Nibbles: Potaghurt, Yams, New fodder crops, Enset, Cowpea migrations, Trees

Nibbles: Goats, Seed Fairs, Banana genebank, Prunus africana plans, Forage grass, English food, Talking heads

The backstory to finding sodium exclusion genes in wheat

Attentive readers may remember a piece we Nibbled a couple of weeks back about salinity tolerance genes (Nax1 and Nax2) making their way from a the wild relative T. monococcum to durum wheat. I asked around and it turned out that the monococcum cross in question was originally made decades ago, so I thought there might be an interesting backstory there. Some quick research quickly led me to this: “Parental material used in crossing and in Na+ uptake and flux experiments were durum wheat (Triticum turgidum) Line 149 and cv Tamaroi, and the parents of Line 149, Triticum monococcum C68-101 and durum cv Marrocos. Seeds were provided by Dr. Ray Hare of the Tamworth Agricultural Institute, New South Wales Department of Primary Industries.” So I contacted Dr Hare, who is now retired, and he was kind enough to send me the following, and allow me to reproduce it. It illustrates not just the importance of genebanks and crop wild relatives, but also how that importance sometimes becomes apparent through luck coupled with perseverance. Interestingly, that combination can be patented. My main question to Dr Hare was where the T. monococcum accession that started it all came from.

The C68-101 Triticum monococcum accession I believe came from the University of Sydney’s collection. It is known to carry the stem rust resistance Sr21. It is the stem rust resistance gene present in the Stakman differential set, ‘Einkorn’. Dr Dante The, a post graduate student at Sydney University, had been given the task to transfer Sr21 to hexaploid wheat so that this gene could be used in breeding rust resistant breadwheat cultivars.

Originally this accession was used as a source of Sr21, transferred from the diploid through a bridging cross (interspecific) with Marrocos (stem rust susceptible durum) to the hexaploid level. The Line 149 a stable tetraploid line carrying Sr21 (i.e. C68-101/Marrocos). It has the Australian Winter Cereal Collection (AWCC) accession number AUS 17045. This line is freely available. I am sure Greg Grimes and team, at the AWCC, will provide you with seed.

Now what has all this got to do with the salinity research, you may ask. To cut a long story short, I selected this tetraploid accession because I felt that it represented a potential divergence from the normal tetraploid genetic diversity, in that I was certain that it had a considerable content of monococcum genes. I was endeavouring to assemble a relatively small collection of tetraploid accessions (subspecies) representing the broadest range of genetic diversity from the Australian Winter Cereal Collection. At this time I was keen to look at the range of phenotypic expression for a number of breeding traits in durum wheat. I was concerned that the breeding program could be running out of genetic variability.

Being the Australian National durum breeder at the this time, my varieties were being grown on soils that we knew to contain transient salinity. Durum wheat yields were relatively poor on these soils. Durum wheat was known to be sensitive to elevated sodium levels in the soil.

My long time friend, Rana Munns, is a plant physiologist and an expert in plant/salinity research. She had all the experiment techniques sorted out nicely. So we got together and started a small project to see if there was any salt tolerance in durum.

All reports in the press were not positive. But nevertheless we pushed on. Our starting point was my collection of tetraploid subspecies. To our pleasant surprise, we found a few lines that appeared to exclude sodium from the leaves. Confirmation experiments showed that we were really onto something (i.e. high potassium and low sodium in leaf tissues, the reverse of normal when grown in elevated sodium media; this was a highly significant and repeatable reversal).

As the Marrocos line was rather wild and far from an ideal cultivar type, I commenced crossing it to my durum breeding materials. The cross with my variety ‘Tamaroi’ formed the research population for inheritance studies and subsequent molecular research. All these studies are published. Search under R. A. Munns.

I have no idea where the monococcum accession came from originally. I could check out the register of the Sydney University collection when I am at the Plant Breeding Institute, soon. I am on the staff of the PBI. I can also check Dante’s thesis when next at PBI Cobbitty. Dante’s thesis may carry more details on the source of the monococcum.

A bit long winded but I think that it is a nice little story on the value of genetic resources centres. Outcomes like this clearly demonstrate the value of such centres, many times over. A colleague of mine (Richard James in Plant Industry, CSIRO, Canberra) is transferring the two sodium exclusion genes (Nax1 and Nax2) to hexaploid wheat. Who knows what other genes for important traits can be found in monococcums and other progenitors. There are so many possibilities and exciting opportunities for gene exploration without going outside the Triticeae.

Nibbles: New genebank, Urban ag, Cassava, Justice, School gardens

How not to debunk anti-GMO propaganda

Graham Brookes and Bruce Chassy wrote a detailed rebuttal of a paper by G.F. Botta et al. in the American Journal of Plant Science, which questioned the value of GMO soybeans in Argentina. On the basis of their analysis, Brookes and Chassy conclude that:

The major deficiencies identified in this paper lead us to question the thoroughness of the review process undertaken by the American Journal of Plant Sciences, as it is our professional assessment that this paper should not have been accepted for publication in any reputable peer review journal.

