi se razumjeli procesi koji uzrokuju mitohondrijsku bolest, kao i potencijalni tretmani, Barrowova laboratorija ovisi o nepristranim, visokopropusnim mehanizmima pregleda, poput kemijskog ciljanja malih molekula i ablacije gena CRISPR-Cas9 na cijelom genomu. “Naš cilj je identificirati sve gene ili proteine ​​koji bi mogli biti povezani s mitohondrijskom bioenergetikom, a zatim ih značajno iskoristiti da vidimo možemo li ih potaknuti na terapiju”, kaže Barrow.

      Proučavanje genetike i biohemije u osnovi mitohondrijalnih poremećaja

      Istraživači koriste kombinaciju ćelijskih i mišjih modela, pored tkiva pacijenata, kako bi istražili genetiku i biohemiju iza ovih bolesti. „Naši tipični eksperimenti počinju tako da vidimo koliko dugo možemo održati ćelije sa oštećenim mitohondrijama u životu“, kaže Barrow. “Stavili smo ih pod određene nutritivne uvjete za koje znamo da će ih ubiti jer ne mogu proizvesti ATP. Tada pokušavamo promicati preživljavanje tretirajući ih malim molekulima ili modificirajući određene gene. ”

      Nakon što su utvrdili koji spojevi mogu spasiti stanice, Barrow i njeni suradnici prelaze na fazu otkrića svog istraživanja. "Moramo točno shvatiti šta spoj čini", kaže Barrow. „Šta obavezuje? Kako cilja na ovu funkciju? Kako to podstiče proizvodnju ATP-a? Da bismo povećali potencijal terapije, moramo odgovoriti na takva pitanja. U isto vrijeme, mogli bismo otkriti i druge dodatne faktore koji pokazuju terapeutski potencijal na tom putu.”

      "Moja laboratorija proučava genetske i molekularne komponente kako bi otkrila imaju li neki ljudi predispozicije koje ih čine manje ili više gojaznima."

      Barrow nastavlja svoj raniji rad kao postdoktorski istraživač na Univerzitetu Harvard, gdje je profilirala 10.015 malih molekula - prirodnih i sintetiziranih spojeva koji ciljaju različite proteine ​​u tijelu. Ona i njene kolege identificirale su više od 100 obećavajućih kemijskih spojeva. Sada ih njena laboratorija karakterizira da procijene njihovu sposobnost da ispravljaju oštećenje mitohondrija, posebno u mišićnim ćelijama. So far, a significant subset has a positive effect, and the researchers are trying to pin down exactly how they work.

      Obesity and Metabolic Diseases, Mitochondria-Related

      Continuing her research connected to mitochondria, Barrow also explores metabolic disease in the context of obesity. Worldwide, 1.9 million, or one in three people, are overweight, and 41 million of them are children under the age of five. With obesity comes associated metabolic diseases such as cancer, cardiovascular disease, and hypertension.

      “Every year we do the statistics on obesity, and no matter how much we counsel on diet and exercise, no matter how easy it should be to maintain an energetic balance, something is amiss,” Barrow says. “So my lab is looking at genetic and molecular components to discover if some people have a predisposition that makes them more or less obese or to see if we can take advantage of the molecular system to increase energy expenditure. This could offer another form of therapy to fight against obesity in conjunction with diet and exercise.”

      Thermogenic Fat

      The researchers have turned their attention to thermogenic fat. This subset of fat cells, also called brown and beige fat, is prevalent in animals that go through hibernation, but scientists recently discovered it in humans as well. “Brown and beige fat don’t only store fat molecules, like white fat does, they have a special ability to burn them to produce heat,” Barrow explains.

      Thermogenic fat has a protein known as uncoupling protein 1 that pokes a hole in the membrane of mitochondria, allowing protons to leak out. These protons are part of a proton gradient that is integral to the production of ATP. Without them, mitochondria are no longer able to effectively make the chemical. “Your body’s response is to start burning everything it can to try to maintain the proton gradient,” Barrow says. “And as a result, your energy expenditure goes through the roof.”

      Brown fat is prevalent in newborn humans where it serves to keep infants from going into thermal shock as they exit from maternal body temperature to the much colder temperature outside the womb. Later, other mechanisms, such as shivering, serve to keep adults warm while maintaining their body weight. “But adults still have brown fat that we can activate to increase energy expenditure components,” Barrow explains.

