No they aren't the same as suicide genes. They are the reason we have suicide genes. Telomeres are the ends of chromosomes. Every time a chromosome is replicated, a few bases are lost at the end (a consequence of DNA always needing a primer with a 3' OH group to attach the next base to). Telomeres are repeated sequences at the end that are just some extra garbage DNA with a sequence that varies between species. That way, when some bases are lost from the end of linear chromosomes, it is just junk DNA instead of valuable genes. They are replenished by the enzyme telomerase. Most cells in humans don't replenish their telomeres, which is why they undergo apoptosis after a set number of replication cycles.

Telomeres are thought to be one of the causes of aging. As the chromosomes undergo replication during mitosis, the end replication problem causes a shortening of the chromosome in somatic cells. Eventually, the shortening of the chromosomes cuts beyond the TTAGGG repeated segments created by telomerases in germ cells, cuting into the coding segments of the genome.
Thus, Dolly, the cloned sheep, is expected to have a shortened lifespan, equivalent to that of the remaining expected lifespan of the original maternal sheep.


Unsurprisingly, Webster (1913) doesn't mention the word telomere. It's a fairly new term from the realm of biochemistry. However, Webster's modern descendent, the Merriam-Webster OnLine Dictionary1 has this to say:

Main Entry: telo·mere
Pronunciation: 'te-l&-"mir,  'tE-
Function: noun
Etymology: International Scientific Vocabulary
Date: 1940
: the natural end of a eukaryotic chromosome

A minimally more eloquent definition comes from another source2:

Telomeres are the physical ends of linear eukaryotic chromosomes.


Recursing into the components of this definition brings us most of the way toward understanding the topic:

  • Chromosomes are strands of genetic information. Consider a chromosome as something like an open necklace, a long kind of rope with genes attached to it like totems on a pole or beads on a string.

    Each human cell contains 23 chromosomes in its nucleus, or inner core. Microphotographs of most chromosomes look like fuzzy, bent little X's, or like pairs of curved sticks siamese-twinned in the middle.

    • Genes are sequences of nucleic acids, perhaps a few dozen to a few hundred of them. The particular combination of nucleic acids in a gene is a kind of biological code. Each of these codes, or genes, is not just a representation of a particular protein, it actually serves as a chemical template for its construction. The presence of one or more genes results in a particular feature in the physical makeup, or phenotype, of a living being.
      • proteins are the building blocks of all living cells. Cell membranes are made of particular proteins, and there are many different proteins inside. Different cells are made up of different proteins; this makes the difference between muscle fibres, hair follicles and bone cells. Viruses are made of proteins, and eggs are mostly proteins as well. The selection of proteins which make up a cell is determined by the composition of the genes on the cell's chromosomes. All proteins are made up of amino acids.
      • amino acids are the organic molecules that make up all living matter. Comprised of between a dozen and a few dozen atoms, amino acids are fairly complex as far as molecules go, but they are just the building blocks of super-complex molecules called proteins.
  • linear means essentially straight. In the context of chromosomes, this means not necessarily straight as an arrow, but it's essential that this precludes a closed loop, such as a circle. Thus, linear chromosomes are straight like sticks: Some are really straight, others are a bit bent.
  • eukaryotic is a term which biologists apply to cells which are well-organized, such as those of humans, plants and animals. The cells which make up the "higher lifeforms" have a clearly defined nucleus, held together and protected by a membrane, and also functional units called organelles. In more primitive cells, genetic material and other components of the cell just drift around in the cell's protoplasm.
  • The ends of chromosomes are, then, exactly what you'd imagine if you think of linear chromosomes as more-or-less straight sticks: Simply short pieces of the chromosomes near their two tips.


Given this background, it becomes possible to understand the significance of the ends of chromosomes.

Chromosomes are the structures that hold our genetic material together, Nature's blueprints for all the proteins in all living things, and how they connect together. The process of protein construction is called expression, and it essentially works by means of cellular proteins specialized as "construction machines" which inch along on the chromosome and use its structure as a template for constructing new proteins. I'm skipping some steps here that aren't too relevant to this explanation.

Although the protein "construction" business is essentially chemical, chromosomes are big enough to be considered mechanical entities too, and like the corners of furniture, the ends of chromosomes are most likely to get "bumped into" by the other contents of a cell, and damaged. Also, chromosomes aren't fully covered end-to-end in genes; there are bare spots, and inactive genes. In particular, the "construction machines" are adapted to constructing proteins from somewhere along the length of a chromosome; the end has a different geometry. So the ends are essentially "dead" zones as far as genetic information is concerned, and protective end pieces to the structure of each chromosome. They also work like bookends, holding the information between them together.

