The New York Times reports today on the opposite idea: that human culture may actually intensify the selective pressure on our genes. This idea is known as gene-culture co-evolution, since although our genes and our culture evolve through separate processes (biological reproduction vs. sharing of ideas), these two processes interact and affect each other.

The Times article surveys how culturally evolved changes in diet, lifestyle, and social norms could have influenced the genetic evolution of our digestive systems and brains. But as a discussion starter, I’m interested in more speculative questions: is our evolving culture still shaping our genetic evolution? If so, in which directions are we being pushed?

Related posts:

1. What is a Gene?
2. Evolution & Emergence
3. Evolution Favors Cooperation Over Competition

One preface I think will help is to understand that genome, karyotype and chromosome refer roughly to the same thing.  Here are several schematics that I will present without explanation that together illustrate how genes relate to genome/karyotype/chromosome structure, and how that in turn relates to the so-called genetic network (loosely equivalent to the “proteome”).  Of course “gene” is an outdated and inaccurate concept, so don’t get too hung up looking for genes here, just understand that they are sub-structural elements of the genome.

From MSU website

From eapbiofield.wikispaces.com

From Heng’s paper titled”The genome-centric concept: resynthesis of evolutionary theory”

Now onto the paper.  I’ll point out that I’ve eliminated the scholarly references in the original text simply for clarity, but I don’t want readers to think that the authors have not properly credited the research that goes into the statements/claims made below.  If you’d like to read the original paper, email Henry Heng whose address is on the abstract above.  Also note that all emphasis in the quotes below is mine.

Somatic Evolution

…cancer progression is an evolutionary process where genome system replacement (rather than a common pathway) is the driving force.

It has become clear that a correct theoretical framework for cancer research is now urgently needed and the concept of somatic evolution represents just such a framework.

The increased NCCA frequencies reflect increased survival advantage while increased CCAs reflect a growth advantage. [NCCAs and CCAs are chromosomal aberrations, like gene mutations but at the genome level]

This last quote is reminiscent of the RNA autocatalysis experiments reported on earlier this year which showed divergent evolution towards two co-existing phenotypes, one that more quickly gobbled up available resources and another that was more efficient at using resources to reproduce quicker.  Perhaps there is a basic principle at work in both systems (autocatalytic RNA populations and somatic cell populations).

Instability / Heterogeneity / Diversity

Clearly, as there is no defined cancer genome (the vast majority of cancer cases display different karyotypes representing different genome systems), there is no defined cancer epigenome either.

…the most common feature in tumors is a high level of genome variation…

Understanding the importance of heterogeneity is the key to understanding the general evolutionary mechanism of cancer.

…the true challenge is to understand the system behavior (stability or instability)…

When closely examining the contribution of various genetic factors, it is clear that many of the genetic loci or events are only significantly linked to tumorigenicity when they contribute to system instability (which is closely linked to genome level heterogeneity).

…it is relatively easy to establish a causative relationship between system heterogeneity and cancer evolution, as heterogeneity is the necessary pre-condition needed for cancer evolution to occur….

…instability imparts heterogeneity, which is acted on by natural selection.

The predictability of cancer can be accomplished by measuring the system heterogeneity that is shared by most patients rather than characterize each of the individual factors that contributes to cancer.

Virtual Stability / Chaotic Synchronization

Heterogeneity provides a greater chance of success that a system can adapt to the environment and survive.

…heterogeneity ‘‘noise’’ represents a key feature of bio-systems providing needed complexity and robustness.

…epigentic alteration is an initial response when the genome system is under stress.

It turns out, lower levels of ‘‘randomness’’ are essential for higher levels of regulation when facing a drastically changed environment.

In a human-centric version of a perfect world, within the multiple levels of homeostasis, environmental stress should be counteracted by epigenetic regulation; disturbances of metabolic status should be recovered; the errors of DNA replication should be repaired; altered cells should be eliminated by cell death mechanisms; abnormal clones should be constrained by the tissue architecture; and the formed cancer cells should be cleared up by the immune-system. In a cancer defined perfect world, in contrast, the break down of homeostasis is the key to success. Unfortunately, continually evolving systems are the way of life and cannot be totally prevented. In a sense, cancer is the price we pay for evolution as an interaction between system heterogeneity and homeostasis….