      Using proteomics, metabolomics, and genomics, Barrow and her colleagues seek to unveil factors that will activate brown and beige fat cells. “We have discovered a host of novel genes that are involved in turning on the thermogenic pathway that protects you against obesity,” Barrow says. “Now it will be fascinating to discover how these genes work so that they can be targeted toward therapy.”

      For Barrow, who has a doctorate in biochemistry and molecular biology, with clinical expertise as a registered dietitian, mitochondria are a perfect target for research. “The mitochondria are the metabolic hub of the cell,” she says. “No matter what aspect of metabolism you study—lipids, carbohydrates, vitamins—they all feed back into whether or not you can effectively produce energy. Everything my lab works on centers around this very mighty, tiny organelle that’s so important to life.”


      Why we Age: Mitochondrial Dysfunction

      Mitochondrial dysfunction is one of the root causes of aging as described in the Hallmarks of Aging [1]. As they age, mitochondria lose their ability to provide cellular energy and release reactive oxygen species that harm cells.

      What are mitochondria?

      Mitochondria, which are often called the powerhouses of cells, act like miniature factories, converting the food we eat into usable energy in the form of a chemical called adenosine triphosphate (ATP) [2]. ATP provides energy to fuel a myriad of cellular processes, such as muscle contraction, nerve impulse propagation, and protein synthesis. ATP is common to all forms of life and is often referred to as the “molecular unit of currency” of intracellular energy transfer.

      Interestingly, mitochondria did not originate as part of multicellular life they are stowaways in our cells and have their own unique DNA, which is separate from our own. It is widely thought that they merged with a very early ancestor of all multicellular life to form a symbiotic relationship [3]. Mitochondria become dysfunctional as we age and are host to their own separate (though similar) forms of damage.

      How do mitochondria become dysfunctional?

      As we age, our mitochondria go through changes that harm their ability to provide us with chemical energy while causing the release of harmful reactive oxygen species [4], which can cause DNA mutations leading to cancer [5-6] and even harm proteostasis [7]. Reactive oxygen species also drive muscle weakness [8], a further smoldering level of background inflammation (inflammaging) [9], and the associated bone frailty [10], senescent cell load [11] and immune suppression [12] of old age. Mitochondria from elderly people even look different [13] they swell while their numbers dwindle, unable to replace themselves as quickly in their dysfunctional state [14-15].

      These problems aren’t all that reactive oxygen species can cause, however they can also cause mutations in mitochondrial DNA. [16] While some studies suggest that this damage is not done directly [17], it must be remembered that reactive oxygen species can damage the very proteins that would control the reproduction of mitochondria and introduce additional errors into the copies by extension [7].

      While most of these issues are detected by quality-control mechanisms in the cell [18], causing damaged mitochondria to be destroyed through a process called mitophagy, these systems become less and less effective with age, decreasing in activity and eventually allowing errors to slip through. In some cases, this isn’t so bad each cell contains a large number of mitochondria, so ten or even a few hundred being mutated isn’t a problem. However, some of these errors can make the dysfunctional mitochondria survive longer than healthy mitochondria. In this way, some types of dysfunctional mitochondria build up and eventually become more common than healthy ones [19].

      Additionally, as aging progresses, NAD+ levels in human cells decrease, causing a breakdown in communication between the human nucleus and mitochondrial DNA, again leading to decreased energy production and increased reactive oxygen species production [20].

      How could we prevent or reverse this?

      A number of methods have been proposed for preventing this. First of all, the issues with NAD+ could be solved by some method of NAD+ supplementation, slowing down the accumulation of this damage. In addition, the most vital parts of the mitochondrial DNA could be moved to another part of the cell – the nucleus – giving it access to better DNA repair mechanisms and keeping it away from the source of reactive oxygen species [21]. This approach has been demonstrated for some of this vital code [22]. Of particular note, the study proving that this is possible was funded on our crowdfunding platform Lifespan.io!

      Zaključak

      Mitochondrial dysfunction is an important part of the aging process. These miniature chemical engines, while capable of self-replication, gradually become more dysfunctional with age through a variety of mechanisms, causing harm to our cells and encouraging more dysfunction in a vicious cycle. Quality control mechanisms hold this at bay for a time, but they eventually fail, leading to multiple diseases of aging and a long-lasting, chronic background level of inflammation called inflammaging.

