chadn737

Wrong about glyphosate resistance? I challenge you to show any comment I have ever made that says I was "wrong" about glyphosate resistance. Herbicide resistance is an old problem that predates GMOs by decades. It also does not make the weeds more "weedy" in a traditional sense. It only means that the handful of species that are resistant must be controlled by other means. Meanwhile, there are hundreds of weeds that are not resistant. In the absence of GMOs, glyphosate is limited only pre-plant usage and tillage or more toxic herbicides must be used during the growing season....both having huge disadvantages. If weed resistance develops, then how are we worse off than before the use of GMOs? We aren't. We couldn't use glyphosate post-plant before GMOs. At one time humans farmed (and still do in most crops) without glyphosate period. To listen to you and others complaining about this, one gets the impression that all of farming is and always has been completely dependent upon glyphosate. If its a matter of the "amount" used. While Glyphosate usage has gone up, it has largely been at the expense of using LESS of other herbicides that are far more toxic environmentally and too human health. The overall effect is that we are using more of a much safer product which is a net benefit. Glyphosate resistance is only a problem in that it keeps us from using glyphosate. I agree that it is a problem from this perspective, but it is only a problem if you already support using glyphosate in the first place. If you are opposed to its use, then you are proposing a farming system that would never use it anyhow, in which case resistance is irrelevant. For those of us who applaud the use of a safer more effective herbicide that allows one to use better farming methods like no-till, it is a problem and I advocate using a diverse mixture of herbicides to reduce/eliminate resistance. However, typically those complaining of superweeds don't want us using glyphosate period, in which case, the presence of weeds who are only resistant to glyphosate and not mechanical means of control amounts to a circular argument. GMOs are also a broad class of products. Talking about the use of a single herbicide like glyphosate when you have other GMOs like Bt, virus resistant Papaya, virus resistant squash, acrylamide reducing potatoes (Innate potatoes), non-browning apples, vitamin-A enriched crops (rice, maize, bananas), drought resistant corn, etc is to miss the forest for the trees and an attempt to reframe the debate.

1) No, you don't need selection to evolve. Basic population genetics demonstrates that to be absolutely false. 2) The notion that we are still not under selection is also absurd. Advances have allowed us to overcome many historical selective pressures (starvation, certain diseases), although this is not true of the entire world. But to presume that these are the only types of selection at work is to take a very narrow and naive view of selection. Sexual selection can play a very large and important role in human evolution still. 3) Natural selection is about differences in reproductive success, not "survival of the fittest". Rich, successful, atheletic, beautiful people that we would typically think as "the fittest" who never reproduce are losers in the evolutionary game. Their genes have failed to be passed on. High birth rates amongst other populations, such as those who are poor...they are successfully passing on their genes. You now have nations with decreasing birth rates and inverted demographics. These are all factors that will continue to shape human evolution. The movie is a comedy and inaccurate on many levels, but watch the first 5 mins of Idiocracy. It gets basic Evolution right and more so than any other movie I have ever seen. Selection is all about reproduction. Doesn't matter if the characteristics those reproducing possess what most people think of as those of the "fittest".

An open access paper negates any profit from subscriptions and somebody has to pay for the maintenance of servers, editorial staff, web designers, etc.

You mean all political parties?

Science, Nature, PNAS, PLoS One...there are several reputable non-specialist journals. In the Life Sciences I know of no journal that does not carry publication fees. As pointed out, a figure will cost you money. So does making it open access. Even if you publish in a highly reputable open access journal, like eLife (which is very high quality) or one of the PLoS journals, you will pay money....in some of the BMC journals, expect to pay ~$2000 for an open access paper.

Last night there was a great debate on Intelligence Squared over Genetically Modified Food. The science came out on top with audience overwhelmingly voting in favor of GMOs. Great information, very civil debate, well worth a watch. http://intelligencesquaredus.org/debates/upcoming-debates/item/1161-genetically-modify-food

That is not typically what is referred to as "synthetic biology".

synthetic biology = genetic engineering. Same thing, different name

As we keep pointing out, these tests DO EXACTLY THAT. Tests like Tajima's D screen for alleles that pass the threshold. In any experiment there is always a certain chance of false positives and false negatives...hence statistics. If you test an allele and it passes the threshold, on what basis do you reject it as being acted upon by selection? What you are suggesting smacks of cherry picking and confirmation bias....rejecting results that you don't agree with. The beauty of these tests is that they are not biased by any assumptions of what the selective force is or how adaptation should operate. If Evolution has taught us anything, its that the adaptations don't always fit how we expect them to. Sickle Cell anemia seems like a pretty bad adaptation, yet that is what it is. If you apply these tests to those alleles, they show that they have been selected for in those populations.