Facilitated Variation / Baldwin Effect

When changes are selected by the evolutionary process, these changes can be fixed either at a specific gene level or at the genome level (achieving the transition from epigenetic to genetic changes).

This is corroborated by Spencer, et al and Brock, et al, the latter of whom says, “‘pre-selection’ of non-genetic variants would markedly increase the probability of producing a random genetic mutation that may provide the basis for the survival capability of the original non-genetically variant outlier population.”

Path Dependence

…cancer cases are genetic and environmentally contingent. The pattern of specific gene mutations can only be used within a specific population with a similar genome, mutational composition as well as a similar environment.

…the stochastic events referred to here are not completely random but rather are less predictable due to differences in the initial conditions reflected by the multiple levels of genetic and epigenetic alteration.

From a system point of view, significant karyotypic changes represent a ‘‘point of no return’’ in system evolution, even though certain gene mutations and most likely epigenetic changes can influence karyotypic changes.

Upon establishment of a new genome through karyotypic evolution, it is impossible to revert back to a previous state through epigenetic alteration.

As long as the genome does not significantly change, epigenetic reprogramming could work to bring the system to its original status.

Multiple Levels

…the multiple levels of homeostasis are more important than genetic factors in constraining cancer, as alterations of system homeostasis rather than individual genetic alterations are responsible for the majority of cancers. Accordingly, the robustness of a network, the reversible features of epigenetic regulation, tissue architecture, and the immune-system will play a more important role than individual genetic alterations.

…genome level alteration within tumors is a universal feature.

Note that although physically the epigenetic level sits “above” the genome, functionally it’s really below, as indicated in this last figure.  Of course, it helps to remind ourselves that “level” is a convenient but not quite accurate concept, and they are not always clearly distinct and non-overlapping, as in this case.

Current Methodological Weaknesses

It should be noted that these weaknesses stem from an inherent paradigmatic conflict that exists in science as it’s practiced today.  These weaknesses will not be addressed until complex systems thinking pervades science in general.

…methodologies of DNA/RNA isolation and sequencing from mixed cell populations artificially average the molecular profile.

…current methods used to trace genetic loci heterogeneity are not accurate, as the admixture of DNA from different cells will wash away the true high level of heterogeneity and only display the heterogeneity of dominant clonal populations.

There is a need to change our way of thinking by focusing more on monitoring the level of heterogeneity rather than attempting to identify specific patterns in this highly dynamic process.

…the benefit of cancer intervention depends on the phase (stable or unstable) of evolution the somatic cells are in.

The strategies of attempting to reduce heterogeneity to study the mechanisms of cancer represent a flawed approach.  Without heterogeneity, there would be no cancer. That is the reason why many principles discovered using simplified homogenous experimental systems do not apply in the real world of heterogeneity.

…cancer progression is fundamentally different from developmental processes…. The terminology ‘‘cancer development’’ implies an incorrect concept and needs to be changed.

…we recommend focusing on correlation studies rather than search for a specific ‘‘causal relationship’’.

…the understanding of the overall contribution of epigenetic regulation should not focus solely on tumor suppressor genes, but rather focus on system dynamics and evolve-ability.

A true genome project would focus on the way genomic structure and topology form a genetic network and should also include epigenetic features of the genetic network.

Related posts:

1. The Conflict Between Complex Systems and Reductionism
2. Cancer as Evolution — 2008 Summary
3. Cancer as Evolution, part 3

Second, via Prometheus, Wired reports on a robot-software combination that was able to generate, test, and refine it’s own hypotheses to identify coding for orphan enzymes in yeast. Obviously, this is a very special purpose kind of science.  But the fact they got a closed loop is very impressive.  I also like the fact that it’s in the biological sciences. Hey, maybe some descendant of this program can solve the aformentioned cancer problem.