      Literature

      [1] López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. Cell, 153(6), 1194-1217.

      [2] Lodish, H., Berk, A., Zipursky, S. L., Matsudaira, P., Baltimore, D., & Darnell, J. (2000). Electron Transport and Oxidative Phosphorylation.

      [3] Gray, M. W., Burger, G., & Lang, B. F. (2001). The origin and early evolution of mitochondria. Genome biology, 2(6), reviews1018-1.

      [4] Lesnefsky, E. J., & Hoppel, C. L. (2006). Oxidative phosphorylation and aging. Ageing research reviews, 5(4), 402-433.

      [5] McAdam, E., Brem, R., & Karran, P. (2016). Oxidative Stress–Induced Protein Damage Inhibits DNA Repair and Determines Mutation Risk and Therapeutic Efficacy. Molecular Cancer Research.

      [6] Suzuki, D. T., & Griffiths, A. J. (1976). An introduction to genetic analysis. WH Freeman and Company..

      [7] Korovila, I., Hugo, M., Castro, J. P., Weber, D., Höhn, A., Grune, T., & Jung, T. (2017). Proteostasis, oxidative stress and aging. Redox biology, 13, 550-567.

      [8] Alway, S. E., Mohamed, J. S., & Myers, M. J. (2017). Mitochondria Initiate and Regulate Sarcopenia. Exercise and sport sciences reviews, 45(2), 58-69.

      [9] Rimessi, A., Previati, M., Nigro, F., Wieckowski, M. R., & Pinton, P. (2016). Mitochondrial reactive oxygen species and inflammation: molecular mechanisms, diseases and promising therapies. The international journal of biochemistry & cell biology, 81, 281-293.

      [10] Lane, R. K., Hilsabeck, T., & Rea, S. L. (2015). The role of mitochondrial dysfunction in age-related diseases. Biochimica et Biophysica Acta (BBA)-Bioenergetics, 1847(11), 1387-1400.

      [11] Kamogashira, T., Hayashi, K., Fujimoto, C., Iwasaki, S., & Yamasoba, T. (2017). Functionally and morphologically damaged mitochondria observed in auditory cells under senescence-inducing stress. NPJ aging and mechanisms of disease, 3(1), 2.

      [12] Frasca, D., & Blomberg, B. B. (2016). Inflammaging decreases adaptive and innate immune responses in mice and humans. Biogerontology, 17(1), 7-19.

      [13] Gerencser, A. A., Doczi, J., Töröcsik, B., Bossy-Wetzel, E., & Adam-Vizi, V. (2008). Mitochondrial swelling measurement in situ by optimized spatial filtering: astrocyte-neuron differences. Biophysical journal, 95(5), 2583-2598.

      [14] Seo, A. Y., Joseph, A. M., Dutta, D., Hwang, J. C., Aris, J. P., & Leeuwenburgh, C. (2010). New insights into the role of mitochondria in aging: mitochondrial dynamics and more. J Cell Sci, 123(15), 2533-2542.

      [15] Figge, M. T., Reichert, A. S., Meyer-Hermann, M., & Osiewacz, H. D. (2012). Deceleration of fusion–fission cycles improves mitochondrial quality control during aging. PLoS computational biology, 8(6), e1002576.

      [16] Lee, H. C., & Wei, Y. H. (2007). Oxidative stress, mitochondrial DNA mutation, and apoptosis in aging. Experimental biology and medicine, 232(5), 592-606.

      [17] Itsara, L. S., Kennedy, S. R., Fox, E. J., Yu, S., Hewitt, J. J., Sanchez-Contreras, M., … & Pallanck, L. J. (2014). Oxidative stress is not a major contributor to somatic mitochondrial DNA mutations. PLoS genetics, 10(2), e1003974.

      [18] Srivastava, S. (2017). The mitochondrial basis of aging and age-related disorders. Genes, 8(12), 398.

      [19] Luo, C., Li, Y., Wang, H., Feng, Z., Li, Y., Long, J., & Liu, J. (2013). Mitochondrial accumulation under oxidative stress is due to defects in autophagy. Journal of cellular biochemistry, 114(1), 212-219.

      [20] Gomes, A. P., Price, N. L., Ling, A. J., Moslehi, J. J., Montgomery, M. K., Rajman, L., … & Mercken, E. M. (2013). Declining NAD+ induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell, 155(7), 1624-1638.

