A Tale of Two Theories: The Mossy Earth and The Flower Conquerers

A Long, Long Time Ago on Planet Not So Far Away

What were the first plants to colonize the land on Earth? And when did this occur in the history of the biosphere?

Why did a burgeoning of flowering plant species come to dominate their gymnosperm and fern predecessors so quickly?

The Mossy (Algal and Fungal) Earth

Most biology textbooks state that plant life emerged on land about 450 million years ago (e.g, see p.4, The Biology of Plants by Raven, Evert & Eichhorn).

A new study suggests that plants colonized land much earlier than this.

As summarized here, the authors L. Paul Knauth and Martin J. Kennedy think that their geochemical data suggests that photosynthetic life forms (largely mats composed of mosses and algae, accompanied by fungi) carpeted the land over 800 million years ago.

Their evidence, albeit indirect, may help to explain the increase in atmospheric oxygen levels that allowed for the evolution of relatively large respirating animals about 600 MYA.

This green “welcome mat” may have set the stage for animal colonization of the land.

The “Abominable Mystery” of the Flower Conquerers

It’s been over 100 years since Charles Darwin described it as an “abominable mystery”.

What was perplexing Darwin was the fossil evidence that flowering plants (angiosperms) rapidly diversified and spread across the planet. (This was at odds with his belief that evolution was a gradual process.)

A new theory has been proposed in an attempt to solve this “mystery”.

As brilliantly summarized here, flowering plants may have taken advantage of changes in soil fertility, which were due largely to the higher growth and turnover rates of angiosperms compared to gymnosperms. Thus, a sort of positive feedback loop was created that allowed for the rapid proliferation of flowering plant species.

The originators of this theory, Frank Berendse and Marten Scheffer, published this ecological explanation of Darwin’s “abominable mystery” in Ecology Letters.

Bottom Line: Looks like studying the soil can provide answers to botanical questions.

Wicked Plants?

Toxic? Yes!….. But wicked?

Wicked (wik’id) adj. [Middle English wikke, evil, akin to Old English wicce, witch] “1. morally bad or wrong; acting or done with evil intent; depraved; iniquitous.” – Webster’s New World Dictionary

A wonderful new book Wicked Plants: The Weed That Killed Lincoln’s Mother and Other Botanical Atrocities by Amy Stewart, which I just finished reading, describes the myriad of chemical compounds found in some plant species that are toxic to animals – especially humans. Of course, such toxic plants aren’t evil or “wicked”. They’re just passively defending themselves against herbivores.

But calling them “wicked” certainly attracts more attention and sells more books, no? And isn’t it a good thing that more people would then learn about plants? So, fair enough.

Perhaps an interesting question to consider is why these plants have come to produce such toxic chemicals.

These “Wicked” Toxic Chemicals are Plant Secondary Compounds

It may come as a surprise to you that most of the basic metabolic pathways found in your cells – glycolysis, respiration, protein synthesis, etc. – are also found in most plant cells. Plant and animal cells likely share a common ancestor – a primitive eukaryotic cell. Thus, both plants and animals have many of the same so-called primary (a.k.a., “housekeeping”) metabolic pathways.

But, since plants don’t eat stuff, they have to make all the specialty organic compounds, such as amino acids, vitamins, pigments, etc., that they need to function well.

Therefore, plants not only have the “primary” metabolic pathways, but also so-called “secondary” metabolic pathways. That is, plants have special (secondary) metabolic pathways to achieve special functions, such as protecting themselves from UV light, chemically attracting pollinators, surviving periods of drought, etc.

Plants Can’t Pee, So They Have to Recycle or Store Their Secondary Metabolic Byproducts

If you ever took an organic chemistry class, you make recall that in chemically synthesizing an organic compound, you would sometimes generate chemical byproducts. Plants do this, too. But how do they get rid of them?

Often, they store these byproducts of secondary metabolism or “secondary compounds” in the vacuole of plant cells. The vacuole sometimes functions as the plant cell’s “garage”.