I cannot dispute that. I can, however, point out that in seeking to orchestrate an invincible attack, Brookes and Chassy are perhaps guilty of stressing a single, not very helpful view of the nature of diversity, which is also entirely unnecessary to discredit the Botta et al. paper.

The main thrust of their rebuttal is to challenge the statements surrounding the use of the weedkiller glyphosate, and as an outsider that convinced me that the original paper was indeed deeply flawed. The two experts then go on to address another claim in the original paper.

‘Up until not recently agrarian diversity had always been increasing. However, in industrialized countries, plant and animal genetic engineers, trading houses and governments themselves combined forces to supply new varieties and uniform breeds that would replace the tremendous heterogeneity already existing’. 1

That’s easy enough to skewer, and Brookes and Chassy do so well enough.

From the very beginning of agriculture biodiversity of crops has, in fact, been continually contracting as farmers and breeders selected the most desirable crops (see for example, L.T. Evans. Feeding the 10 Billion, Cambridge University Press).

Sloppy to confuse crops and varieties, but hardly criminal. Unfortunately, from my perspective, instead of leaving it at that, they go on to help readers to do something that they say Botta et al. have not done, viz.

to comprehend the nature of breeding modern crop varieties. While a single or limited number of varieties may be grown in one region at a particular time, this does not mean biodiversity is being lost. Quite the contrary, since modern varieties have complex combinations of parents this results in the incorporation of numerous diverse traits from many ancestors.

Yes. And, what is your point?

This argument deliberately or ignorantly confuses the differences among genetic diversity in a pedigree, genetic diversity within a population, and genetic diversity among populations planted at a given time in a given place. Brookes and Chassy then go on to show how crop failures that the rest of us associate with “reductions in ‘genetic variety’” are in fact no such thing. Forget their view of the Irish potato famine. Consider instead their account of Southern Corn Leaf blight, which halved maize yields in the US in 1970. Here is how Brooks and Chassy describe the cause of the epidemic:

In 1970, all US corn had, what is known as N cytoplasm (a designation of the genotype of the mitochondria).  Around this time a second cytoplasm called T was introduced which facilitated male sterility for hybrid seed production.  Ironically, it was the new cytoplasm that was susceptible to blight.

So far, so true. As a result of the widespread adoption of Texas cytoplasm to confer male sterility – because it makes the production of F1 hybrids easier and cheaper – almost all the maize planted in the US shared a single type of mitochondrial genome that rendered them all susceptible to Southern Corn Leaf blight. As far as that susceptibility is concerned, there was genetic uniformity in the crop, no genetic diversity at all. So how do Brookes and Chassy describe that?

So, in this case, it was an increase in diversity—not a decrease—that caused the problem.

How can they possibly say that?

Before the widespread adoption of Texas cytoplasm, there was a range of genetically-based susceptibilities among maize varieties. Afterwards, all varieties were susceptible. Because they all shared one set of genes.

Here is how a panel of the US National Academy of Sciences described what happened:

The corn crop fell victim to the epidemic because of a quirk in the technology that had redesigned the corn plants of America until, in one sense, they had become as alike as identical twins. Whatever made one plant susceptible made them all susceptible.
Uniformity is the key word–the plants were uniform in that special sense, and uniformity in a crop is an essential prerequisite to genetic vulnerability.

There are other aspects of the Brookes and Chassy rebuttal that I am unhappy with 2 but I’m sufficiently self aware not to pursue them here.

Instead, I’ll just conclude that genetic diversity in a pedigree is not the same as genetic diversity in a population, a species, or an ecosystem. Especially not as far as resilience is concerned.

Just the facts, ma’am
Friends will, I know, be wondering why on earth I’m bothering. Indeed, after a little digging, I wondered why Brookes and Chassy bothered too. The American Journal of Plant Sciences is published by Scientific Research Publishing, which has been described as a scam and which “borrowed” papers published elsewhere and called them its own. It may be peer-reviewed, in the strict sense, but it is also clearly a joke. So why bother debunking a joke? Equally, Academics Review, the site where Brookes and Chassy (who is one of the founders) published their debunk, seems to be withering on the vine. The debunk itself isn’t dated, although on 20 March David Tribe (another founder of the site) gave notice that Chassy and Barfoot have just put out a dissection of Botta et al. 3 Few of the pages at Tribe and Chassy’s site seem to have a date, and there hasn’t been any “news” since May 2010. It’s all a bit sad, because a repository of countervailing facts would be useful, especially if not sullied by internal errors.