The significance of these genetic bookends becomes dramatically apparent when cells reproduce: Before a cell splits into two new ones, it must duplicate all of its chromosomal material so that there are (nearly) identical copies for both of the new cells. In this duplication process, the chromosomes are not perfectly copied. Partly because of the geometric particularity of the tips, part of the end pieces, or telomeres, is lost with each duplication. Thus, over the course of (cell) generations, the chromosomes become shorter and shorter until at some point the "book ends" are gone. At some point, genetic information from the ends of the chromosome is lost in duplication and the cells inheriting these defective chromosomes lose some of their function, eventually becoming defunct, or more simply: dead. What this all leads up to is this: The gradual shortening of telomeres is the process we know as aging.

Research is still ongoing, of course, but there are clear signs that telomeres, along with some essential cellular mechanisms that deal with them, are the keys to aging and longevity. With their physical length, telomeres measure out the lifespan of most living things.

Naïve thinking might lead us to believe that a bit of chemical refurbishing is all that's needed to make humans immortal; but like everything in nature, the truth is more complex than this.

Philosophically, death of old age is Nature's way of recycling living protein and of keeping the planet from getting overcrowded. In some ways, it's simply not healthy to keep on living forever. For striking evidence of this statement, consider cancer. Yes, malignant tumors are simply masses of cells that multiply without bound. The body's natural tendencies in this direction are usually checked by the shortening of telomeres, but in cancer this mechanism somehow fails. What's good for individual cells is not always good for the organism as a whole.

But if telomeres shorten each time a cell divides, how can cancer come about? Again, the paths of evolution have led to some interesting mechanisms. In many kinds of cells, an enzyme, a cellular chemical tool called telomerase, has the job of patching up chromosomes damaged in duplication. Apart from cancerous cells, whose life cycle isn't yet fully understood, there are also some very clear examples of cells which employ this mechanism:

So, in their ongoing research for the secrets of longevity while avoiding the hazards of cellular explosion, scientists may yet have a lot to learn from the humblest of organisms.

Results, present and future

On another front3, scientists have discovered a protein they call TRF2 which somehow bonds to telomers in the cells of higher animals and keeps them from harm. They found that so long as this substance is produced and available in abundance in cells, telomeres do not shorten and aging does not set in. So at least in some organisms, aging seems to be a precise mechanism of checks and balances intended to measure out the life span of living beings.

These findings, though, probably represent no more than the tip of an iceberg of exhaustive scientific research that will be necessary before eternal youth will be a finished, labelled, FDA approved product sold at your local drugstore. In the meantime, a sensible diet and moderate exercise will probably be most effective in helping you attain a healthy old age.


    was unfortunately not available when I tried it, except for a brief excerpt from a search engine's cache.

Further reading


Telomeres! They're the aglets on the shoelaces of eukaryotic chromosomes. They cause cancer, and prevent cancer, and probably have a whole lot to do with "aging". Can't live with 'em, can't live without 'em. They're the poster children for dynamic equilibrium.

DNA is made up of four bases — adenine, cytosine, guanine and thymine — on a sugar-phosphate backbone. The backbone is directional. One end terminates in a phosphate group (the 5' end, for the 5th carbon of the nucleotide to which the phosphate group is attached), and the other (the 3' end) in a hydroxyl group. By convention, DNA sequences are written 5' to 3', so a single strand of DNA looks something like this:


Single strands bind — A to T, G to C — to make the familiar double helix, and they do this in opposite ("antiparallel") directions:


A given run of DNA that actually codes for some protein might be on either strand, and might have associated regulating sequences on the opposing strand. It's all biological and messy, but it works, so hey.

The directionality is thus insignificant as far as "genes" are concerned, but it's a big deal for cell division. Chromosomes are replicated by unzipping the two strands and synthesizing new strands that complement each:

   |||||||||||| yoink!

5'-agtcgatcgata cggtcactctga-5'
3'-tcagctagctat gccagtgagact-3'

DNA polymerases — the enzymes that "read" the original strands and synthesize the new ones — can only do so by attaching nucleotides to an exposed 3'-OH. In other words, DNA is always read 3' to 5', and always extended 5' to 3'.

This has the inconvenient side effect that a single-strand of DNA, all by itself, is never enough for a cell to reconstitute a double-stranded chromosome. All the information is there, but the process can't get started without at least one complementary nucleotide with a 3'-OH for DNA polymerase to latch on to.

3'-tcagctagctatcggtcactctga-5'     (frickin' useless!)

5'-a-3'-OH                         (good to go)

How does it get that little bit of "primer" sequence? Using very short sequences of RNA instead of DNA. RNA has the same exposed -OH, but unlike DNA polymerase, RNA polymerase can start a chain from nothing.

3'-tcagctagctat gccag-3'-OH     ← ta-da!