Related posts:

1. Stray Thought About the Singularity
2. Singularity Summit: Thoughts on AGI
3. Superorganism and Singularity

I don’t know too much about it except that it’s an autoimmune disease and has a complex, multi-causal etiology and pathology.  In my reading on autoimmune diseases in general there seems to be a direct link between latitude an incidence.   Specifically, the farther from the equator you live the more likely you are to get Crohn’s, Type 1 diabetes, rheumatoid arthritis, and so on.

This being our wont in Western society, we try to isolate it down to a single cause: farther from the equator means less sunlight, which means vitamin D deficiency, so it must be vitamin D.  So we try to feed people vitamin D, but this doesn’t cure the condition since it’s notoriously hard for your body to get utility from vitamin D supplements (and in fact it’s easily toxic) and even hard to get enough in food.  Plus there’s the issue that maybe it’s not just the vitamin D itself but some combination of biochemistry that happens when you expose yourself to sunlight (the main way humans have gotten a majority of their vitamin D throughout history).  But wait, what about skin cancer?  Let’s put on sunscreen and go outside for 15 minutes a day.  Nope.  Sunscreen blocks vitamin D production.  Plus in northern climates it’s very hard to get enough sunlight to produce enough vitamin D, especially in the winter months.  A number of studies suggest that over half of Americans are deficient.

My guess is that vitamin D is not the issue, but more generally sunlight is.  Or more precisely, given your ethnic background, there’s a range for optimally healthy sunlight exposure, and if you go too far out of that range in one direction or the other, you end up with health problems.  Autoimmune and other disease on one end, cancer and poor skin health on the other.  But I doubt it’s even that simple because lifestyle in general can predispose you or provide resilience — diet, exercise, exposure to environmental insults, and patterns of activity that affect emotional and mental state.

One thing that I think is overblown is the portion of the equation that is genetically predetermined.  The pendulum in science has swung too far towards genetics in terms of explanation in general, and this completely contradicts the evidence.

If I were diagnosed with Crohn’s or any other autoimmune condition, here’s what I would do personally.  First, devote several hours a day to physical fitness and conditioning, as if I were a professional athlete.  Second, experiment with diet like a mad scientist: try every supposed “good health” diet out there, but mixing it up and listening to my body and mental state.  Third, I would experiment with daily sunlight exposure, using guidelines based on my natural skin tone (darker = need more sun).  Next, I would examine my interpersonal relationships and eliminate/reduce contact with anyone who I even suspected of being a “net negative” emotionally in my life.  Finally, if I didn’t see dramatic results, I would move closer to the equator and to a locale that’s very different from my current one (different culture, different daily patterns, etc), and change up my daily routine, esp. if I spent more than a few hours a time doing the same thing (like staring at a computer screen).

Related posts:

1. Should You Use Sunscreen?
2. Celiac Disease on the Rise
3. Egyptian Mummies Yield Ancient Secrets of Good Journalism

Related posts:

1. Should You Use Sunscreen?
2. Crohn's Disease
3. Behavior and Emotions as Virus

Like does this mean you can cure heart disease?

She’s hesitant.  Nobody wants to say they can defeat the industrialized world’s number one killer.  Nobody wants to make promises about life, or quantify salvation.  But she fervently believes she’s got a shot.

This is what the 2008 Genius edition of Esquire Magazine had to say about Hina Chaudhry.  Her approach is to switch back on the mechanism that causes cells to divide in the heart, which doesn’t normally happen after birth in any mammal.  This is not a stem-cell approach, despite what it might sound like.

Looking on the web there appears to be very little written about this work, so I’m wondering how Esquire found her or chose her work to highlight.  I’d like to learn more if anyone has information they’d like to share.

Related posts:

1. Approaching the Singularity from Two Points
2. Approaching a Cure for Cancer
3. Killing Cancer Stem Cells

The key insight needed to make sense of this mystery involves the aforementioned principles evidenced in the Spore universe, but it also requires the notion of real world as encoding device.  By this I mean that the genome itself is not a complete, self-contained piece of code with all that is required to generate (for instance) an adult human.  Rather, implicit in the genetic code is a model of the real-world environment that the code will operate in once activated (i.e. “expressed”), and this implicit model is absolutely crucial for life to have originated and continue to thrive.  Imagine, for instance, if all of a sudden the laws of chemistry were altered and carbon could only form 2 bonds.  Life as we know it would cease to exist; our DNA (and all DNA for that matter) relies implicitly and thoroughly on existing features of the world.  And thus our DNA does not need to explicitly encode how to fold proteins since protein-folding is an automatic reaction given the structure and environment of the particular protein molecule.