      [21] Boominathan, A., Vanhoozer, S., Basisty, N., Powers, K., Crampton, A. L., Wang, X., … & O’Connor, M. S. (2016). Stable nuclear expression of ATP8 and ATP6 genes rescues a mtDNA Complex V null mutant. Nucleic acids research, 44(19), 9342-9357.

      [22] Boominathan, A., Vanhoozer, S., Basisty, N., Powers, K., Crampton, A. L., Wang, X., … & O’Connor, M. S. (2016). Stable nuclear expression of ATP8 and ATP6 genes rescues a mtDNA Complex V null mutant. Nucleic acids research, 44(19), 9342-9357.


      Introducing the Mitochondria

      In order to survive and thrive, microorganisms require energy. Microorganisms need energy to be able to keep up homeostasis (inner cell environment stableness), making sure a well-working metabolism, also to keep the body's essential functions working [1]. Mitochondria (mitochondrion = singular) established fact as the power place of the cell. Its name was produced by the Greek phrase "mitos" (thread) & "chondros" (granule). Therefore, the name mitochondria mean "thread-like granule" [2].

      The first recorded recognition of mitochondria was initially detected back in 1857 by way of a Swiss physiologist and anatomist, Albert von Kolliker as "granule-like" constructions within muscle cells. During this time, microscopes were very simple so scientists that time can only see and observe the several organelles in a cell scheduled to very harsh morphology observations. This means scientists that time have yet to find the value of mitochondria in cell life. In later years, German pathologist and histologist Richard Altmann utilized a dye approach in order to stain the structures to make them easier to imagine under a light microscope. This technique ended up being successful and he could distinguish the first mitochondria from other cell organelles. Altmann then known as this organelle the "bioblast" and he presumed this organelle to be essential in cellular activity. Later in 1898, German scientist Carl Benda eventually copyrighted the name mitochondria to displace bioblast. Further researches regarding the functions, roles, mechanisms, and dysfunctions of the mitochondria in cells are still continuing even until today [2]. The breakthrough of mitochondria was called one of the biggest science discoveries ever matching to Kendall Haven's reserve, "100 Greatest Science Discoveries ever" [3].

      Mitochondria are dual membrane-enclosed organelles, indicating it is covered with an unbiased membrane. It has an outside membrane and also an internal membrane. These membranes are made up of any bilayer of phospholipids. These two membranes then enclose two compartments which will be the intermembrane space and the mitochondrial matrix (for more info, see the subsequent section). The shape of mitochondria resembles a kidney or a sausage. These are around 1-10 m long making them the greatest organelle found free in the cytoplasm [5].

      Mitochondria are available in almost all eukaryotic cells and their figures differ in each cell. The number of mitochondria in a cell depends upon how much energy the cell needs. It can range from just only one to a few thousand per cell. If a particular cell needs more energy than another cell, the amount of mitochondria within the specific cell would be greater than that of the other cell. For example, muscle skin cells require more energy than kidney skin cells because muscle cells perform more work than kidney skin cells because of their contraction quantities and power. The mitochondria can occasionally be found situated between your myofibrils of muscles or at the base of the sperm cell's flagellum [6]. Through the use of an electron micrograph, mitochondria can be seen forming a sophisticated 3 dimensional branching network inside the cell with the cytoskeleton [7].

      Due to its independent bacteria-like DNA and ribosomes, mitochondria are presumed to be once an external bacterial symbiote that was then engulfed by a more substantial procaryotic cell. This bacterial symbiote then wasn't broken down in reality, it was maintained alive within the bigger cell which then goes through a mutualism symbiosis with the symbiote. The symbiote provides energy for the bigger cell and the bigger cell provides coverage and the right living environment for the much smaller symbiote cell. This specific incident was thought by many scientists as the beginning of modern eukaryotic cells. This specific theory is called the endosymbiosis theory. North american biologist Lynn Margulis was the individual who developed and outspreaded the theory worldwide. Due to its 3rd party DNA & ribosomes, the replication of mitochondria can be done independent from the mom cell this implies its replication can be done independently from the normal nuclei replication that largely occurs [8].


      The Psychological Powerhouse

      It’s likely that you remember this statement to be important enough that your teacher drilled this idea into your brain.

      Well there might be a bit more to this generalized statement of Biology. What if I told you that how you feel and think and deal with stress actually involves the mitochondria?

