The Carrot and the Stick

Sex is so important to the health of a breeding community that natural selection has arranged to encourage everyone to participate.  There’s a conflict here, because the selfish gene does not want to share.  The strongest and most fertile individuals–anyone who has an advantage in the present environment–is tempted not to dilute her genes by sharing, but to reproduce clonally instead.  Avoid the competition for mates; avoid the energy expense, the dangers and deceptions to which mating is prone; transmit all your genes to the next generation, not just half.


Sex is not reproduction.

Sex originally had nothing to do with reproduction, and how the two became bound so tightly together is a subject of ongoing debate in the evolutionary community for a hundred years.  Sex is the sharing of genes.  Your children get half your chromosomes and half from your spouse.  What is more, individual genes within a chromosome can cross over between a mother’s chromosome and  a father’s in an exchange that greatly enhances the possible combinations.  Sex serves a profound evolutionary purpose, boosting evolvability by broadening the competition, making possible trials of many diverse combinations.  Sex is a democratizing force in opposition to the selfish gene, tying together the fate of an entire community.  Any selfish gene that wants to get very far in evolutionary competition has to learn to work well with a variety of other genes in the community.  This puts a damper on the selfish advantage of any gene that provides only a temporary advantage, or whose advantage depends on stealing from others.

In “higher organisms”–that’s you, me, and the cockroach–sex and reproduction have been so tightly integrated that it’s not possible to reproduce without sharing genes. Ultimately, it’s the prospect of reproduction that provides the “carrot” (not what you were thinking?)  In some animals, including humans, sexual activity modestly enhances life expectancy.  That might be a carrot if you think of it as a motivation to have sex, or a stick if you think of early death as punishment for abstience.

In many protozoans, the functions of sex and reproduction are completely separate.  Sex occurs between two protozoans of the same species via conjugation, and it may occur only once in a few hundred lifetimes.  But reproduction is something every protozoan does individually, by dividing in half.

Paramecia conjugating

In conjugation, two cells sidle up to each other and the membranes between them dissolve.  Two cells actually fuse, and then the nuclei of those cells (containing the genetic material) fuse as well.  The identities of the two are thoroughly scrambled to create two new individuals.  Then two cells emerge from conjugation, but the cells that emerge cannot be identified individually with the original cells.  You and I have both become ‘half me and half you’.


Sex and the Single Protozoan: What’s in it for Me?

In animals and plants, sex and reproduction have been tied tightly together so that organisms can’t revert to reproduction on their own.  But in protozoans, where is the motivation to participate in conjugation?  What carrot or stick assures that cells take time out from the serious business of reproduction to share their genes?

The carrot is entirely subjective.  Disclaimer: I, myself, have never had personal experience as a protozoan.  But several protozoans whom I know and trust have told me that it is an experience like no other.  I mean, like cosmic, man, really far out.  The feeling of that cell wall dissolving and new cytoplasm pouring in is an experience of a lifetime–once in a hundred lifetimes, actually.  Even though they are merging with just one other individual, what they describe is an experience of sublime oneness with all of creation.  Groovy.

Still, in case the experience itself is not sufficient reward for sharing, nature has provided a stick as well as a carrot.  And that is that if you go for too many generations just reproducing clonally, never sharing genes, then you die.  This is the origin of replicative senescence, another name for telomere shortening.

Every time the cell reproduces, the telomere gets a little shorter (in both daughter cells).  If the daughter cells go on like this for more than a few hundred generations, they run out of telomere.  The remedy: sex=conjugation.  When two cells conjugate, the two cells that emerge have long telomeres again, and a fresh lease on life.  Telomerase is brought out of deep storage to rescue the chromosomes and restore their telomeres to full length.  The cells that emerge begin life anew and can replicate hundreds of times more before their descendants have to worry again about a shortage in the telomere department.


Telomerase Rationing Enforces Gene Sharing in Protozoans

The interesting thing is that telomerase is right there in the genome, always available to be expressed.  The cell could, in principle, get out a little telomerase every time it replicated, so it would not lose telomere length at all, ever.  In this sense, it is an artificial shortage.  Telomerase is withheld by evolutionary programming, and the cell is coerced into sharing genes every so often in order to get its hands on the telomerase it needs to continue living and reproducing.  The temptation to cheat must be enormous.  The telomerase gene must be hidden away (by epigenetic programming) so well that a chance mutation can’t create a rogue daughter cell that is “immortal” in the sense that it can go on dividing and dividing, never sharing its genes.

We are the descendants of these cells, a billion years on, and we have inherited the same system of telomerase rationing that the protozoans have to live with.  In protozoans, the artificial shortage of telomerase is the “stick” that enforces the imperative to Share Genes!  In humans (and most other mammals) our stem cells divide during an individual lifetime, and very little telomerase is available, so the telomeres of our stem cells gradually shorten with age, and this is one of the primary aging clocks, one of a handful of deep roots of human aging.

Oxytricha trifallax

Last week, ScienceBlog featured an article about one such protozoan that reproduces by simple mitosis without telomerase, and conjugates occasionally to exchange genes and renew its telomeres.  This is the pond-dwelling cilliate Oxytricha trifallax.