This implicit encoding or reliance of the genetic code on its environment has been likened to scaffolding that is used in construction (genes being the blueprint of course).  But the scaffolding analogy doesn’t do justice to the immensity of information (both in absolute terms and as a percentage of the total) that is implicitly encoded by the environment for use by the genome.  Not that this is some giant happy coincidence mind you; the genome evolved in a world where physical and chemical principles pre-existed.  And as lifeforms increased in complexity, each new level of organization was a pre-existing condition to be relied upon for the evolution/emergence of the next.

It is worth pointing out that by “genetic environment” I don’t just mean the environment that the whole organism finds itself in, but rather the extended and recursive environment that the genetic code will find itself in as it does its work.  This includes increasing levels of complexity that are generated by, or on top of the DNA level: chromosomes, epigenetic markers, proteome, cellular structures, multicellular structures, and on up.  One level begets the next, and your genetic code expects these levels to emerge in due course or it won’t function properly (or at all).  Consider, for example, how useless the part of your DNA that describes brain structure would be if it were not for the encoding of how to make neurons and axons.

By grasping the significance of the extended, recursive genetic environment (ERGE) it becomes more clear why genetic fatalism is misguided and why the nature/nurture debate misses a large portion of the action.  By intervening in the expression of the genome through the ERGE to the mature human animal — for example, via early intervention in childhood — genetic “predispositions” become largely irrelevant in practice.  By the same token, there’s no such thing as a purely natural or purely environmental effect: it all a matter of controlling the ERGE.

Related posts:

1. Cancer as a Complex Adaptive System
2. What is a Gene?
3. The Conflict Between Complex Systems and Reductionism

As you’ll recall, I hypothesized that the Frugality Meme has its roots in evolutionary psychology. Given the conditions present on the savanna where we evolved, it’s easy to see how this meme might creep beyond the bounds of mere frugality. In the ancestral environment, tribes were almost certainly caught in a Malthusian Trap: any significant improvement in their material standard of living would quickly be countered by an increase in their population (see Chapter 2 of Gregory Clark’s excellent Farewell to Alms for a thorough, yet accessible explanation of the Malthusian Trap) .

Therefore, except for those few at the very top of the dominance hierarchy, everyone lived close to the subsistence level. There simply wasn’t much surplus that could be saved, so it would have been difficult to save too much without literally starving. Under these conditions, the Frugality Meme didn’t require any modulation; just save whatever you can. However, in modern industrialized societies, there is plenty of surplus. Sure, saving some is great. But the marginal benefit of saving decreases as you save more. At some point, the benefit of consumption today exceeds the benefit of saving for tomorrow. However, when the Frugality Meme degenerates into the Ascetic Meme, people seem to discard any notion that consumption today is desirable. Their intertemporal utility functions are their own business of course. But people in the grip of the Ascetic Meme typically also try to enjoin others from consuming today.

I think one of the primary reasons people worry about the consumption of others is hierarchy. As most of you undoubtedly know, humans are wired for hierarchy. An interesting aspect of the Frugality Memeis that people at the top of the hierarchy seem to be exempt. There’s no clear direction of causality here. Does hierarchy override the Frugality Meme? Does hierarchy enforce the Frugliaty Meme? Does the Frugality Meme promote hierarchy? I think the answer is that we have two mutually reinforcing dynamics. Hierachy and frugality both conferred some competitive advantages to our ancestors and they became intertwined.