If one such secondary compound turns out to be nicotine, for example, which just so happens to be toxic to some insect herbivores, then it’s a lucky break for the plant. By chance, an evolutionary selective advantage for the plant has occurred.

And if this compound also turns out to affect humans, then this also may be a lucky break for the plant. (Nice to be cultivated.)

So most, if not all, of the toxic compounds mentioned in “Wicked Plants” are secondary plant metabolties stored in the vacuoles of plant cells. When the plant is eaten, or if trichomes on the plant surface are crushed by contact, the toxic compounds are released, which deter (or, in some cases, inter) potential herbivores.

All just by chance.

No evil or “wicked” intent involved.

Less Nutritious Plants as a Result of Higher Atmospheric CO2?

No Controversy Here

Despite the denials of global warming caused by increased atmospheric CO₂ from the scientifically ignorant or from the oil/coal corporations (or from politicians bought or rented by these corporations), there is one thing they can not deny.

The level of atmospheric CO₂ on Earth has been steadily increasing for the past century and will continue to increase. Indeed, the rate of increase may actually be accelerating.

Because plants rely on CO₂ as their carbon source for photosynthesis, how does/will this increased CO₂ affect green plants?

Less Nutritious Plants in a High-CO₂ World?

In a previous post, I briefly discussed the possible effects of higher CO₂ on plants.

A recent report indicates that under high CO₂ conditions some crop plants may produce higher levels of toxins and lower levels of protein, rendering them less nutritious.

The lower levels of protein as a component of plant biomass may be due to a decreased production of the protein RuBisCo in response to higher levels of CO₂. RuBisCo may account for up to 40% of the protein in leaf tissue, for example.

Despite early predictions that higher CO₂ would lead to increased crop yield more recent information suggests otherwise.

Bottom line: Increasing levels of atmospheric CO₂ will be a significant factor affecting plants now and in the future. We need more research into the effects of increased levels of CO₂ on crop plants in order to better prepare for a high-CO₂ world.

Is Sex Necessary?: For Dandelions, Apparently Not.

Send In The Clones

Few plants generate such annoyance among suburban homeowners with immaculate lawnscapes as the common dandelion (in North America, most likely Taraxacum officinale).

Despite efforts to eradicate them using chemical warfare (see here for info on such herbicides), the dandelions exhibit a remarkable ability to proliferate.

And they do so likely because they produce seeds asexually, that is, without the complications of sexual reproduction, such as pollination.

This is because most dandelions reproduce by a process called apomixis.

Unlike other forms of asexual reproduction in plants such as vegetative plant propagation via cuttings, apomixis is asexual reproduction via seeds.

In the case of most dandelions (i.e., Taraxacum officinale), the embryo in the seed forms without meiosis, thus the offsping are genetically identical to the parent.

Hence, most, if not all, of the dandelions in your neighborhood may be clones.

What are the benefits of apomixis?

Well, despite the lack of the evolutionary benefits of sexual reproduction (lack of diversity), apomixis allows for the “mass production” of seeds, which appears to be an effective strategy for dandelion propagation.

Bottom line: By rapidly producing cloned offspring, sex is certainly not necessary for the common dandelion.

Bees and Flower “Velcro”

Getting a Grip

Ever wonder how a bee or a butterfly can land on a flower and not fall off?

Me neither.

But thanks to researchers in the UK, we now have another reason why flowers are so marvelous.

Flowering plants have evolved chemical signals to attract pollinators to their flowers. Such signals include volatile chemicals to produce attractive odors and pigments to produce attractive flower colors or even so-called “honey guides”. For a brief review please see here (PDF).

Years ago, investigators noticed a difference in cells on the surface of some flower petals. Instead of the typical flat, tile-like surface of leaves, some of the petal epidermal cells were cone-shaped, producing a much rougher surface.

This led some biologists to hypothesize that such flower petal microtexture is a tactile cue for bees.

In a recent issue of the journal Current Biology Heather Whitney and colleagues present evidence that the flower petal microtexture allows bees to grip flowers and increase foraging efficiency. (Summaries of the paper can be found both here and here.)