      Before going into that, let’s refresh our memories about what exactly “the powerhouse of the cell” generally means for the Mitochondria.

      Our body is made up of trillions of cells! Ćelije are the Lego pieces that fit together to create the structure that forms us as humans. In cells, there are different subunits that help the cell called organele. These tiny parts of cells each have a specific function. Mitochondria are one of those organelles– and I am sure you might have an initial guess about what they do!

      These small but mighty organelles are organized by the different regions created by their two membranes – the outer and inner membranes. These membranes are boundaries that keep together parts of the mitochondria and determine what can enter into the mitochondria. The outer membrane is focused on housing proteins and enzymes, the pieces that provide structure, regulate processes, and transport materials throughout the cell. The inner membrane, which includes the cristae (the folds) and the matrix (the space), include space for chemical reactions, production of ATP (energy), and mitochondrial DNA (genetic information).

      We call these little organelles the powerhouse because of one of its central functions: energy production. Think of where you would be without energy: on your bed, lazily watching Netflix? Yes – in the colloquial sense. But, without your mitochondria’s energy production, your cells are not going to function to keep you alive.

      Mitochondria are like windmills that convert energy into power for the farmhouses they break down sugar into energy, and this useable energy is utilized by all the other important cells to make our bodies function.

      You might now be asking if mitochondria are the source of physical energy, what do they have to do with a Psychological Powerhouse? Well, while Biology, Neuroscience, and Psychology have always been friendly, these fields are often afraid to interact too much. A lot of factors contribute to this disconnect between the fields, but it is important to understand this broader interaction to understand that how we function as humans physically impacts us mentally.

      When we take a step back and examine a larger picture, we find that this powerhouse organelle, whose main focus is energy production, actually has a very interesting relationship with psychological stress.

      The mitochondria’s functions extend far past energy production. In the course of producing energy, mitochondria have the ability to sense stress mediators, such as its ability to sense environmental, metabolic, and neuroendocrine stressors, whether they are a lack of nutrients or particular hormones. Picard & McEwen (2018) explored this relationship between psychological stress and mitochondria.

      When a stressor occurs, there is an effect on the way mitochondria interact with each other and undergo morphological and function changes. Think of how the way you and your Uncle interact differently at a funeral. You dress, talk to each other, and hug differently than when you normally see her on a regular basis because you are in a different and stressful environment mitochondria also look and act different with each other when undergoing stress.

      In the short-term these types of changes may result in adaptation, but in the long term, stressors can result in chronic alterations within the mitochondria (Picard et al., 2015).

      When multiple stressors cumulate to the dysregulation of the immune system in the body, allostatic load occurs, and it contributes to long-term effects on the body – both physically and mentally.

      What exactly is an allostatic load? Have you ever started to make a pile of semi-clean clothes on that one particular chair in your room? They are dirty enough not to make it into your dresser, but clean enough that you don’t need to put them in the laundry. Allostatic load is when that pile eventually gets so high over time that it becomes too heavy to physically carry and you mentally cannot determine how to fix the pile as it is overwhelming the clothes are the different types of stress that pile up metaphorically in your body, physically and mentally. This concept can occur in the mitochondria as well.

      When the mitochondria sense the stress mediators (such as increases in the stress hormones cortisol and catecholamine), changes occur to its structure and functions. Over time, these constant changes damage the mitochondrial DNA that is stored in the organelle and diminish its capacity for energy production. Thus, the important systematic processes that are in connection with the mitochondria are negatively influenced, meaning that your body’s cells are no longer recieving all the energy they need. This effect of chronic stress on mitochondria is termed mitochondrial allostatic load (MAL).

      Mitochondrial Allostatic Load (MAL)

      Think how if you kept attending those funerals as well as had other stressful events, you would feel physically and emotionally drained from all the changes in behavior you have when interacting with other people. Your relationships would be negatively affected by your lack of energy and mood changes from the cumulation of stressful events.

      Just like this cumulation from stress would have many negative consequences for your life, chronic stressors have many negative affects to mitochondria because of MAL.

      MAL can result in cellular dysfunction, which can lead to health effects like high blood pressure, cardiovascular disease, diabetes, cognitive issues, among others.

      MAL can also impact brain structure and function, such that areas of the brain like the hippocampus (responsible for explicit memory) and the medial prefrontal cortex (responsible for decision-making) are atrophied (shrinking quality).