Obviously, those at the very top are immune from attempts to enforce frugality. They already dominate. But those angling to make it to the top can use a lack of frugality to signal their perceived higher status. If they can then defend themselves against enforcement, they consolidate that status. Those higher up the chain probably try to enforce more frugality on those lower down the chain as a way of demonstrating their dominance and capturing more of the surplus for themselves. Those at the bottom also have a reason to maintain frugality among their ranks. They want to prevent too many people from being above them in the hierarchy. Obviously, those at the bottom who don’t want to suffer an enforcement sanction from either their superiors or their peers have a strong incentive to signal their frugality somehow.

So what does this have to do with environmentalists? Quite a bit I think. Environmentalism creates a fertile ground for the Frugality Meme to transform into the Ascetic Meme. With environmentalism, there really is a problem that requires conservation. We can absolutely over consume our environmental assets. But the environment is so complex, it’s hard to rationally determine what “over consume” means. So it’s easy to recursively appeal to the Frugality Meme: The world could end unless you save! How much? A lot! Is that enough? Is the environment being degraded in any way? Yes. Are you close to starving yet? No. Then you can save more! Welcome to asceticism.

I’m not sure if my hypothesis is correct. But it explains a lot of strange behavior surrounding environmentalism. First, we have the people that want to use environmentalism as an excuse to live a primitive, subsistence life. Second, we have leaders at the top of the hierarchy who are exempt from saving even as they exhort others to. Third, we have the call for severe sanctions against those who fail to signal their willingness to save. Fourth, we have people trying to signal their environmental frugality by buying Priuses (BTW, I believe the reason the Prius outsells the Civic Hybrid is that it looks distinctive and thus sends a stronger frugality signal) and putting out lawn signs advertising how they’re buying green energy. Lastly, it explains some of my own internal dialogs where my knowledge of economics conflicts with an instinct to appear environmentally conscious.

So the next time you hear someone telling you about some grievous environmental harm and how you have to change your life to prevent it, you feel the need to impress people with your environmental consciousness, or you sneer at someone because they are doing something that appears environmentally unfriendly, ask yourself, “Did I really think that through or did the Ascetic Meme just take me for a ride?”

Next up, my thoughts on the implications of the Ascetic Meme for environmental policy.

Related posts:

1. Follow Up on the Ascetic Meme
2. Environmental Ideology and The Ascetic Meme
3. Policy Implications of the Ascetic Meme

First, I must warn you that these thoughts are pretty preliminary, highly speculative, and undoubtedly controversial. It will also likely require more than one post to flesh them out. So bear with me. The crux of my hypothesis is that the polarization we are currently seeing on environmental issues is an emergent phenomenon stemming from some deep evolutionary psychology. Developing workable policies will require getting past this psychology and rationally examining what is actually in long term best interests of the human species.

My insight began by observing a common internal dialog of mine, “That’s cool! I want one. Yeah, but it’s really too flashy for me.” There seem to be competing personalities in my head when it comes to luxuries. I see similar behavior in my family and friends. These well off people forgo small luxuries that are pretty clearly a benefit to them with the rationalization that, “Oh, I don’t really need that.” Then for the big luxuries they do finally cave in to, they have to convince themselves that it’s alright to get them, which seems to require long drawn out conversations with me.

I see similar behavior among environmentalists. Take the “locavore” movement. The thinking here is that eating food grown close to you is better for the environment because it reduces the emissions from transporting food. Unfortunately, it turns out that the dirt-to-table emissions attributable to food are dominated by the production phase. So it’s better for the environment to produce foods in areas that require the least intensive methods and then ship them. For example, we should grow a wide variety of foods in New Zealand and ship them to England rather than grow them in England. But emotionally it seems more extravagant to eat food from far away. That’s why when you point out the efficiency argument to avowed locavores, they come up with all sort of other reasons why you should eat local–not why they eat local, but why you should. If they’re willing to bear the costs of eating local, more power to them, but leave me out of it.

It’s this combination of internal pressure and the incidence of proselytizing that leads me to believe evolutionary psychology may be involved. Humans appear to be wired for cooperation and enforcing cooperation. It’s easy to see how a bias against luxuries could also be adaptive in the ancestral environment. There’s already pressure to accumulate luxuries to signal status . Without some countervailing factor, early groups of humans may have dissolved into a counterproductive escalation of selfish accumulation. Note that I’m not claiming strong evidence for this effect, just putting it forward as a hypothesis.

