To understand how superweeds survive, we first have to understand why normal weeds (the Jimmy Olsens and Lois Lanes of the plant world) die. <– last superhero reference of this post I promise.

Plants are not like people. The list of differences goes on and on, but today the difference we’re concerned about is where amino acids come from. Amino acids are the building blocks of proteins, the same way Adenine (A), Thymine (T), Guanine (G) and Cytosine (C) are the building blocks of DNA. Both our bodies and plants (and almost every other living thing) use the same twenty amino acids to build proteins. Our bodies can make ~12 of the twenty animo acids for themselves, but there are at least eight amino acids that the human body cannot produce (called essential amino acids). Our only source of these amino acids is from protein in our food.

It’s all well and good for us to get amino acids from our food, but plants don’t eat. They’re made of pretty much nothing more than water, sunlight and air. And trust me, none of those things are a good source of protein.

Unlike us, plants have to be able to make all twenty amino acids from scratch. That means they need whole biochemical pathways* that aren’t found in animals. But a biochemical pathway is like an assembly line. Break one of the steps in the middle and the whole thing falls apart. That’s what glyphosate/round-up does.

This part of the story starts with an enzyme called 5-enolpyruvylshikimate-3-phosphate synthase (or EPSPS for short). Do you don’t have to understand what EPSPS does specifically**, what is important is that its job is an important step in making the three amino acids Tryptophan, Phenylalanine, and Tyrosine***.  When EPSPS can’t do its job, the next protein in the biochemical pathway won’t get the parts it needs to do its job, and in short order the whole pipeline shuts down, none of those three amino acids get produced, and the plant dies.

How does glyphosate keep EPSPS from doing it’s job? It imitates one of the the chemical building blocks EPSPS normally works with, so EPSPS proteins will bind to it like they would to the actual chemical compound. But since glyphosate isn’t the compound EPSPS actually work with, it sticks in the protein. If it helps you can think of this as feeding the wrong sort of paper into a printer, causing a paper jam. Lots of individual molecules of glyphosate get into each plant cell. They stick in EPSPS proteins floating within the cell, which keeps EPSPS from doing its job, and once EPSPS stops working, the plant cell can’t make the amino acids it needs to survive, and dies.

Glyphosate is very good at doing what it does: killing plants. And as weed-killers go, it’s a lot less nasty for animals since it works by breaking a protein animals don’t need or even have. But there is one problem. Some weeds are becoming less effected by the herbicide, able to survive larger and large doses.  There are a number of ways plants can evolve to survive large doses of glyphosate. Let’s talk about three:

1. The first, and probably most obvious, is to change the shape of the EPSPS protein so glyphosate can no longer jam the mechanism. As it turns out mutations that change which amino acid is used at one specific point can produce a version of the EPSPS gene that is less likely to be broken by glyphosate. Think of it as changing the design of a print so paper that would jam the mechanism either won’t fit in the printer at all or passes through harmlessly. This method of getting “superweed” powers has been used by malaysian goose-grass and and australian ryegrass.
2. A second way for plants to become superweeds is to stop transporting glyphosate around the plant. I don’t have a good printer metaphor for this one. Cells in the leaves of plants are mostly completely grown and don’t need to make as many new proteins as the rapidly dividing cells in meristems and newly developing leaves. When a farmer sprays glyphosate it will mostly land on the mature leaves of the plant. If plants can keep the herbicide in those leaves and keep it from traveling throughout the rest of the plants, they stand a better chance of survival, and that’s exactly what has been found in resistant stiffstalk rye and pigweed.
3. The first two methods are all well and good, but I probably wouldn’t have bother to write this post if it wasn’t for the method of resistance discovered in Amaranthus palmeri (one of the many species that share the common name pigweed). Palmer amaranth’s approach to resisting glyphosate is charming in its brute force. Resistant plants have duplicated the gene for EPSPS many times (up to 160 copies in some plants!). All those extra genes mean the plants produce a lot more EPSPS protein, so no matter how many individual EPSPSs get jammed by glyphosate molecules, there are still plenty more working EPSPSs to keep doing the job, and the biochemical pathway never stops. Sure a problem with paper jams can be fixed by more advanced printers, or more strict controls on what kind of paper is allowed into the building… but Palmer amaranth’s solution was simply to build a lot more printers.