That is what all of these tests mentioned do. They determine if an allele is selective rather than stochastic. Alleles that fail to pass the threshold are assumed to be neutral rather than under selection. This happens to be the VAST majority of any genome. In humans, ~10-15% of alleles through the genome appear to be under selection, while the majority are not and thus neutral. I would recommend that you take some time to learn about evolutionary and population genetics. Specifically the models of HWE and tests of selection. This debate really wont progress otherwise.

This is true of any scientific experiment. Even if you know potential selective pressures, you still have a problem of reliably showing that they are indeed selective and that the selection on a particular allele is even caused by it in a first place. Error is inherent in all of science no matter how much information you have. This is why we use statistics and set minimum thresholds that any test must pass before we call it significant. By definition, that is what Genetic Drift is. Its the stochastic alteration of allele frequencies. You don't have to include them specifically. Neutral allele frequencies fluctuate stochastically, regardless of the source of that stochasticity. This can either be mathematically modeled or inferred directly from the sequence data itself. No assumptions about causative events are necessary.

Deviation from the null is EXACTLY what selection is. Its population genetics 101. Hardy-Weinberg Equilibrium. Given a large enough population size and absence of various factors LIKE selection, allele frequencies do not change. This is has been mathematically worked out and demonstrated. Changes in allele frequency are always do to one of four forces....genetic drift, natural selection, gene flow, and mutation. Genetic drift and mutation are inherent in the null model which selection is tested against. gene flow can be identified by multiple signatures. That leaves only selection to explain the deviations observed. In this, the tests are actually superior because they are not biased in anyway by any presumption of what the selective force is or what adaptation should look like.

In what way is a catastrophic event selective? Natural selection is a factor of reproductive success over time. Rare catastrophic events like an asteroid impact or a massive volcanic eruption are not something that can be adapted to nor do they occur over long enough time periods to impose the sort of pressure necessary to manifest itself as differential reproductive success. The long-term changes of such events, such as climate change CAN provide that sort of selective pressure, but the initial event itself is immediate, not multigenerational. You have not provided anything other than your continued assertion to the contrary coupled with a profound misunderstanding of very fundamental population genetics. The ability to trace backwards the effective population size and date bottlenecks is pretty well established in the field. Yet somehow you are going to challenge all of this? No, I don't agree. It is possible for a rare allele to replace a common allele, but for that allele to survive a catastrophic event creating a bottleneck would be by pure dumb-luck, i.e. a stochastic event. This is all a matter of very basic probability. Say you have a bag of a hundred colored balls, 48 red, 48 blue, 1 green, 1 yellow. You then blindly toss 90 balls away, what is the probability of each ball surviving? With 10% remaining, you are guaranteed to have at least either a blue or red ball remain, there is absolutely no guarantee that a green or yellow one will. In fact the odds are against picking a green or yellow ball. Even if a rare allele provides some selective advantage to the catastrophic event, the mere fact that it is a RARE allele makes it improbable that it will survive. Its a pretty well established in population genetics that at small population sizes, even adaptive rare alleles stand a good chance of being wiped out simply by genetic drift. The conservation genetics literature is full of this. The best way for a rare allele to survive and spread through a population is to exist in a large population under steady or at least slowly changing conditions. Catastrophic events forcing a population through a bottleneck negate both of those factors. The population is very quickly reduced (hence a bottleneck) and conditions are changing rapidly. In such cases, common alleles have the best survival. No you don't. You keep asserting this, but there are many methods of looking for natural selection on an allele without knowing anything about the stochastic events. You simply don't have too. There are other measures of stochasticity beyond environment which to test against. Stochastic environmental effects will treat neutral mutations the same as mutations under selection. If an asteroid randomly falls on an animals head, it kills off both the advantageous, disadvantageous, and neutral mutations that organism carries. You test against the rate of neutral mutations to determine if a particular allele is above or below some threshold, indicating selection has been at work. Knowing the actual events causing any of these things is completely unnecessary.