In and of itself, this bias is probably a good thing even in modern times. Max Weber described how frugality was part of a highly successful work ethic in The Protestant Ethic and the Spirit of Capitalism. I owe my existence to this work ethic (all four of my grandparents are/were paragons of Protestantism), so I’m a fan. Also, people are generally bad at predicting the future, so “saving for a rainy day” is still good advice.

Let’s call this adaptive bias the Frugality Meme. Where we get into trouble is when it mutates into an extreme form: the Ascetic Meme. In this version, the goal is not to savings or modesty, it is suffering through deprivation, typically to achieve some sort of spiritual goal. Asceticism is a recurring theme in many world religions. More offensive is that it sometimes includes a compulsion to see other people join in this suffering. You can flog yourself, but please don’t flog me.

I see some environmentalists going down this extreme path. There are people dedicated to “sustainable living“, which appears to bear an uncanny resemblance to living like a monk. But hey, that’s their choice. What really worries me are environmentalists that don’t seem satisfied unless everyone suffers. You can find plenty of environmental extremist quotes on the Web, but here are my top three scariest:

“Phasing out the human race will solve every problem on earth, social and environmental.” — Dave Forman, Founder of Earth First!

“If I were reincarnated, I would wish to be returned to Earth as a killer virus to lower human population levels.” — Prince Phillip, World Wildlife Fund

“We, in the green movement, aspire to a cultural model in which killing a forest will be considered more contemptible and more criminal than the sale of 6-year-old children to Asian brothels.” — Carl Amery

Obviously, these guys are wackos. What worries me more is that regular people often seem to reflexively behave as if anything that protects the environment is good. I plan on exploring how the propagation of this meme stifles debate in future posts.

Related posts:

1. The Insidious Ascetic Meme
2. Policy Implications of the Ascetic Meme
3. Follow Up on the Ascetic Meme

At the very least, it would look much different than “a locatable region of genomic sequence, corresponding to a unit of inheritance” (call this the “standard definition”).

Gerstein’s definition, “a union of genomic sequences encoding a coherent set of potentially overlapping functional products,” while more accurate, is not really a useful definition. It just says there is structure to the information on a DNA sequence which corresponds to higher level function in the cell or organism. But we knew that already, it doesn’t tell us anything about the structure or how it relates to function.

The standard definition is a stronger claim, but it’s harder to reconcile with the evidence. Simply read the rest of the Wikipedia page to see the contradictions. Locatable regions of sequential base pairs only partially correspond to identifiable function. And as far as I can tell — somebody please explain if I’m wrong here — these locatable regions are not units of inheritance. Inheritance involves a very accurate copying of the entire genomic sequence, and in the case of sexual reproduction a very preservative recombination operation called crossover. The heterogeneity conferred by mutation (and crossover) acts either on points in the sequence or sequential regions, but these are mostly random occurrences, not limited to supposed gene boundaries. So if during inheritance, a gene can be chopped in two, partially deleted, inserted into, etc, in what sense is a gene a unit of inheritance? You could argue that an individual base-pair is a unit of inheritance, and you could argue that the entire genomic sequence (modulo a few mutations and crossover) is a unit of inheritance. But not a gene.

Then there’s the mystery of “junk” DNA, the portions of the genome which don’t directly code into identifiable products like proteins. In many species (including humans) the non-coding portion of DNA comprises over 98% of the genome. Wayt Gibbs in a Scientific American article points out that certain segments code for RNA which doesn’t get turned into protein, but which are actively functional in a number of ways not previously appreciated:

To avoid confusion, says Claes Wahlestedt of the Karolinska Institute in Sweden, “we tend not to talk about ‘genes’ anymore; we just refer to any segment that is transcribed [to RNA] as a ‘transcriptional unit.’”