Potentially there’s potentially a fourth way to develop glyphosate resistance, which would be for the resistant version of the EPSPS protein engineered into glyphosate resistant crops**** to be introgressed into wild relatives allowing those wild crop relatives to become herbicide resistant “super weeds”. This gets talked about a lot and clearly the risk is going to depend on a lot of factors*****. In researching this post I couldn’t find any papers describing herbicide resistant weeds that owe their resistance to a gene from an herbicide resistant crop. And given how much ink has been spilled on the subject, I would expect any such papers to makes a big splash.

*Biochemical pathways are just a bunch of steps needed to get from some molecule an organism already has, to some other molecule the organism wants. Usually each individual chemical change is performed by some specific protein, like workers on an assembly line. (Sometimes its even arranged like an assembly line with intermediate molecules being passed directly from one protein to another, although it isn’t always that way)

**Although if you’re interested you can read more about the details of the EPSPS protein here.

***The first two are certainly essential amino acids. Our bodies can produce our own tyrosine, but all we do is modify phenylalanine. We can’t make it from scratch.

****Weeds that resist glyphosate are “super weeds”, but I can’t imagine ever hearing the crops that resist the exact same herbicide called “super crops” .

*****How the crop reproduces, whether its being grown near any wild ancestors, how weedy those wild ancestors are to begin with, which crop alleles are in close linkage with the resistance gene (crop-like traits tend to make weeds much less successful).

Gaines, T., Zhang, W., Wang, D., Bukun, B., Chisholm, S., Shaner, D., Nissen, S., Patzoldt, W., Tranel, P., Culpepper, A., Grey, T., Webster, T., Vencill, W., Sammons, R., Jiang, J., Preston, C., Leach, J., & Westra, P. (2009). Gene amplification confers glyphosate resistance in Amaranthus palmeri Proceedings of the National Academy of Sciences, 107 (3), 1029-1034 DOI: 10.1073/pnas.0906649107

POWLES, S., & PRESTON, C. (2006). Evolved Glyphosate Resistance in Plants: Biochemical and Genetic Basis of Resistance Weed Technology, 20 (2), 282-289 DOI: 10.1614/WT-04-142R.1

Photo: ekpatterson, flickr (click photo to see in original context)

There are more differences in the genomes of two unrelated corn plants than between the genomes of a human and a chimpanzee (two species separated by 3.5 million years of evolution).

On the other hand, two unrelated human beings, members of the same species, have more than four times as many genetic differences as two unrelated heirloom tomatoes.

Genetic Diversity:

Corn vs. Corn > Human vs. Chimpanzee >> Human vs. Human >> Heirloom Tomato vs. Heirloom Tomato

Now the fact that any two human beings are more closely related to each other than either is to a chimpanzee should be obvious to anyone who gives it a moments thought.

I plan to poll my sections tomorrow to see how many of them would put corn and heirloom tomatoes in the opposite positions, but many have figured out my feelings about corn, so they’ll probably guess it’s a trap.

3:20-7:54: Introducing the subject, developing drought tolerant varieties of maize in Africa, and the fact that the researchers working on it as using conventional breeding, marker assisted breeding and a genetically engineered trait Monsanto. When battling starvation, you use any tool that comes to hand.

18:40-21:20: This part is almost hard to listen to. You can hear the raw emotion in the researcher’s voice as the reporter keeps trying to make genetic engineering sound, at best, like a last resort. Couldn’t they just try irrigating more crop land she suggests?

25:10-end. Conclusion. I also thought this part was very powerful.

A few complaints:

“It’s philanthropic but it can also be seen as a publicity stunt by {inset any person or organization here}” <– this statement would apply to pretty much any philanthropic act that’s not done anonymously wouldn’t it?

Marker assisted breeding is not “a kind of half-way house between breeding and genetic engineering”! Think of marker assisted breeding as GPS for plant breeders. All that changes is that plant breeders get more useful information faster.