1) Extreme events like volcanic eruptions or asteroid impacts are not selective. They have an immediate impact of eliminating huge swaths of a population indiscriminately. The effect of this is that populations typically are forced through a bottleneck very quickly. Rare or less common alleles having less probability of surviving simply as a matter of the sampling effects, while common alleles will face nearly equal chances of being eliminated. These population bottlenecks can be dated and effective population sizes at the time of the bottleneck estimated using various methods, including those based in coalescent theory. Long term changes in climate caused by such effects will be selective, but the initial event itself will not be. 2) You do not need to know the selective pressure to know that a trait or allele has undergone selection. The tests for selection are unbiased in this respect and independent of whatever the selection pressure is. Its one of their strengths.

The mechanisms we typically associate with "epigenetics", DNA methylation and certain histone modifications, are most highly concentrated in heterochromatin, in particularly targeting repeats and transposons. It really appears that they evolved with the purpose of preventing the spread of parasitic elements like transposons. Any other function then in actual protein coding genes is more of a co-option after the fact or an accidental spreading from silencing of some of these parasitic elements. Epigenetics is too often thrown around as some mystical magical answer for any hard to explain phenomena...its not.

Homework question?

These are still genetic differences and thus still behave in the ways described by evolutionary and population genetics that underlie the modern synthesis.

They are talking about differences within protein-coding genes and arguing that much of the differences between species are due to genetic differences in coding regions. This is still genetic variation and requires no rethink of evolutionary theory.

I know of no study that has shown that the genetic diversity is not proportional to the phenotypic diversity. This issue is particularly complicated by the fact that the phenotype is factor of both genetics and environment, i.e. gene x environment interactions. If you have the genetic potential to be 6ft tall but spend your childhood malnourished, you wont be 6ft tall. Furthermore, different variants interact with each other in different ways. This is known as epistasis and this can greatly increase the number of possible combinations and resulting potential phenotypes. Finally, initial studies have missed a lot of genetic variation. SNPs are the easiest to identify via sequencing. There are also chromosomal rearrangements, Copy Number Variants, insertions, deletions, many non-coding variants that have yet to be identified....not to mention that we don't know the extent of rare variants or their effects. Most GWAS studies rely on using known common SNPs and will miss unknown rare variants. So there are many possible reasons for any missing heritability that does not require an invocation of epigenetics.

Yes. One of the worst violators of this is Michael Skinner, who has made a lot of news claiming that various herbicides and other chemicals cause transgenerational epigenetic effects. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0102091 However, in this study, they use an outbred strain of rats, as opposed to an inbred strain. This means that there is going to be considerable genetic variation floating around from rat to rat and generation to generation. At no point do they test any genetic markers or control for any effects of genetic variation. They test for methylation differences, they find some...which is guaranteed to happen by chance alone, particularly when comparing genetically segregating individuals....and then assert that the effects observed are epigenetic. This is the sort of study one sees time and again, particularly from animal and human community, to a lesser extent in the plant community. Even in some of the better studies that get published in Science or Nature, there is a failure to do this sort of control fro genetic variation. This is exactly the point that Tim Bestor, one of the leading scientists in the field from the animal side has made about many high-profile studies, such that diet of the mother affects the children and subsequent generations. "Other factors could explain the new Science findings, cautions Timothy Bestor, professor of genetics and development at Columbia University. For one, he suggests that the researchers choice of mouse strain could have influenced the study results. Radford and colleagues did not study inbred mice because those mice had more trouble surviving the restrictive diet needed for the experiment. (Inbred mice are often studied because they are genetically homogenous across generations.) Instead, Radford studied more genetically diverse mice that could better survive the poor nutrition regime. In turn, the health issues seen in the second generation of mice (which were born free of the sperm DNA changes seen in the first generation of the mice) could be somehow genetically inherent to this mouse model, he suggests." http://www.scientificamerican.com/article/diet-during-pregnancy-linked-to-diabetes-in-grandchildren/

Funny thing is that at least in the plant community, those that are considered leading the field of plant epigenetics (old and new scientists) are typically pretty adamant about how this ultimately ties back to genome evolution (in particular transposons) and is not really environmentally variable. I see a lot more of that come from certain people in the animal community and few of them experts in epigenetics. For years there has been a problem (and continues to be a major problem) that studies looking at DNA methylation or histone modification differences between populations or generations fail to test or control for genetic variation. They make huge claims that they found a DNA methylation difference and therefore its epigenetic and yet not once did they look for any genetic variation that might be causing it. In the cases where genetic variation is also looked at...often its linked to the variation in DNA methylation or histone modification and likely causative.

