Editing Telomere (section)

=== Telomerase ===
[[File:Synthesis of chromosome ends by telomerase.svg|thumb|Synthesis of chromosome ends by telomerase]]
{{Main|Telomerase}}

Many organisms have a ribonucleoprotein enzyme called telomerase, which carries out the task of adding repetitive nucleotide sequences to the ends of the DNA. Telomerase "replenishes" the telomere "cap" and requires no ATP.<ref name=":2">{{cite journal |vauthors=Mender I, Shay JW |date=November 2015 |title=Telomerase Repeated Amplification Protocol (TRAP) |journal=Bio-Protocol |volume=5 |issue=22 |pages=e1657 |doi=10.21769/bioprotoc.1657 |pmc=4863463 |pmid=27182535}}</ref> In most multicellular eukaryotic organisms, telomerase is active only in [[germ cell]]s, some types of [[stem cell]]s such as [[embryonic stem cells]], and certain [[white blood cell]]s. Telomerase can be reactivated and telomeres reset back to an embryonic state by [[somatic cell nuclear transfer]].<ref>{{cite journal | vauthors = Lanza RP, Cibelli JB, Blackwell C, Cristofalo VJ, Francis MK, Baerlocher GM, Mak J, Schertzer M, Chavez EA, Sawyer N, Lansdorp PM, West MD | s2cid = 37387314 | display-authors = 6 | title = Extension of cell life-span and telomere length in animals cloned from senescent somatic cells | journal = Science | volume = 288 | issue = 5466 | pages = 665–9 | date = April 2000 | pmid = 10784448 | doi = 10.1126/science.288.5466.665 | bibcode = 2000Sci...288..665L }}</ref> The steady shortening of telomeres with each replication in somatic (body) cells may have a role in [[senescence]]<ref name="WhittemoreVera2019">{{cite journal|last1=Whittemore|first1=Kurt|last2=Vera|first2=Elsa|last3=Martínez-Nevado|first3=Eva|last4=Sanpera|first4=Carola|last5=Blasco|first5=Maria A.|title=Telomere shortening rate predicts species life span|journal=Proceedings of the National Academy of Sciences|volume=116|issue=30|year=2019|pages=15122–15127|issn=0027-8424|doi=10.1073/pnas.1902452116|pmid=31285335|pmc=6660761|bibcode=2019PNAS..11615122W |doi-access=free}}</ref> and in the prevention of [[cancer]].<ref>{{cite journal | vauthors = Shay JW, Wright WE | title = Senescence and immortalization: role of telomeres and telomerase | journal = Carcinogenesis | volume = 26 | issue = 5 | pages = 867–74 | date = May 2005 | pmid = 15471900 | doi = 10.1093/carcin/bgh296 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Wai LK | title = Telomeres, telomerase, and tumorigenesis--a review | journal = MedGenMed | volume = 6 | issue = 3 | pages = 19 | date = July 2004 | pmid = 15520642 | pmc = 1435592 }}</ref> This is because the telomeres act as a sort of time-delay "fuse", eventually running out after a certain number of cell divisions and resulting in the eventual loss of vital genetic information from the cell's chromosome with future divisions.<ref>{{cite journal | vauthors = Greider CW | title = Telomeres, telomerase and senescence | journal = BioEssays | volume = 12 | issue = 8 | pages = 363–9 | date = August 1990 | pmid = 2241933 | doi = 10.1002/bies.950120803 | s2cid = 11920124 | doi-access = free }}</ref><ref>Barnes, R.P., de Rosa, M., Thosar, S.A., et al., ''[https://www.nature.com/articles/s41594-022-00790-y Telomeric 8-oxo-guanine drives rapid premature senescence in the absence of telomere shortening]'', Nature, June 30, 2022; Nat Struct Mol Biol 29, 639–652 (2022). https://doi.org/10.1038/s41594-022-00790-y</ref>