I’m pretty sure the BBC reporter at one point calls ears of corn kernels, but if this is just a difference between american and british english, I’ll withdraw that complaint.

Obligatory greenpeace quote:

“We really question the use of say molecular markers and gm in the same plant together … And what would concern us, that is, that it would be undoing all the good effects of conventional breeding by then also crossing it with a GM crop.”

I talked about another BBC story that addressed the lack of acceptance of genetically engineered crops in europe back in December.

* = tied for number of citations

** = some mutant alleles have kernel phenotypes.

If you want to become one of the famous mutant corn genes, it helps if you have an effect that is visible in corn kernels instead of only from fully grown plants.

And here is why:

• A geneticist could determine that the version of c1 that creates yellow kernels is recessive to the version that creates purple kernels just from looking at the ear of corn on left.
• Furthermore, they could tell you that both the male parent (the plant that provided the pollen) and the female parent (the plant on which the ear of corn grew) were both heteryzygous for the c1 genes (they each had one dominant version of the genes and one recessive version), and therefore the corn kernels the parent plants were grown from were both purple.
• They would know with certainty that all of the yellow kernels contain two recessive versions of the c1 gene.
• While they couldn’t predict with absolute certainty whether a specific purple corn kernel on that ear carried two dominant versions of the c1 gene or one dominant and one recessive version, they would know there was a 1/3 chance that kernel has two dominant copies, and a 2/3 chance it had one dominant and one recessive copy.
• That geneticist could make all sorts of predictions about what ears would look like in future generations depending on what colors of corn kernels were planted and which plants were mated with each other.

All this from a single picture of an ear of corn. For a phenotype seen in corn plants but not in kernels (like Knotted1), a geneticist would have to plant a row or more of corn seeds from an ear and examine the growing plants to get the same quantity of information.

And that is why mutations with kernel phenotypes have been so popular over a century of maize genetics research.

MAT points out another more pragmatic reason yellow corn may not be favored in Africa that I hadn’t heard of before. Apparently the extra carotenoids make yellow corn more susceptiable to spoilage than white corn varieties, a very pertenent issue in areas without access to the kinds of storage facilities we take for granted in American agriculture.

Jeremy at the Agricultural Biodiversity Weblog picked up the torch, highlighting a number of their own previous posts relevant to the discussion, including one by fellow blogger Luigi that relates the reaction of his own wife, originally from Kenya, on ordering polenta** at a restuarant and receiving a yellow dish.

Fortunately breeds of corn that contain even more beta carotene (the carotenoid most easily converted into vitamin A by our bodies) aren’t even yellow all the time. Although I wasn’t able to find a freely available picture, sometimes they’re ORANGE.*** While it turns out the correlation between color and beta carotene content isn’t perfect****, there’s still reason to hope varieties bred for the highest pre-vitamin A content will end up a striking orange color. For a visual examples of how orange corn can get, check out check out Dr. Rocheford’s lab website.

Will the distinction between orange and yellow***** be enough to get over the Africa’s lack of enthusiasm for yellow corn? Will the benefits of a diet with more vitamin A be enough to outweight the issues with yellow corn going “off” if stored improperly? I certainly hope the answers to both these questions are yes, but we won’t know for sure until we try. And there are some hopeful signs. For example this segment in a story from NPR:

Winter-Nelson and one of his graduate students took some of this orange corn to an open-air market in Mozambique for a taste test. The market-goers still preferred their white corn, but almost half of them agreed to exchange it for bags of orange corn when they heard it was more nutritious.”Probably the most encouraging part of it for me was that people who reported that they didn’t have much dietary diversity,” Winter-Nelson says. “People who reported that they didn’t eat very many fruits and vegetables, [or] that they very rarely ate animal products of any kind — eggs, meat, or chicken — were the most likely to take the trade.

“So, the ones who need it were attracted to it.”

So that’s a hopeful sign.