Reference:
Whitney et al., Conical Epidermal Cells Allow Bees to Grip Flowers and Increase Foraging Efficiency, Current Biology (2009), doi:10.1016/j.cub.2009.04.051

Bottom Line: In addition to attracting pollinators using olfactory and visual cues, flowers may also provide tactile cues to facilitate pollination.

Plant Versus Plant: Some Plants Kill Other Plants Using Natural Herbicides

Alien Invader Uses Chemical Warfare

Spotted knapweed (photo left) is an invasive plant in North America.

It is native to Central Europe, east to central Russia, Caucasia, and western Siberia, but was accidentally introduced to North America through contaminated seed or ballast beginning in the late 1800’s.

Since then, spotted knapweed has spread throughout most of Canada and the U.S. (see map here).

In 2003, a study was published that suggested that Knapweed produces a chemical that makes other plants self-destruct.

The chemical is (-)-catechin, which is the stereoisomer of (+)-catechin – a chemical that may play an important role in the health benefits of green tea.

If spotted knapweed kills other plants by producing (-)-catechin, this would be an example of allelopathy, an often controversial subject in plant ecology.

Or Does It?

Upon further examination, the idea that spotted knapweed displaces other plants mainly by using (-)-catechin has been seriously questioned by a study published in 2009.

One of the chief arguments against (-)-catechin involve its effective soil concentration in native environments versus greenhouse studies.

In other words:

How valid is it to extrapolate greenhouse studies of allelopathy to native ecosystems, which are, of course, much more complex systems?

This question is often at the center of controversies regarding the actual significance of allelopathy in plant ecosystems.

Chemical Warfare in the Plant Kingdom

Aside from the controversy regarding spotted knapweed, there are many examples of plant-plant allelopathy.

Some examples are described at this excellent website provided through Cornell University’s Science Inquiry Partnerships and at this website from the U. of Florida and also at this website.

Alleopathy may also be relevant with regard to the subject of companion planting.

Sometimes fact, sometimes fiction, companion planting has been embraced by organic gardeners. (A popular book on the subject is Carrots Love Tomatoes.)

Bottom Line: It’s clear that some plants produce chemicals that are toxic to some other plant species, but the significance of allelopathy in affecting the nature of plant ecosystems has been questioned.

Why Herbicides Kill Plants (But Not You) – Part 2: Roundup®

The Last Roundup?

The herbicide that most Americans are likely familiar with is Roundup®.

Unlike the auxin-based herbicides I discussed in the previous post, Roundup® is not a selective herbicide. That is, it usually kills all green plants (except if the plant is Roundup Ready® or if the plant is a naturally Roundup®-resistant “superweed” – see below for more).

Roundup® is the Monsanto brand of the artificial chemical glyphosate, which was first synthesized in the 1970’s by Monsanto as a so-called “broad-spectrum” herbicide (i.e., kills all plants).

Glyphosate kills plants by specifically blocking the action of a key enzyme (5-enolpyruvylshikimate-3-phosphate synthase or EPSPS) that plants use to synthesize three amino acids (tyrosine, tryptophan and phenylalanine) that are essential components of all proteins. Without the ability to synthesize these amino acids, the plants will die.

Why doesn’t glyphosate similarly affect animals?

Humans and most other animals don’t have this enzyme, so glyphosate has no specific target as it does in plants*. (Since they do not have this enzyme, animals do not synthesize these three essential amino acids. They get them from their food.)

*Please note: This is NOT to say, however, that glyphosate is totally non-toxic to animals – more below.

Roundup may be losing its effectiveness, however, due to several factors.

Are Your Plants “Roundup Ready®”?

During the 1980’s there was a revolution going on in the plant sciences. Scientists discovered how to insert genes into the genome of some plants by using the bacterium Agrobacterium tumefaciens (At) as a genetic vector. Here’s how:

Scientists were able to use recombinant DNA technology to load genes into the Agrobacterium. And the bacteria were then able to “infect” susceptible plant tissue and deliver the genes straight into the plant cell’s genome. These foreign genes were actually “hard-wired” (stably inserted) into the plant’s genome. Moreover, these genes were able to be passed along to the plant’s offspring.

