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Answer by Richa Mishra:
Telomeres protect against genomic instability. Telomeres are also quoted as source of genomic instability. Interesting, isn’t it?
Our DNA holds our genetic information. DNA is packaged and arranged in form of chromosomes. At the end of chromosomes, we find stretches of DNA called telomeres.
So what are telomeres?
Telomeres are TTAGGG repeats, 9-15 kb in length in humans. The actual end of the telomere is recognised by the presence of a 50–300 nucleotide extension of single stranded repeats from the 3′ end, termed the G-tail or G-overhang . Telomeres protect our genetic data, make it possible for cells to divide, and hold some secrets to how we age and get cancer.
Telomeres have been compared with the plastic tips on shoelaces, because they keep chromosome ends from fraying and sticking to each other, which would destroy or scramble an organism’s genetic information.
Yet, each time a cell divides, the telomeres get shorter. When they get too short, the cell can no longer divide; it becomes inactive or “senescent” or it dies. This shortening process is associated with aging, cancer, and a higher risk of death. So telomeres also have been compared with a bomb fuse.
Fig 1: telomeres protecting end of chromosomes. image source:
The role of telomere length in end protection: Telomeres essentially serve three important functions:
1.Protecting natural chromosomal DNA ends from being inappropriately recognized as double-stranded breaks (DSBs) and therefore initiating an inappropriate DNA damage response (DDR),
2.Protecting chromosomal ends from inappropriate enzymatic degradation and
3.Preventing chromosomal end-to-end fusion. 
Telomeres as sources of genome instability :
In 1938, McClintock noticed that chromosomes in plants that had previously been irradiated with X-rays engaged in spontaneous chromosome breakage–fusion–bridge cycles. This laid the foundation for the hypothesis that aberrantly fused chromosomes will break in the subsequent cell division, thereby leading to the unequal and random distribution of genetic material into the daughter cells  Dysfunctional telomeres that fail to be distinguished from broken DNA lend themselves perfectly to the hypothesis that loss of chromosome end protection leads to genome instability through McClintock’s breakage–fusion–bridge cycles. This hypothesis was formally proved in mice, in which targeted deletion of the RNA subunit of telomerase rendered the telomerase complex inactive for telomere length maintenance. As a consequence, telomeres shortened progressively by approximately 5 kb per generation and, after four generations, telomeres lacking TTAGGG signals were detected. Loss of telomeric sequences led to chromosome end-to-end fusions, chromosomal abnormalities and aneuploidy, supporting the suggestion that loss of chromosome end protection can be the basis for genome instability in mammals.
Telomeres and ageing:
Some organisms grow cells indefinitely, but human tissues do not. Even tissues that renew constantly in adult life, including skin and intestine, eventually run out of steam. Part of this limit is genetically encoded as a gradual erosion of the protective cap at each chromosome end called telomeres. An enzyme, called telomerase is essential in synthesis and maintenance of telomeric repeats. Telomerase is fully active in cells of the human embryo but not in adult human tissues, triggering a countdown of telomere amount with each cell division that ultimately impedes tissue renewal.
Telomere length shortens with age. Progressive shortening of telomeres leads to senescence, apoptosis, or oncogenic transformation of somatic cells, affecting the health and lifespan of an individual. Shorter telomeres have been associated with increased incidence of diseases and poor survival. The rate of telomere shortening can be either increased or decreased by specific lifestyle factors. Better choice of diet and activities has great potential to reduce the rate of telomere shortening or at least prevent excessive telomere attrition, leading to delayed onset of age-associated diseases and increased lifespan. 
Telomeres and cancer: Telomere length has been associated with development of cancers and telomerase over-expression as marker for many malignant cancers.
As cells proliferate, TTAGGG repeats are lost from telomeres unless they have an active telomerase enzyme — a reverse transcriptase that adds TTAGGG repeats onto pre-existent telomeres [17-19] Most normal somatic cells do not have sufficient telomerase activity and suffer telomere attrition. When telomeres shorten below a critical length, this results in telomere fusions and cells lose viability. This phenomenon is evident with increasing passages of cultured primary cells and is known as ‘telomere-induced senescence’ 
Telomerase activity is necessary to maintain the integrity of telomeres, which in turn prevent chromosome ends from being processed and signaled as damaged DNA. Cancer cells rely on telomerase to maintain functional telomeres and to divide indefinitely 
Telomeres and other diseases: Telomere function has been directly implicated in two additional diseases:
- dyskeratosis congenita and,
- idiopathic pulmonary fibrosis.