Two ears where some kernels received C1 from both parents, some from one parent and some from none. In a whole field full of C1 homozygotes, almost the kernels would be dark purple/black. Image courtesy of MaizeGDB and MG Neuffer

As I was proofing this post today, one other thing occurred to me. If the objection to yellow corn is primarily based on the color (let’s leave aside the issue of flavor for a moment), wouldn’t the simplest solution for the biofortified corn be to breed in an allele like C1 that turns corn kernels purple/black? There’d be absolutely no chance of the corn being mistaken for normal yellow corn, and since C1 acts on the production of anthocyanins, a completely different kind of plant pigments, it shouldn’t impact the level of beta carotene in the biofortified corn. Please point out in the comments if I’ve missed something obvious.

*This isn’t to say the food aid itself is unpopular, only that people prefer not to eat corn that resembles it when they’re NOT starving.

**A dish made of boiled corn meal, see photo below. A few years ago my mother discovered a lasagna recipe that substituted well cooked polenta for lasagna nuddles. About which, all I can say is that if you otherwise couldn’t eat lasagna (for example people who avoid eating gluten found in grains like wheat, barley, and rye by choice or necessity), polenta lasagna is a lot better than no lasagna at all.

Polenta. photo: Marilyn M., flickr (click to see photo in its original context)

***The amazing genetic diversity of maize also means these varietes can be produced without the need for genetic engineering. Which means getting the seeds to those would could most benefit from them would be faster and cheaper than something like golden rice which governments will hopefully approve someday.

****Harjes, C.E., Rocheford, T.R., Bai, L., Brutnell, T.P., Kandianis, C.B., Sowinski, S.G., Stapleton, A.E., Vallabhaneni, R., Williams, M., Wurtzel, E.T., Yan, J.B. and Buckler, E.S. (2008). Natural genetic variation in lycopene epsilon cyclase tapped for maize biofortification. Science DOI: 10.1126/science.1150255

****It occurs to me one factor in whether the distinction between yellow and orange is important may turn out to be whether different local languages contain a word for orange. Languages have been studied that contain as few as two words for colors (roughly: dark and light) and a color name describing orange is almost never found in languages with less than 7 color names. … sorry a distribution requirements class that I had to take in college just became arguable relevant. This is exciting!

Read about it in:

• The Economic Times
• The Times of India
• The AP

How much difference a comma makes:

“It is my duty to adopt a cautious, precautionary, principle-based approach.” <– Sounds like a reasonable person dealing with vocal discontent with the genetically engineered eggplants. Indian Environment Minister Jairam Ramesh quoted in Times of India

“It is my duty to adopt a cautious, precautionary principle-based approach.” <– Irrational standard* that can never be met. Indian Environment Minister Jairam Ramesh quoted in AP.

I don’t know what else to say about this story. Letting facts that should be settled by science becoming matters of opinion is one of the prices we pay for democracy, a form of government that’s still a head and shoulders above anything else yet discovered by modern man. Also, I totally called it:

This would seem to be the week for vegetables I hated as a kid. Yesterday was onion, today tomato, if there’s a story about brinjal/eggplant in the next few days we’ll have hit all the big ones.

*The precautionary principle as it has been quoted to me in the past: “Activities that present an uncertain potential for significant harm should be prohibited unless the proponent of the activity shows that it presents no appreciable risk of harm.” In other words, any and every action can be considered guilty until proven innocent of all accusations levels against it, and since people can come up with new accusations a lot faster than science can disprove them, it would seem that adhering to this version of the precautionary principle would mean not doing anything. Event

An anonymous indian tomato vendor in Chennai, Tamal Nadu. photo mckaysavage, flickr (click to see photo in it's original context)

First, since I didn’t explicitly state it in my previous post, the paper on the longer lasting tomatoes developed by India’s National Institute for Plant Genome Research didn’t report any data on how the RNAi knock-down tomatoes actually taste.* The tomatoes are nearly twice as firm as tomatoes in which these genes are NOT knocked down, so it’s possible they’d seem unpleasantly crunchy, I don’t know how doubling the firmness of a tomato translates into the feeling when a person bites into one.