Simply put, Agrobacterium was like a taxicab, and the DNA was the passenger.

Using such technology, Monsanto scientists discovered a bacterial version of the enzyme EPSPS (see above) that was not affected by glyphosate, isolated the gene coding for it from the bacteria, and then inserted this bacterial gene into soybeans.

Roundup Ready® soybeans were born. Followed by Roundup Ready® cotton and canola. And when scientists learned how to genetically engineer grasses (Agrobacterium doesn’t work so well on grasses) using the so-called gene gun, along came Roundup Ready® corn. And maybe even Roundup Ready® turfgrass for lawns!

Roundup® Ready crops have certainly contributed to the extensive use of glyphosate, making it the most widely used herbicide in the U.S. This has likely increased the evolutionary selective pressure on “weeds”, leading to the generation of naturally glyphosate-resistant plants, a.k.a., “superweeds”. (Figs. 1 & 2 from Ref. 1 below)

Here Come the Superweeds.

Recent articles, such as this one in, of all places, Business Week have discussed implications of the appearance of so-called “superweeds”.

Examples of more recent reports of Roundup®-resistant weeds can be found here, here, and here. The increase in the number of such glyphosate resistant plant species has elicited warnings from environmental groups such as the Union of Concerned Scientists, as well as the international press.

In addition to naturally occurring gylphosate-tolerant weeds, there also is the risk of the spread of the genes conferring herbicide tolerance from GM (genetically modified) plants to native plants. Such events have recently been reported to have occurred in test plots of Roundup Ready® turfgrass in Oregon.

Briefly, the artificial gene conferring gylphosate-tolerance was discovered to be present in some native grass species growing adjacent to the test plots. (The genes presumably traveled via pollen from the GM plants to pollenate the native grasses.)

Thus, the possibility of the creation of superweeds via the escape of herbicide-resistance-conferring gene constructs is a very real possibility indeed.

May Increased Use of Glyphosate Also Be Toxic to Animals?

Though glyphosate has been considered one of the more benign pesticides, its environmental impacts are being reconsidered in light of some recent evidence to the contrary.

Reference
1. Boerboom, C. and M. Owen (2006) “Facts About Glyphosate Resistant Weeds”, Purdue University Extension, publ. GWC-1. (PDF)

Bottom Line: Though glyphosate kills plants by targeting an enzyme not present in animals, its overuse – due in part to GM Roundup Ready® crops – may be harmful to agriculture, to the environment, and, ultimately, to human health.

Why Herbicides Kill Plants (But Not You)

What Do Suburban Lawns and the Vietnam War Have in Common?

Answer: The herbicide 2,4-D.

You may be familiar with this herbicide as an active ingredient in “Weed ‘n Feed®”, “Weed B Gon MAX®”, Turf Builder® With Weed Control”, etc..

During the Vietnam War, it was an active ingredient in Agent Orange.

On lawns it’s used to kill the dandelions, but NOT the grass. (Find out how it does this below).

In the Vietnam War the U.S. military used it to defoliate the trees (so that they could more easily spot the Viet Cong).

You’re likely familiar with the term “Agent Orange” because of the controversy regarding the tragic health problems it caused to U. S. soldiers. (For current info re. this issue see here).

The serious health issues to both Americans and Vietnamese caused by Agent Orange are due to contaminants called dioxins produced during its chemical synthesis. (For more info on this see 2,4-D and dioxins and also here.)

But since this post is about how such herbicides work on the plants, let’s leave dioxin issues aside (for now).

Herbicides Such as 2,4-D are Auxins

Auxin in perhaps the most well-known plant hormone. (I’ve previously discussed auxin in this blog here.)

The herbicide 2,4-D is a synthetic auxin first produced in the 1940’s. It is one of many so-called phenoxy herbicides. These herbicides all are both structural and functional analogs of the natural auxin indole-3-acetic acid (IAA). That is, these synthetic auxins not only are structurally similar to IAA, but they are also biologically active as auxins in plants.