Still, these RNA-only genes are only likely to double the number of identified functional units in the genome, leaving in humans 96% or more of the genome unaccounted for. Recently, the ENCODE project made a startling revelation:

“The majority of the genome is copied, or transcribed, into RNA, which is the active molecule in our cells, relaying information from the archival DNA to the cellular machinery,” said Tim Hubbard of the Wellcome Trust’s Sanger Institute…. [From COSMOS article, emphasis mine]

The pilot project posits:

Perhaps the genome encodes a network of transcripts, many of which are linked to protein-coding transcripts and to the majority of which we cannot (yet) assign a biological role. Our perspective of transcription and genes may have to evolve and also poses some interesting mechanistic questions. [From Nature article]

In other words, most of the so-called non-coding DNA does code after all (just not directly into proteins), and there is good evidence that these genetic products are not junk after all, but rather constitute nodes in a multi-level genetic, epi-genetic, proteomic and metabolic network. Sole, et al outline both theoretical and empirical bases for this line of thinking, which not only agrees with the above findings but also gives a plausible explanation for one of the biggest questions about the gene model having to do with robustness. More generally, Sole, et al represent a shift in thinking towards systems biology which is long overdue.

With all this in mind, we turn to a real genetic headscratcher about recent experiments in which ultraconserved (and thus presumed critical) portions of mouse DNA were deleted but to no apparent effect. While the network theory could in principle solve the mystery, it’s worth going through the comments on the blog because (a) plausibility doesn’t imply veracity, and (b) there could easily be more than one relevant cause/dynamic. I’ve summarized what I feel are the main arguments and referenced the corresponding comments by number:

• The deleted genes serve functions that are latent (21,26,32, 35, 52, 55, 63, 78, 82)
• Gene-level information interacts with other types of information in a complex, indirect way (71, 86, 87) [ precursor to the network theory ]
• Genes are selfish and look out for their own preservation; the deletable sections could have been introduced by random mutation, viral or recombinatory injection (33, 59, 62, 72, 74, 76)
• They are useful in recombination, but not alone (4, 75, 76, 77)
• They play an important role in the physical structure of the chromosome (4, 54, 71)
• Redundancy is achieved by a form of “checksum”, possibly probabilistic, or other cryptographic mechanism (6, 12, 76)
• Certain genes if mutated properly could be harmful, but if deleted entirely have little effect (59, 76, 84)
• The ultraconserved segments piggyback on the critical genes they are next to (29, 33, 54)
• Some of the genome acts as a latent heterogeneity reserve which evolution thrives off of (53)
• They protect critical genes by reducing the chance such genes will be mutated (75, 76)
• The ultrapreservation has to do with negative selection (37) [ I have to admit to not understanding this argument (or whether it's a counterargument for negative selection), perhaps someone can explain it ]

Notwithstanding the ultraconserved parts, it is worth pointing out that there doesn’t necessarily need to be any function for non-protein-coding DNA; it could just be junk after all. Alternatively, we are often just looking at an evolutionary snapshot (as suggested by some of the comments above) and it’s hard to say what is functional without looking at the longer context and looking at the evolutionary system as a whole. After all, nothing in biology makes sense except in the light of evolution.

So, why does all this matter, and why am I picking on the gene model even though we all know that it has its flaws? For one, because we don’t all know that it is so terribly flawed. I certainly didn’t until I looked into it. But more importantly, even if we admit at some level that a “gene” is a quaint concept — accurate to describe only a small portion of the genome — by continuing to use the term, we (a) propagate misunderstanding to the vast majority of the population, and (b) continually reinforce flawed thinking and logical fallacies in our own minds that blocks better understanding and insidiously undermines fruitful new ways of thinking of the problems. Ultimately we keep having to narrow the gene definition, add caveats to apologize for its poor explanatory power and come up with post hoc explanations for why empirical results don’t fit the model.

Perhaps it is time to stop using the term “gene” entirely and come up with a lexicon for the elements and processes of the genome which incorporates and integrates models for the informational content beyond that of protein coding, including chromosomal structure, epi-genetic information, and biomolecular and cellular networks.

Related posts:

1. Cancer as a Complex Adaptive System
2. Gene-culture Co-evolution
3. Encoding Life's Complexity