Two Cell Nuclei

Oxytricha and other protozoans (but not higher life forms) actually have two cell nuclei.  There is a micronucleus that contains the original copy of all the chromosomes.  Then there is the macronucleus that contains many working copies.  In the course of the cell’s metabolism, it is the macronucleus that directs all the cell’s activities.  The original copies of the genes are preserved in the micronucleus, which is only active during reproduction and conjugation.  Genes in the micronucleus are organized strictly onto chromosomes.  Genes in the macronucleus are cut apart for easy access.  The number of copies of each gene is proportional to the amount of activity that that gene needs to contribute to the cell’s metabolism.

During clonal reproduction, chromosomes in the micronucleus are copied to make two identical new micronuclei.  But the macronucleus is simply split in two, half going to each clone.  After reproduction, the micronucleus fortifies the macronucleus with new gene copies.

But conjugation brings a truly fresh start.  After conjugation, the two macronuclei are destroyed and digested!  This is so new instructions can be read from the new library of genetic material, coming from two organisms that are slightly different.  The old macronuclei are destroyed, and new ones are created separately in each daughter cell, with faithful copies of that daughter’s genes.

In Oxytricha,

the level of DNA processing in the formation of a new macronucleus is extraordinary: the original micronucleus chromosomes are fragmented at tens of thousands of positions, 95% of the DNA complexity is lost, and the resulting chromosomes– sometimes referred to as “nanochromosomes”–are amplified to thousands of copies each. Each macronucleus chromosome typically contains a single gene flanked by very short telomeres. The size of these molecules ranges from 0.25 to 35 kb, and each is present at an average of 1000 copies.  [Genome Inst, Washington Univ St Louis]

The ScienceBlog summary referred to a recent article by Laura Landweber’s group at Princeton:

Here, we report the Oxytricha germline [micronucleus] genome and compare it to the somatic [macronucleus] genome to present a global view of its massive scale of rearrangement.  The remarkably encrypted genome architecture contains >3,500 scrambled genes, as well as >800 predicted germline-only genes expressed, and some posttranslationally modified, during genome rearrangements.  Gene segments for different somatic loci often interweave with each other.  Single gene segments can contribute to multiple, distinct somatic loci. Terminal precursor segments from neighboring somatic close to each other, often overlapping.

The message is that the genome evolves by assembling pieces of genes that had been found useful in different circumstances in the past, and that much of the genome is assembly instructions for piecing together parts from different locations to form a functional whole.  Many of the pieces are re-used.

This presages the fact for higher organisms that only 5% of our DNA is genes, and the rest is epigenetic instruction, dictating when and where each gene is to be expressed.


Brief Updates

I did another 4-day fast this week.  It seemed easier than my first long fast last spring.  There were no craving or headaches.  I’m not able to run or to swim or do interval training while fasting, but I can bicycle and do yoga and walk for hours on end.  I bicycled more than 20 miles (to attend a conference) on my fourth day, and didn’t feel drained.  I’m not very productive during a fast, and my concentration is pretty diffuse.  Sleep is often interrupted by hunger.  But on the positive side, there’s a calm and peace that comes over me, and it’s easy to be content just being where I am.

Science Magazine had 2 feature articles [Ref1, Ref2] and a summary news article on CRISPR dynamics in E. coli bacteria.  The articles describe how CRISPR RNA is able to locate stretches of foreign DNA, planted there by an invading virus, and excise it from the genome.  I still can’t say that I understand how the cell knows what to look for.



6 thoughts on “The Carrot and the Stick

  1. Far as I know the gamete sex cells are immortal already as the telomerase gene is already switched on ensuring that 1. the DNA expression capacity is protected, and 2. children are born with a full life and not at the age of their parents. In fact I understand that in the male of the species the telomere length gets longer the older they get making older men the ideal mates for passing on greater longevity to their offspring. Old men with young women being the ideal.

  2. If any therapy designs to be reversal of aging or aging prevention, or whatever anti-aging term you choose to use, you CANNOT go about it without addressing telomere shortening foremost.

  3. You may be right. The evidence on this isn’t completely clear. It doesn’t seem to be true in mice, for example. But I’m inclined to agree with a slightly toned-down version of your statement.

  4. Josh notes…

    “Still, in case the experience itself is not sufficient reward for sharing, nature has provided a stick as well as a carrot. And that is that if you go for too many generations just reproducing clonally, never sharing genes, then you die. This is the origin of replicative senescence, another name for telomere shortening.”

    I believe telomere shortening is not an accident…it is an evolved aging system which could easily be overcome by simply causing chromosomes to assume a circular shape (plasmids) and voila replicative senesence caused by telomere shortening- solved

    in humans many telomere lengths are under hormonal control…..various hormones activate telomerase

    • I agree it’s an evolved system. I’m working at present on a model of how that system may have originated.
      Jeff – what hormones are you thinking of? I thought that all known hormones only promote telomerase in minuscule amounts.

  5. Superb research; thanks for all your excellent work, in all your blogs.

    Also enjoy the expert responses.

    Very best regards,


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