On the other hand, if the tomatoes do turn out to be tasty and delicious, it’s quite possible the trait could be replicated without genetic engineering. And if that turns out to be true, it’s absolutely the approach anyone developing longer lasting farmers to Indian farmers, or farmers anywhere, should take (for why I’m saying this, check out the bit in bold further into this post). The synthetic microRNAs used in their experiments reduced gene expression by at least 99%, so, if it turns out that remained <1% isn’t playing a key role, the researchers at NIPGR have effectively created knock out lines for each of the two genes they were studying. Knocked out genes (genes so broken they don’t work anymore) has been a key part of genetics since before the word gene even existed. (Mendel in the 1850s and 1860s and Wilhelm Johannsen in 1905 respectively) With a couple of known targets, and a target phenotype that’s known to be worth the effort, creating tomatoes with “naturally” broken copies of the gene is possible and probably worth the effort to avoid the expense and controversy associated with trying to commercialize a new genetically engineered trait.

The mutant (left) and wildtype (right) tomatoes from mutant line e2615m1 from the mutant population cited below. Photo from the searchable database of identified mutant phenotypes at: http://zamir.sgn.cornell.edu/mutants/

Back in 2004 a paper** from two research groups in Israel described a saturation mutagenesis population*** of tomatoes created using EMS**** and fast neutron***** techniques. Screening 13,000 inbred lines for knock outs of either of these two genes would take a fair bit of time and money, but less than is involved trying to get approval of a genetically engineered trait (especially in India, where a political battle over their first genetically engineered food crop, an insect resistant breed of eggplant is still ongoing).

If it weren’t for (what I consider to be) irrational fears about genetic engineering and actions of people who exploit those fears, the arguments of speed and cost would instead rest with the genetically engineered RNAi knock downs already created in this study. Given the world we live in, and given there is an way to get the same benefits without genetic engineering in this particular case, getting the benefits of cheaper produce to people who could use the vitamins, and higher effective yields to farmers who could use the money must take priority. In the mean time people like you and I will just have to keep doing our best to combat that ignorance and fear so someday the deciding factor will be whatever technique is safest, fastest, and makes the most efficient use of scarce resources, not what people have, apparently arbitrarily, decided to natural or unnatural.

And as I said above, we don’t even know if the tomatoes are tasty, or if the NIPGR is or will be working on creating varieties of tomatoes with this trait for use by India’s farmers in the first place, so speculation on this paper may have gotten a bit too far ahead of itself.

*If they people who worked on the project are at all after my own heart, I’m sure they’ve tried the tomatoes for themselves, but subjective judgements like taste aren’t going to make it into a PNAS paper on fruit ripening (and its possible consuming genetically engineered tomatoes that haven’t been approved would technically be breaking the law in India, in which case the researchers would even less inclined to publicize any off the books tasting they did on their own.)

**Menda, N et al “In Silico Screening of a Saturated Mutation Library of Tomato” The Plant Journal DOI: 10.1111/j.1365-313X.2004.02088.x

***A mutagenesis population is a group of plant lines that have all been exposed so some mutating agent (see the footnotes on EMS and fast neutron). A saturation mutagenesis population is one where,  based on the number of lines of plants in the population and an estimate of the number of mutated genes in each line, a mutation of (almost) any gene in the genome will likely be found somewhere in the population. The exception being really genes that are so bad to lose that plants carry even one broken copy, or gene and pollen cells (which only have one copy to begin with), die without being able to reproduce.

****EMS stands for Ethyl methanesulfonate, a chemical that creates a specific kind of mutation in the genome of a plant (changing some Gs into Ts). Exposing plants to specific doses of this chemical creates (on average) predictable numbers of mutations in the genome.

*****Fast neutron mutagenesis is less common than EMS, likely because creating fast neutrons involves the use of radioactive substances (one source I found specifically cited uranium aluminum alloys). The advantage of fast neutron mutagenesis is that as the neutrons tear through cells they tend to rip away large chunks of DNA (hundreds or thousands of As, Cs, Ts, and Gs at once) which makes the resulting mutants more likely to completely lose the function of a gene (imagine using EMS to create mutations as changing a couple of key letters in a recipe, and using fast neutrons as tearing out a whole page of a cook book and throwing it away).