Dyskeratosis congenita is an inherited disease that is marked by
bone marrow failure, abnormal skin pigmentation, nail dystrophy and leucoplakia [7,8].
X-linked recessive dyskeratosis congenita is caused by mutations in dyskerin, a protein that associates with a subgroup of small nucleolar RNAs and also with the RNA component of telomerase (TeRC) — an association that stabilizes the shelterin complex. Autosomal dominant dyskeratosis congenita has been linked to mutations in TeRC itself 101, in the catalytic telomerase subunit TeRT and in the shelterin component TIN2[11,12]. One unifying feature in dyskeratosis congenita is short telomeres, and the importance of limiting telomere length has been emphasized by the observation that mice that suffer from extensive telomere shortening because of a lack of POT1B suffer from clear signs of the disease [3,13,14]
Idiopathic pulmonary fibrosis is a lung disorder that is marked by progressive scarring, which leads to destruction of lung architecture with a frequently fatal outcome. 
The discovery that short telomeres correlate with idiopathic pulmonary fibrosis eventually led to the finding that heterozygous mutations in TeRT or TeRC can be the cause of the disease [15,16]
Hence, are telomeres special?
References and further reading:
 Verdun, R. E. & Karlseder, J. Replication and protection of telomeres. Nature 447, 924–931 (2007).
 A very interesting article written in very simple and comprehending manner, must read for basic information.
Roderick J. O’Sullivan and Jan Karlseder, : most of the content of this answer, is derived from this article.
 McClintock, B. The fusion of broken ends of sister half chromatids following chromatid breakage at meiotic anaphase. Mo. Agric. Exp. Stn. Res. Bull. 290, 1–48 (1938)
Blasco, M. A. et al. Telomere shortening and tumor formation by mouse cells lacking telomerase RNA. Cell 91, 25–34 (1997). This manuscript is the first one to describe the effects of telomerase inhibition on a chromosome and organism level in mammals.
Mason, P. J. Stem cells, telomerase and dyskeratosis congenita. Bioessays 25, 126–133 (2003).
 Mason, P. J., Wilson, D. B. & Bessler, M. Dyskeratosis congenita — a disease of dysfunctional telomere maintenance. Curr. Mol. Med. 5, 159–170
Mitchell, J. R., Wood, E. & Collins, K. A telomerase component is defective in the human disease dyskeratosis congenita. Nature 402, 551–555
Vulliamy, T. et al. The RNA component of telomerase is mutated in autosomal dominant dyskeratosis congenita. Nature 413, 432–435 (2001).
 Vulliamy, T. J. et al. Mutations in the reverse transcriptase component of telomerase (TERT) in patients with bone marrow failure. Blood Cells Mol.
Dis. 34, 257–263 (2005).
 Savage, S. A. et al. TINF2, a component of the shelterin telomere protection complex, is mutated in dyskeratosis congenita. Am. J.Hum Genet. 82, 501–509 (2008).
 Walne, A. J., Vulliamy, T., Beswick, R., Kirwan, M. & Dokal, I. TINF2 mutations result in very short telomeres: analysis of a large cohort of patients with dyskeratosis congenita and related bone marrow failure syndromes. Blood 112, 3594–3600 (2008).
 Hockemeyer, D., Palm, W., Wang, R. C., Couto, S. S. & de Lange, T. Engineered telomere degradation models dyskeratosis congenita. Genes Dev. 22, 1773–1785 (2008).
 Alder, J. K. et al. Short telomeres are a risk factor for idiopathic pulmonary fibrosis. Proc. Natl Acad. Sci. USA 105, 13051–13056 (2008).
 Armanios, M. Y. et al. Telomerase mutations in families
with idiopathic pulmonary fibrosis. N. Engl. J. Med. 356, 1317–1326 (2007).
C.B. Harley, A.B. Futcher, C.W. Greider ,Telomeres shorten during ageing of human fibroblasts ,Nature, 31 (1990), pp. 458–460
K. Collins, J.R. Mitchell, Telomerase in the human organism,Oncogene, 21 (2002), pp. 564–579
A.G. Bodnar, M. Ouellette, M. Frolkis, S.E. Holt, C.P. Chiu, G.B. Morin, C.B. Harley, J.W. Shay, S. Lichtsteiner, W.E. Wright ,Extension of life-span by introduction of telomerase into normal human cell, Science, 279 (1998), pp. 349–352
M. Serrano, M.A. Blasco Putting the stress on senescence Curr. Opin. Cell Biol., 13 (2001), pp. 748–753