      Overall, it is apparent through this framework of MAL, that our favorite powerhouse of the cell is also a psychological powerhouse – one that has interactions with psychological stressors and impacts our brain as well as our physiological functioning.

      If you want to pretend you are in Biology class again, below are some videos and websites to learn more about Mitochondria:


      Live mitochondria seen in unprecedented detail: photobleaching in STED microscopy overcome

      Inner membranes of live mitochondria under a STED microscope imaged using the MitoPB Yellow fluorescent marker molecule created by researchers at the Institute of Transformative Bio-Molecules (ITbM) at Nagoya University. The outer membranes of the mitochondria are invisible. The marker molecule can withstand the STED beam for a relatively long time, which allows time-lapse imaging of the live subject. Sample preparation is much easier for an optical microscope than a Transmission Electron Microscope (TEM), requiring about an hour rather than a day. Cells cannot be imaged alive using TEM. The mitochondria have been treated with a reagent that suppresses DNA replication, inducing dysfunction, in order to see their survival (left) and dying (right) processes. Being able to see the dysfunction processes occurring inside mitochondria will lead to a better way of diagnosing human mitochondrial disease - and perhaps even a cure. Credit: © ITbM, Nagoya University

      Light microscopy is the only way in which we can look inside a living cell, or living tissues, in three dimensions. An electron microscope only gives a two-dimensional view, and the organic sample would quickly burn up due to the extreme heat of the electron beam, and therefore cannot be observed alive. Moreover, by marking the biomolecules of the structure we are interested in with a specially designed fluorescent molecule, we can distinguish it from the surroundings: this is fluorescence microscopy.

      Until the mid-1990s fluorescence microscopy was hampered by basic physics: due to the diffraction limit, any features on the sample closer together than about 250 nanometres would be blurred together. Viruses and individual proteins are much smaller than this, so they could not be studied this way. But around 1994, in a wonderful lesson teaching us that we must take care when applying fundamental physical principles, Stefan Hell discovered Stimulated Emission Depletion (STED) microscopy, which is now one of several optical microscopy approaches that achieve "super-resolution," resolution beyond the diffraction limit. He received the Nobel Prize in Chemistry in 2014 "for the development of super-resolved fluorescence microscopy," together with Eric Betzig and William Moerner.

      To see why the diffraction limit is a problem, imagine the structure of interest is very small, say, 50 nanometres across, like a virus, and has been marked with a fluorescent biomolecule. Now imagine illuminating it with a laser spot, say, 200 nanometres in diameter. The illuminated marker molecules emit light spontaneously, at random times, by fluorescence, with the probability dropping rapidly with time. The photons from many fluorescing molecules are focused onto a detector using lenses, creating a single featureless pixel. It's not fully bright because only a small proportion of the sample in the illuminated circle contains fluorescent molecules. If you were to move the laser 200 nanometres in any direction, to where, in this example, no fluorescent molecules are present, the signal will certainly go dark. So, this rather dim pixel tells us that something is present inside this sample area 200 nanometres in diameter. The diffraction limit prevents us forming pixels from smaller areas, if we use the basic approach.

      The physical idea of STED microscopy is very simple. With the laser spot illuminating the region around the small fluorescing structure again, suppose you somehow stop light being sent to the detector from as large an area as possible within the spot—leaving a much smaller spot, say, 60 nanometres in diameter. Now if you move the laser 60 nanometres in any direction and the signal goes dark, the pixel in the image represents the presence of structure up to 60 nanometres across. The diffraction limit has been beaten. Of course, one such pixel is featureless, but a sharp image of mitochondria can be built up by scanning across and recording many pixels of varying brightness. (See Figure 1. "Time-gated STED Microscopy" was used to capture most of the images in this paper.)

      Stefan Hell's Nobel Prize-winning discovery consists of two insights. First, he thought of the idea of stopping light being sent to the detector from as large an area as possible within an illuminated spot whose size matches the diffraction limit. Second, he figured out how to actually achieve it.

      Two lasers illuminate the same spot. The first laser excites the marker molecule electrons and they decay spontaneously back to their ground state, each emitting a visible photon of a specific wavelength. (This is fluorescence.) The process is random, with the emission probability decreasing with time fairly quickly, meaning that most photons are emitted within the first few nanoseconds of the sample being illuminated. A second laser, the "STED beam," shaped with a hole in the middle so as not to affect the marker molecules there, is tuned to stimulate emission of a photon by the excited marker molecule in the outer ring. But how are these photons distinguished from photons emitted from the middle?