Author’s note: This would seem to be the week for vegetables I hated as a kid. Yesterday was onion, today tomato, if there’s a story about brinjal/eggplant in the next few days we’ll have hit all the big ones.

Ripening tomatoes. Photo: Photos_by_Lina, fickr (click to see photo in its original context)

I was recently pointed to an early publication paper that went up on the Proceedings of the National Academy of Sciences website on Monday, where a research group at India’s National Institute of Plant Genome Research describes two genes from tomato that, when knocked down by RNAi*, result in tomatoes that can remain ripe but not spoiled for up to three times as long as tomatoes where these two genes function normally.

Their approach targets specific genes involved in breaking down certain proteins found in the cell walls of tomatoes (in fact in the cell walls of all plants). Breaking down the cell wall is a key part of ripening in fruits (which the tomato is, botanically if not culinarily). Which makes sense if you’ll think about it for a moment. One of the traits we associate with ripening is getting softer, from bananas to peaches if it’s still crunchy when you bite into it, it wasn’t ripe. What makes plants stiff and crunchy? The strength of their cell walls. Since, unlike vegetables, fruits WANT to be eaten**, as they ripen they begin to break down their cell walls to make themselves more appealing to passing animals. Unfortunately, ripening and spoiling are, in a lot of ways, the same process. If fruits aren’t eaten when they become ripe, they continue to get softer, transitioning from delicious looking -> unappetizing -> inedible -> a puddle of mush on your kitchen counter.

Preventing ripening entirely is relatively easy, and there are plenty of known mutants in tomatoes and other species that never ripen (these naturally mutant tomatoes stay green and hard no matter how long you wait). But getting part of the way to ripeness but stopping before crossing the line into spoiled is a much less tractable problem.

A spoiled tomato. A rotting tomato is visible in the bottom left, but that's the result of the growth of microorganisms which is a more complex process. Cropped version of a photo from goldberg on flickr. Click to see the original photo on flickr.

To the non-cell wall biologist like me, one of the most attention grabbing parts of this paper was figure 3A, which simply shows photos of tomatoes that have been sitting at room temperature for 10, 20, and 45 days***. At ten days all the tomatoes look fine. By twenty days, the control (normal) tomatoes are shriveled. After 45 days sitting on the scientific equivalent of a kitchen counter the control tomatoes are basically brown balls of goo, while tomatoes with either of the two genes identified in this paper knocked down show no change in appearance over the same period of time. So what are these awesome genes?

Both genes studied in this paper are glycosyl hydrolases, a kind of enzyme that breaks the chemical bond holding a sugar to either another sugar or some other molecule, like a protein. Specifically the two genes, which are normally expressed in ripening tomatoes, each break specific kinds of sugar off of a specific kinds of protein found in the cell walls of plants. Plant cell walls are mostly made of hydrocarbon polymers like cellulose and lignin, but plants also use some structural proteins (usually less than 5% of the cell wall) and it is the sugars attached to these proteins that the glycosyl hydrolases studied here act upon.

This is where it gets scientifically cool. The prolonged ripe-but-not-spoiled state of the transgenic tomatoes they produced wasn’t simply a result of preventing the structural damage caused by the break down of the bonds between cell wall structural proteins and the sugars they’re connected to. Instead, when they looked at gene expression in plants where either of these two genes had been knocked out, they found that genes involved in breaking down cellulose, lignin and pectin (the main components of the cell wall) were also less expressed. The authors speculate that the kinds of sugars/carbohydrates these two genes break free from cell wall structural proteins actually serve as a signal to the plant to increase the production of all the other proteins needed to break down cell walls and in their transgenic plants, that signal never comes, letting the tomatoes stop ripening before the process leads to spoiling.

