Crop Comments: Two botanical miracles

The prolific existence of juicy navel oranges is the proof of teamwork employed by Mother Nature and cooperative non-invasive human scientists. The cluster of sections located at the blossom end of a ripe orange resembles a human belly-button, hence the common name of this fruit. But its scientific name is Citrus sinensis. European explorers brought back citrus trees from China and India and transplanted them in tropical and subtropical regions of the western hemisphere New World. The main reason for introducing these fruits to a new home was to provide sailors strategically situated self-sustaining reserves of vitamin C, to counter the outbreaks of scurvy common on long sea voyages.
Orange historian Vince Moses best explains the special personality of navel oranges. Moses states, “That appearance of a navel on the orange is the result of a mutation. The mutation created a conjoined twin — an aborted second orange at the opposite end from the stem — looks like a human navel, but it’s in fact a small, second orange.” Moses explains that the mutation that started it all was a single branch on a sour orange tree in the garden of a monastery in Brazil. A visiting Presbyterian missionary came upon it in the mid-1800s. It intrigued her that not only did the orange have a bellybutton and baby orange inside, its sweetness was a wonderful surprise. She was so impressed that she sent samples of the tree to the USDA in Washington. There, USDA scientists began grafting branch samples into rootstock to catalyze a quantum leap in navel orange multiplication.
The citrus production industry began in earnest in 1873, thanks to that Presbyterian missionary living in Bahia, Brazil. Quoting Moses again, “Because the navel orange through that mutation is seedless, all of the navel oranges that we see today and we eat today are genetically identical with the original orange.” Thus the produce aisle in food markets is filled with clones of that one mutation.
Of course, since a seedless orange has no way to reproduce naturally, a nurseryman gives Mother Nature assistance by grafting sprouted buds onto another tree’s trunk and roots… just the way USDA workers did back in the late 1800s. I just described what I consider to be a positive miracle.
The second miracle, unfortunately, isn’t positive, namely, botanical monsters, the most notorious of which is herbicide-resistant Palmer’s amaranth. In tackling this subject, let me hit the high spots of Marc Brezau’s April 24 online paper found on the website of the Genetic Literacy Project:
But first let me give a little background to this herbicide-tolerant noxious super weed called Palmer’s amaranth (Amaranthus palmeri… let’s just call it A.p.). To begin with it is a sibling to regular old pigweed (Amaranthus retroflexus), and it’s a cousin to the trendy South America-based food seed quinoa.
A.p. boasts two very important botanical assets. First, it’s a C-4 type plant. C-4 means that its carbon building blocks are crafted with four carbon modules. Without getting too technical, this means that the ability of the plant to retain moisture… as regulated by stomates (openings on leaf surfaces)… is much more efficient than is the case for non-C-4 plants. The C-4 class boasts such members as corn, sorghum, Sudangrass, millets, sugarcane, and… obviously amaranth family species.
The other asset which A.p. enjoys is that it’s dioecious, meaning (with plants or invertebrate animals) that the species in question has the male and female reproductive organs in separate individuals. This trait basically doubles the gene pool, compared to species in which male and female reproductive organs are housed in one individual. Brazeau wrote that even in scientific circles there is an almost universal mind-set “that herbicide resistance evolves via random useful mutations that happen after the application of herbicide and then natural selection kicks in. While not impossible, that’s not generally what’s going on. What’s happening is that the weeds start selecting for a trait they already have, expressing it in greater degrees as it starts conferring new found Darwinian fitness.”
Taking this one step further Washington State University agronomist Andrew McGuire noted that weeds have evolved resistance to 23 of the 26 known herbicide sites of action and to 163 different herbicides. Quoting McGuire, “These types of statements make it sound like weeds actively did something, but they didn’t. We’re talking about random mutations (491 and counting) that were maintained in weed species until they were sprayed with an herbicide that the mutation interfered with.” McGuire then cited University of Wyoming weed science professor Andrew Kniss who found latent traits for weed-killer resistance to an herbicide that wouldn’t be developed for another 80 years.
Namely, French researchers screened herbarium specimens for a weed called blackgrass (Alopecurus myosuroides). They then tested those blackgrass specimens to see if any of them carried genetic mutations known to confer resistance to a certain type of herbicide (ACCase inhibitors). They found a mutant collected in 1888 near Bordeaux and kept at the Montpellier herbarium that had the same kind of mutation that causes herbicide resistance in blackgrass today. In effect (my words) that weed possessed the protective shield long before the weapon it would fend off was developed.
Kniss further explained: “Weed scientists have long suspected that spraying herbicides doesn’t cause resistance mutations to occur in the plant; it simply removes all of the susceptible plants so that any plants that are resistant can grow and survive. Over time, continued use of the herbicide selects for the resistant plants to become more common, and to eventually dominate the field. Herbicide use selects for the resistant plants that occur naturally within a weed population.” I close with the thought that non-stop use of the same herbicide greatly intensifies that selection process.

2018-06-01T10:30:02-05:00June 1, 2018|New England Farm Weekly|0 Comments

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