The whole question of framing science has passed me by, mostly because I have had nothing to add. But this headline brought me up short.
Researchers Identify Genetic “Fix” for Problem in Some Sweet Corn Hybrids.
A news story from the Agricultural Research Service of the US Department of Agriculture explains that
Several herbicides registered for use on sweet corn kill weeds but not the crop, thanks to protective enzymes in corn that rapidly degrade the chemicals. But some sweet corn hybrids aren’t so lucky; they harbor a genetic defect that impedes the enzymes, causing herbicides to linger in the plants, which suffer stunted growth or other harm.
The researchers discovered that a particular cytochrome P450 gene protects maize from a variety of herbicides. In the ones that are sensitive to the herbicide there is a mutation to that gene, or one very nearby, which makes plants carrying that version sensitive to five distinct classes of herbicide. Knowing that, breeders hope eventually to be able to eliminate the sensitive version of the gene in commercially important maize varieties.
You’ll notice that I tied myself in knots back there trying to avoid calling the herbicide sensitive version of the gene “defective”. Because that is the whole thrust of my argument.
Since when is being sensitive to a chemical designed to kill plants a “defect”?
Only if you think that the normal state of affairs is for some kinds of plants to survive being sprayed with a lethal chemical could the death of those plants be considered defective. But of course, that’s exactly how many plant breeders and researchers do think.
Maybe Michael Pollan, looking through the Extended Phenotype lens he has made his own, would see it as a defect too. It is certainly a minor setback in corn’s march towards global domination. But those clever corn plants have managed to persuade a bushel of plant breeders to do the eugenic thing and fix their defects. All hail maize.
(Of course, what I really want to know is whether Teosinte and farmer varieties of maize carry the protective cytochrome p450 or the “defective” version.)
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Hi Jeremy
Sounds like an interesting project you’ve go there!
You’ve been given a flying start by those Open Helix people…
http://www.openhelix.com/blog/?p=388
The gramene database has some good tutorials if you fancy tinkering yourself (with a crash course in bioinformatics, thrown in for free)
http://www.gramene.org/tutorials/
The sequence viewer linked to by the mary at
http://gramene.org/Zea_mays/cytoview?l=5:1-6365100;h=umc1766
is based on a browser called “ensembl” for which there are also good tutorials.
http://www.ebi.ac.uk/~bert/presentations/genomes_to_systems/
http://www.google.co.uk/search?q=ensembl+tutorial
Needless to say, this would be a lot easier (and perhaps less fun!) if it was genetic “defect” in humans, mice, e.coli or any other better understood model organism… (rather than pesky tetraploid corn)