Although they both look and act like auxins, plants can not metabolize these phenoxy herbicides as they can with IAA, the natural auxin.

This turns out to be the key to why phenoxy herbicides such as 2,4 D are able to kill some plants.

How Does 2,4-D Kill Dandelions…?

Auxin-based herbicides are referred to as “selective” herbicides because they kill so-called “broadleaf” plants (a.k.a., dicots) but not grasses, for example. (Hence, that’s why they’re such popular herbicides with both growers of lawns as well as of wheatfields.)

But how exactly does spraying 2,4-D on susceptible plants kill them?

This turns out to be very poorly understood, and it’s also the subject of much misinformation. For example, I’ve heard people say that such herbicides “grow the plant to death” and read that 2,4-D “…simply confuses the plant to death”. Huh?

At the present time nobody really knows precisely how the auxin-like herbicides kill susceptible plants. As with most effects of plant hormones, it probably has a lot to do with the plant species in question.

However, recent findings have provided important clues. And these clues support the idea that plant death may occur as a result of a combination of factors.

Here’s a summary of the story:

First off, one of the well-know effects of excess amounts of auxin on dicots is to cause them to overproduce the plant hormone ethylene. For example, in 1969, Mary Hallaway and Daphne J. Osborne first showed that ethylene is a factor in defoliation caused by 2,4-D.

Because plants can’t break down 2,4-D, it’s action persists. This action includes the excess production of ethylene, which may result in a number of plant responses, including epinasty and senescence.

Another effect of excess ethylene production in response to 2,4-D is to stimulate the production of yet another plant hormone, abscisic acid (ABA). The effects of ABA on the plant may contribute to eventual plant death. (For an illustration of the complex effects of auxin-based herbicides on plants, see Figure 1 in the reference listed below.)

…and why doesn’t 2,4, D Kill the Grass? (and You?)

Perhaps the simplest explanation for both questions has to do with sensitivity to the plant hormone auxin.

In general, grasses are much less sensitive to auxin than are dicots. That is, a much higher threshold level of auxin is required to elicit physiological responses in grasses versus the so-called “broadleaf” plants. So, at the doses used to kill dandelions, for example, grasses are largely unaffected. (Higher doses of 2,4-D may kill the grass, too, however.)

Aside from the toxic contaminant dioxin, 2,4-D has no physiological effects on animals at hormonal levels, that is, at the concentrations that affect plants. (Indeed, there is no reputable evidence that any of the five main plant hormones affects animals.)

Reference
Grossmann, K. (2007) “Auxin Herbicide Action: Lifting the Veil Step by Step”, Plant Signaling & Behavior 2:421-423. (PDF)

Bottom Line: The herbicide 2,4-D mimics the plant hormone auxin and sets off a complex series of events – involving two other plant hormones – that eventually lead to the death of susceptible plants. At hormonal levels, auxins affect plants but not people.

Next-Time: More on Herbicides (Is Roundup® Losing Its Punch?)

Do Plants Have an Immune System?

It Depends on How You Define “Immune System”

Plants get sick. That is, they can be infected by pathogens.

But after hundreds of millions of years of pathogen attacks, plants are still here. So, they must have ways to get well after being sick.

Plants can defend themselves against disease-causing organisms (pathogens) such as viruses, bacteria, and fungi.

They do so by producing physical barriers (e.g., plant cells walls), some antibiotic compounds (e.g., phytoalexins), and even enzymes that perturb pathogens.

In a broad sense, these are all part of a plant’s immune response, that is, biological processes that an organism uses to defend itself against disease.

But do plants have an immune system similar to that in animals? One that can “remember” exposure to specific pathogens?

Recognizing (and Remembering) Self from Non-Self

Humans, along with most other vertebrates, have a multifaceted immune system called an adaptive immune system, which is the culmination of complex interactions at the biochemical, genetic and cellular levels.

Key parts of this adaptive system are the organism’s ability to (1) biochemically distinguish between it’s own cells (self) and foreign (non-self) entities AND (2) remember specific features of the foreigner.