Tomatoes at a farmers market in NYC. photo: SeenyaRita, flickr (click to see photo in its original context)

The authors themselves point out the huge potential upside to reducing spoilage in the developing world. As much as 50% of produce is lost to spoilage between harvest and diner plate in the developing world. Reducing spoilage is one of those rare almost-a-free-lunch opportunities to increase the food supply without bring more land under the plow, or increasing the inputs (in the forms of fertilizer, pesticide, and all to often back-breaking manual labor).

At this point you may be thinking, haven’t we heard this story before? There are lots of differences between these tomatoes and the Flavr Savr tomato produced by Calgene in the 90s. Scientifically they come at the problem from very different angles, but rather than get into that let me point out two crucial practical differences:

1. The authors present data that the tomatoes with knocked down expression of either of these two genes are twice as firm as normal tomatoes of comparable ripeness. An important trait for transporting ripe tomatoes over any significant distance as illustrated in this segment of First Fruit talking about the Flavr Savr tomatoes of the 1990s:

The shipping test out of Mexico, however, proved to be yet another disaster. It was designed to test, not only whether the Flavr Savr gene would enable vine-ripened fruit to survive 2000 miles in a truck … The test results were clear before the vehicle came to a complete stop. Tomato puree seeped from the truck’s back end.

2. If these research leads to a commercializable fruit, it will likely be grown first in India, where, as described above, spoilage of produce is a major issue. In the United States, the Flavr Savr tomato had to go up against an existing system built on tomatoes that, without any genetic engineering, never ripen on their own, described in this way by MAT_kinase of TheScientistGardener:

Fresh market tomatoes, in nor cal, are all picked green and gassed with ethylene to force ripening (imperfectly). In the midatlantic, virtually all tomatoes have a natural gene mutation that prevents them from ever ripening completely in the first place. Either way, you end up with an inexpensive, pretty, red tomato that’s often hard and white on the inside. Heirloom varieties taste great, but are very susceptible to pests, have to be hand picked and turn to goo shortly after ripening.

When Pamela Ronald of Tomorrow’s Table talks about the development of transgenic crops, she points out that by 2015, it is projected that more than half of transgenic crop varieties will be produced by the national research labs of developing countries like India, China, and Brazil for they own farmers. If this paper is a sample of the sort of research such labs produce, 2015 should be a truly fascinating year for agriculture.

I shouldn’t have to say this, but there are currently no genetically engineered tomatoes on the market. For a short time in the 1990s Calgene sold the Flavr Savr tomato in California grocery stores, but they weren’t able make a profit doing so, so they stopped. The poor taste of most tomatoes for sale in the grocery store today is purely the result of conventional breeding (my post on the subject and Mat_kinase’s)

Meli, V., Ghosh, S., Prabha, T., Chakraborty, N., Chakraborty, S., & Datta, A. (2010). Enhancement of fruit shelf life by suppressing N-glycan processing enzymes Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0909329107

-The gene knocked down in the Flavr Savr tomato was Polygalacturonase.

-The two glycosyl hydrolase genes studied in this paper are alpha-mannosidase and beta-D-N-acetylhexosaminidase.

*Using RNAi means inserting a backwards version of part of a gene into a plant under a strong promoter (so the plant makes lots of RNA copies of the backwards bit.) Those backwards copies will bind to the RNA transcript of the actual gene, creating double stranded RNA. One of the main times a plant cell normally sees double stranded RNA is when it is being attacked by viruses (the genome is made of double stranded DNA and the RNA messages transcribed from the genome are single stranded), so making a double stranded copy of the a particular gene causes the plant to treat that gene itself like an invading virus and keep the protein that gene encodes for from being produced. (<– this is the simplified version of the story, this work actually uses synthetic microRNAs which are a much more refined version of the technique.)

**When a plant produces a sweet and tasty fruit in the wild, its goal is to attract some animal that will eat the fruit and carry the plants seeds to someplace new where the seeds can grow into new plants. Domestication has changed the rules of that bargain somewhat, as we artificially selected for bigger and tastier fruits, but fruiting plants still trade animals (us humans) food in exchange for having the seeds of their species distributed across whole fields by farmers, and have their growth protected and nurtured by human hands and human ingenuity.