      In response to being deprived of nutrients, mitochondria fuse together and increase the number of cristae. (a) Frames from a time-lapse sequence showing two separate mitochondria fusing together to form a single mitochondrion. The outer membranes of the mitochondria are invisible: we are seeing the inner membranes fusing together. (b) Frames from a time-lapse sequence showing two cristae inside a single mitochondrion fusing together. (See Video 2 in the Supplementary Material on the paper's PNAS webpage.) The scale bars represent 2mm. Credit: © ITbM, Nagoya University

      The emission process from the outer ring is also random but happens much more quickly, the probability decreasing rapidly, meaning that most of these photons are emitted within a nanosecond or so. As the two superimposed beams scan across the sample, by the time the centre of the ring is fluorescing, the surrounding molecules have already been forced into their ground state by emitting a photon—they have been "switched off." The STED microscopy technique relies on clever timing in this way. In principle, the size of the glowing central spot can be made as small as you want, so any resolution is possible. However, the doughnut-shaped "STED beam" would then be delivering energy in the form of concentrated visible laser light to a larger area of the living cell, risking killing it.

      Nevertheless, the process is not ideal, and the resulting image loses some sharpness because some marker molecules in the outer ring are not properly switched off—the process is probabilistic, after all—and when they do fluoresce they contaminate the signal from the centre. However, due to the different timing of the spontaneous and stimulated emission, the earliest photons to arrive at the detector are from regions illuminated by the highest STED beam intensity, and the last photons to arrive are most likely from marker molecules located in the central spot. So by waiting a short time (around one nanosecond) before recording the image, most of the photons from the outer ring can be filtered out. This is called "Time-gated STED Microscopy." Further sharpening of the image is achieved through a process called deconvolution.

      The invention of super-resolution microscopy heralded a leap forward in the life sciences. Living organisms could be observed at an unprecedented resolution. However, time-lapse sequences of images could not be made over any decent length of time because the marker molecules would degrade under the intense STED beam and stop fluorescing. This is the photobleaching problem. The damaged marker molecules can also become toxic to the cell.

      The photobleaching problem solved

      Shigehiro Yamaguchi and Masayasu Taki, of Nagoya University's Institute for Transformative Bio-Molecules (ITbM), led a research team that has developed a marker molecule, called "MitoPB Yellow," that is absorbed by the inner membrane of mitochondria, including the cristae—the fold-like structures—and has a long lifetime under a STED beam. The idea for the marker molecule targeting mitochondria came from co-author Chenguang Wang, of the ITbM. Multicolour STED imaging with a single STED laser is also possible and the researchers expect that fluorescent markers similar to MitoPB Yellow should find a wide range of applications in other super-resolution techniques as well (such as those developed by Eric Betzig and William Moerner).

      To demonstrate the practical usefulness of MitoPB Yellow for live-cell imaging, the group placed mitochondria under conditions that are known to cause certain structural changes—but until now these have only been observed using transmission electron microscopy, which cannot be used on live cells. The mitochondria were treated with a reagent that suppresses DNA replication, inducing dysfunction, in order to observe their survival and dying processes.

      Video 1. Live mitochondria imaged in unprecedented detail -- for an unprecedented length of time -- using the MitoPB Yellow fluorescent marker created by Nagoya University-led researchers. The marker molecule is designed to be absorbed by only certain membranes within each mitochondrion, and retains its fluoresescence under the STED microscope for a very long time. This video was shot at 1.5 fps and a resolution of 90nm. Still images were captured at 60nm resolution. In response to being deprived of nutrients, mitochondria fuse together and increase the number of cristae. This time-lapse sequence shows events such as two separate mitochondria fusing together to form a single mitochondrion and a single mitochondrium fusing together. Note that the outer membranes of the mitochondria are invisible: we are seeing the inner membranes fusing together. Zasluge: ITbM, Univerzitet Nagoya

      Then, using Time-gated STED Microscopy, the research team made still images at 60 nanometre resolution (about one thousandth of the width of a human hair), as well as time-lapse image sequences showing the mitochondria responding to a deprivation of nutrients by changing form in order to survive. The long image sequences—of up to 600 images—are the first ever made of mitochondria at the relatively high spatial resolution of 90 nanometres. (See Video 1, which shows a time-lapse sequence recorded over nearly 7 minutes.)