All pathogens – from viruses to fungi – have so-called macromolecules on their surfaces that distinguish them.

Adaptive immune systems (AIS) use these macromolecules as antigens. That is, the immune system uses these characteristic surface features as a way to specifically identify foreign (non-self) entities.

The AIS uses the antigens to generate specific antibodies, which are used to tag the “foreigner” for destruction by specialized blood cells called lymphocytes. These specific antibodies then allow for the rapid detection of subsequent infections with a particular pathogen, which allows for relatively quick defensive responses.

Although plants don’t possess such a sophisticated AIS, there are instances of self/non-self recognition in plants, mainly having to do with issues of self-pollination. (A topic for another time.)

Plants Have an Innate (Passive) Immune System

A more generic, non-specific response to infection characterizes a plant’s immune system.

This type of response is called an innate immune system, in contrast to AIS.

Plants don’t have antibodies or special cells that search for and destroy pathogens.

Plants do, however, have cell-surface receptors to identify certain patterns characteristic of pathogens. Such receptors, when activated, trigger the production of chemical signals, such as methyl jasmonate (think jasmine perfume or jasmine tea) that may elicit both local and systemic defense responses.

Recent News: Researchers Unravel the Role of Priming in Plant Immunity

Further Reading: Recent (2006) scientific review of the plant immune system

Bottom Line: Although plants do have the ability to defend themselves against disease-causing organisms (sort of a rudimentary immune system), plants don’t have an immune system as complex as humans.

How, When, and Where Did Flowers Originate?

The First Flower?

How did flowering plants (angiosperms) evolve from non-flowering seed plants (gymnosperms)? Or did they?

When did the first flower appear on this planet?

And where on Earth did it occur?

These are some of the most hotly debated questions among botanists today. Partly because some of the fossil data is at odds with some of the DNA data.

An article by Elizabeth Pennisi in a recent issue of Science magazine prompted this blog post, in which I’ll try to summarize the current evidence and opinions. (Click here to listen to an interview with Pennisi regarding her essay on the origin of flowering plants.)

(Even though it’s somewhat outside the realm of “how plants work”, it’s still very a interesting topic, no?)

Goodbye Naked Seeds

Non-flowering gymnosperms, such as conifers, bear naked seeds on scales. Angiosperms have seeds encased in remnants of the flower.

Gymnosperms arose about 370 million years ago and dominated the Earth for 250 million years. Then within a few tens of millions of years, angiosperms appeared and their species greatly proliferated. (Currently almost 9 out of 10 land plant species are angiosperms.) This is the “abominable mystery” that confounded Charles Darwin. That is, how flowering plants diversified and spread so rapidly across the planet. (Still, today, 130 years after Darwin’s lament, this remains a perplexing topic among botanists…. a topic for another time.)

The Missing Link?

Where are the intermediates between the gymnosperm to angiosperm transition?

In 2002, there was much excitement over the fossil discovery of Archaefructus (illustration on left). This aquatic seed plant fossil was initially dated to the late Jurassic, about 145 million years ago, making it the earliest example of an angiosperm.

But since 2002 this fossil has been found to be not as old as originally thought, only about 125 MYA, and some scientists think it may be a member of the water-lily family.

This would render Archaefructus less primitive than Amborella, which currently sits at the bottom of the angiosperm family tree.

Amborella (see photo at top of the post) is a small shrub with tiny greenish-yellow flowers and red fruit that grows only in the understory in the rain forests of New Caledonia.

The simple answer to the question “Where is the missing link?” is: currently, there isn’t any.

The fossil data are incomplete and difficult to interpret. The molecular (DNA analysis) data from living plants group the gymnosperms all together and the angiosperms all together, with no plant species in between.

The missing link may have gone extinct. And, short of a very fortuitous fossil discovery, it may never be found.

Pertinent Links:

Nova (PBS) program on the first flower

Smithsonian on Archaefructus

The Deep Time Project (featuring Archaefructus)

Bottom line: Where and how flowering plants arose on Earth about 130 MYA is still very much an unsolved mystery.