***There’s also numerical data which is probably better science (the images only track two fruits of each type which I’m sure isn’t statistically significant), but the best scientific papers will include hooks like that image of unrooting tomatoes to draw the reader in long enough to read the exciting data itself.

Wild turkeys photo: sanbeiji, flickr (click to see in original context)

When I first saw the headline I was hoping I’d find an article describing the first fruits of the turkey genome project (which I talked about back in november.) Instead, and still interestingly, what was just published in the Proceedings of the National Academy of Sciences was a study showing that wild turkeys have been domesticated twice by different cultures in the Americas.

The turkeys we eat today come from a breed domesticated by the Aztecs, living in present day Mexico (or proceeding cultures occupying that region). However this study, looking purely at mitochondrial DNA sequences was able to use DNA isolated from bones and turkey droppings to determine that turkeys kept by indigenous farmers in what is now the American southwest represented an independent domestication of wild turkeys from one of a couple of wild turkey subspecies found in North America. Given the uncertainties of archeological dating, the most recent evidence for the existence of this second form of domesticated turkey could be as early as 1400 AD or as late as 1840 AD.

The Cliff Palace, the largest of the ancient villages in Mesa Verde Park. Photo: j-fi, flickr (click to see photo in original context)

What’s fascinating to me is that, assuming the easier date is more accurate, that would mean these lost domesticated turkeys met their end a little while after villages across the same region begin to be abandoned.* The PNAS article itself mentions that this may be responsible for the discovery of mitochondrial DNA from these lost domestic turkeys in local wild populations:

… conditions in the late 1200s would have favored this process as Ancestral Puebloan groups migrated out of the Colorado Plateau, perhaps abandoning some of their flocks to fend for themselves.

Trying to herd a flock of turkeys while journeying to some unseen place that I’d likely never seen before is one of those life experiences I’m glad I’ll likely never have to experience.

On the other hand if the more recent extreme of dating in correct (1840), it’s not beyond the realm of possibility (although probably unlikely) that the lost domestic turkeys may someday be found on someone’s grandparents farm as can happen for lost breeds of roses and apple trees.

All in all, another interesting story that we’d likely never have known about without the awesome tools of modern molecular biology.

-PNAS paper itself

- Coverage in Wired

*If you ever get the chance to visit Mesa Verde Park in Colorado, I’d definitely recommend doing it. (The park preserves the stone buildings of the Anasazi/Ancient Pueblo people, who lived, farmed, and built stone villages in the region until they either left or died in the 13th century.) Many of the theories for the abandonment of their villages involve failures of agriculture (whether from extreme droughts or exhausting the local soil), so seeing the ruins was, for me, a stark reminder of how vulnerable any society, including our own, is to decreases in food production.

In the early days of agbiotech, regulations were fairly minimal, which kept development costs low. The safety of a product was judged on the product itself and not the method used to develop it. Regulatory agencies have lost some of that focus in the past ten years. … I am very interested in having a regulatory structure that is science based and gets back to what we originally had.

I continue to be impressed with President Obama’s choice to head up the new agency, as I have been since the appointment of Roger Beachy was first announced. Though I will say I got this part wrong in my original post about Beachy’s appointment:

And on top of that, he’s spent his entire life working in the public and non-profit sectors (places like Cornell, Wash U, the Scripps Institute, and most recently president of the Danforth Plant Science Center). Can you imagine the screaming if Obama had picked someone who’d ever worked in industry to head up the NIFA?

As we’ve seen from the reaction to Roger Beachy’s appointment, finding a respected scientist who has done both basic and applied research, with proven skills as an administrator (plenty of great researchers make horrible administrators) and who’d spent his entire like working in the public and non-profit sectors instead provoked so much screams one might have thought President Obama had appointed Hugh Grant (the CEO of Monsanto, not the actor) to head the NIFA instead of Roger Beachy.

*Such funding contributed to the training of, among others, Gebisa Ejeta, who won the World Food Prize in 2009 for his work developing striga resistant sorghum, and who, from his testimony to the senate foreign relations committee, sounds like he would agree with this goal.