      Over a few minutes the inner mitochondrial structure changed dramatically in a number of ways. Initially, elongation and increase in the number of cristae was seen. One image sequence (see Figure 2a) shows inner membranes of neighbouring mitochondria fusing together—in other words, two mitochondria fusing to make one. Another image sequence (see Figure 2b) shows two cristae within a single mitochondrion apparently fusing together. Elongation and creating more cristae is thought to increase the efficiency of energy production (ATP synthesis) while protecting the mitochondrium from "autophagosomal degradation"—a programmed death whose purpose is to remove unnecessary or dysfunctional components from the cell and allow the orderly degradation and recycling of cellular components.

      After the initial period of elongation, the inner membranes of some mitochondria split into globules that swelled and lost cristae (see Movie S2) some globules ruptured (Movie S4). Some formed concentric spheres (Figure 1 and Video 1). The fluorescence intensity remained the same. Noteworthy here is that the cristae and membranes remain as sharply imaged as before, which indicates that the cause of the mitochondrion's death is not toxicity due to degradation of the marker molecule under the beam. The extremely strong STED laser might have damaged the mitochondria, although exactly why they rupture is unknown.

      In these images, after seeing initial survival responses, we are watching the death of mitochondria under the intense STED beam. A future direction of research will be to reduce the intensity of the STED laser beam by creating a fluorescent marker molecule that glows when illuminated by light of a longer wavelength and therefore lower energy. The mitochondria might then live longer.

      However, even with MitoPB Yellow, the dying process—which is not well understood—can be studied. Nobody knows if the morphological (structural) changes observed during the dying process are related to apoptosis (normal, controlled death) or necrosis (death due to injury or malfunction). Apoptosis is known to be triggered by a signalling molecule called cytochrome C: if a reagent can be found that suppresses cytochrome C, then mitochondria—and human cells—could live longer.

      Being able to see the processes occurring inside mitochondria should lead to a better way of diagnosing human mitochondrial disease—and perhaps even to a cure.


      Mitochondria drive cell survival in times of need

      McGill University researchers have discovered a mechanism through which mitochondria, the energy factory of our body’s cells, play a role in preventing cells from dying when the cells are deprived of nutrients – a finding that points to a potential target for next-generation cancer drugs.

      The research, published in Molecular Cell, builds on previous work by McGill professor Nahum Sonenberg, one of the senior authors of the new study.

      Cells in our body grow in size, mass and numbers through a process governed by a master regulator known as mTOR (Mechanistic Target of Rapamycin). Sonenberg discovered years ago that mTOR also controls protein expression in all human cells. In particular, mTOR targets the selective synthesis of proteins destined for the mitochondria, the bacteria-like structures in all our cells that generate the energy needed for cells to grow and divide.

      In collaboration with the research labs of McGill scientists Heidi McBride and John Bergeron, Sonenberg and his team have now shown that mTOR also controls the expression of proteins that alter the structure and function of mitochondria -- thereby protecting cells from dying.

      Their work has implications for cancer therapy, since new drugs that act on mTOR are currently in clinical trials for cancer. While the treatments are effective in arresting the expansion and growth of cancer cells, the cells continue to survive, despite a shortage of nutrients. The new study reveals that mitochondria help keep these cells alive by fusing together and blocking a central point in a cell death pathway, called apoptosis.

      This advance offers clues to develop combination therapies that could promote cancer-cell death by reversing the protection offered by mitochondria, the researchers say.

      Two postdoctoral fellows from the Sonenberg and McBride labs, Masahiro Morita currently at the University of Texas Health Science Center at San Antonio, and Julien Prudent, currently at MRC Mitochondrial Biology Unit in Cambridge, UK, led the collaborative team, working together to map the details of this cellular survival pathway.

      “mTOR Controls Mitochondrial Dynamics and Cell Survival via MTFP1,” Masahiro Morita, Julien Prudent, et al. Molecular Cell, Sept. 21, 2017
      DOI: 10.1016/j.molcel.2017.08.013

      Funding for the research was provided in part by the Canadian Institutes of Health Research, the Canadian Cancer Society Research Institute, the Terry Fox Research Institute, and the National Sciences and Engineering Research Council of Canada.