Replication starts at various places all over chromosomes, with the "unzipping" headed in either direction. Replicating the strand that happens to go 3' to 5' in the same direction the unzipping is headed is easy; only one RNA primer is needed, after which DNA can be synthesized non-stop for as long as the "replication bubble" — the section of unzipped single strands — travels down the chromosome. That's the "leading" strand.

The "lagging" strand is a little trickier. As the replication bubble moves along the chromosome, the leading strand is synthesized continuously, but the lagging strand has to be filled in as short fragments ("Okazaki fragments") extending in the opposite direction. These all have to be started by RNA primers, which are later removed (RNA isn't very stable), leaving short gaps. At the interior of the chromosome, these gaps can then be filled with DNA by DNA polymerase attaching to the -OH from the next fragment down.

The ends of the chromosomes, however, are a problem. There's no next fragment. The RNA primer gets chewed up, as RNA is wont to do, and that's it. There's just a bit of single-stranded DNA sticking out, with no way to add a complementary sequence. This 3' "overhang" is necessarily present on both ends of linear chromosomes, but on opposite strands:

     5'-atcgatagccagtgagact-3'     (world's shortest chromosome!)

More disturbingly, this happens with every replication. Every time your cells divide, your chromosomes get a little shorter; they lose a little more information.

Telomeres — finally, the good part! — are evolution's answer to the "end replication problem", and an elegant hack indeed. They're a short sequence — ttaggg in vertebrates — repeated many times at the ends of chromosomes, acting as a buffer for the rest of the DNA. Since they're repeated, no information need be lost when they fail to completely replicate. Instead, they're replaced by telomerase, an enzyme that includes its own copy of the telomeric sequence as an RNA fragment — 3'-caaucccaauc-5' in humans, matching the 5'-ttaggg-3' repeat (RNA substitutes uracil for thymine). The other component of telomerase is a reverse transcriptase — a special class of DNA polymerase that takes RNA instead of DNA for the source sequence. It still needs a 3'-OH to get started, but, of course, the overhang has one waiting.

ttagggttagggttaggg-3'           end of a chromsome

ttagggttagggttaggg-3'           telomerase RNA binds to telomere DNA
aatccc-5'  caaucccaauc 

ttagggttagggttagggttag-3'       3' overhang DNA is extended,
aatccc-5'  caaucccaauc          complementary to telomerase RNA

ttagggttagggttagggttag-3'       telomerase proceeds down the
aatccc-5'        caaucccaauc    chromosome

ttagggttagggttagggttaggg-3'     overhang is extended by a full
aatccc-5'        caaucccaauc    ttaggg repeat

ttagggttagggttagggttaggg-3'     now there's room for a regular RNA
aatccc-5'       3-aauccc-5'     primer to attach...

ttagggttagggttagggttaggg-3'     and regular DNA polymerase can
aatcccaatcccaatcccaauccc-5'     extend the 5' strand

ttagggttagggttagggttaggg-3'     the RNA gets chewed up, leaving a
aatcccaatcccaatccc-5'           fresh, short overhang and
                                everything has shifted up by one
                                telomeric repeat.

(Let's all stop a moment to marvel that biology works. I mean, damn.)

As long as telomerase keeps this up, the normal DNA replication process won't lose any information that can't easily be recovered. The telomerase caaucccaauc is essentially a backup of what the ends of your chromosomes are supposed to look like. With telomerase expression turned off, you lose ttaggg buffer until you're within a few replication cycles of losing other, unpreserved sequence, and then cellular machinery that notices short telomeres (by, e.g., binding with lower affinity to proteins that normally bind to telomeres — so if they're available, you know there's not enough telomere to go around) kicks in and shuts down replication. Bam. Cellular senescence.

Or, at least, that's how it goes in healthy cells. If something goes wrong with the senescence pathway, a cell might keep on dividing and start losing coding DNA. Then you've got two problems: you're missing chunks of genes, and, possibly worse, you've got chromosome ends that don't look like chromosome ends. Chromosomes occasionally break, but we've got repair mechanisms that ligate free-floating DNA ends together. They know not to do this to legitimate chromosomes ends by recognizing the telomeric repeat. Once you lose that recognition sequence, your own repair systems try to attach your chromosomes to each other. That causes physical strain, which causes more breaks, and more random ligations, and pretty soon you've got a completely rearranged genome.

Most unfortunate cells just stop there. The chromosomes-in-a-blender game tends to not produce viable results. But every so often, you wind up with something that works just enough to activate telomerase. The ends stabilize, replication resumes, but the cell's normal checks and balances are in ruins and it just goes on replicating the new crazy chromosomal arrangement as long as it can. That's a tumor cell.

So telomerase "causes" cancer, in the sense that tumor cells rely on it. But it may also "prevent" cancer, in the sense that if it'd been active all along, the telomeres would never have shortened enough to start the whole mess. Would you have more mildly fucked up cells, but fewer really fucked up cells? Who knows. More funding, more research, plz.

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