It should be noted that strength of selection and effective population size matter. In the case of the moths, I don't think its a problem and its clearly a case of natural selection. Every trait has a selective advantage/disadvantage and is subject to stochastic effects. In this, what matters is the population size and strength of selection. If something has only a weak advantage or disadvantage, then in a small population, random processes can still dominate even over that weak advantage/disadvantage, rendering them irrelevant. However, as a population gets larger, these weak effects can increasingly be distinguished from stochastic processes, and so become subject to natural selection.

No, epigenetics is not central. This is my field. I work on DNA methylation and transgenerational inheritance of DNA methylation in both plants and animals. The overwhelming evidence from both plants and animals is that heritable differences in either DNA methylation or Histone modifications is typically due to genetic variation. For instance, if you find a region of a genome that differs in DNA methylation between two individuals...often times there is some underlying or neighboring genetic variation that is causing this....like a new transposon insertion. In this case, what many people call "epigenetics" actually reduces down to genetics, since DNA methylation and gene expression are phenotypes of a genetic variant. When the variation in DNA methylation or histone modifications are induced by environmental factors, almost never is this heritable, and even then, it is typically stable only for a generation or two. This is not enough time to have long term evolutionary consequences, at least not in anyway to require a rewrite of evolutionary theory. In the field of epigenetics, we do not define it as the environment....gene x environment interactions were known prior to epigenetics and were never part of the original definition. We define it as heritable variation that is not due to underlying differences in the DNA. If that variation is caused by genetic differences...its not epigenetic. If its not heritable and stably inherited...its not really epigenetics. The cases where it is what is called a "pure" epialle (not induced by genetic variation and stably inherited)...these are actually quite rare as a whole and so are the exception, not the rule. We also have little idea how stable they are in the long term. It is also far more likely that if that trait achieves stability, that it is because it becomes a "genetic" trait rather than an epigenetic trait. With the exception of prions, epigenetics operates through the silencing or unsilencing of genes by DNA methylation or histone modifications. While these are common features of development, they are typically tissue specific and reset every generation. Because they are silencing genes, they are actually operating on the DNA already and so ultimately epigenetics is still a function of the DNA. It is hypothesized, and there is some evidence that mutations can accumulate in methylated/silenced genes. Methylated cytosines sometimes become deaminated which can lead to mutation of the cytosine residue. In this way, the silencing of the gene can become encoded genetically through the mutation disrupting that gene function. At this point, the trait becomes genetic. So epigenetics can serve as a transitory phase in evolution, but in the long term, there is no evidence from epigenetic that suggests evolution needs a rewrite. Those who argue that it does, do so not from a standpoint of evidence, but from a standpoint of untested hypothesis and often conviction.

Quite frankly little of what you have argued makes sense to me....particularly the argument earlier that basically said that all tests against null distributions were wrong... Especially when we know how to distinguish natural selection from genetic drift as Arete has already pointed out. In the case of where you have a single large stochastic event....say a meteor hitting the Earth or a volcano going off....we can actually distinguish this from normal genetic drift and natural selection. Thats because events like this force populations into a bottleneck. There is a huge reduction in the effective population size....something that can be directly estimated and timed using both genetic and other sources of data. Such stochastic events like this have genome wide consequences that make them distinguishable from normal genetic drift and natural selection. Quite frankly, I am not sure what you are arguing, unless its to say that all of population and evolutionary genetics is bunk.

What determines proteomic interactions? The specific domains of that protein and sequence of the proteins. Mutate an amino acid in a critical binding site and you eliminate. What determines the lipids, the sugars, the other components of a cell? In order for a cell to have them, they have to be manufactured, moved, and combined. This is all done by the proteins present and what those proteins do. What determines all of this? The DNA sequence. The DNA sequence encodes the proteins, it encodes their interaction, it encodes what products are ultimately made. In the end, it ultimately reduces to the DNA sequence.