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Seeds Inherit Memories of Enemies

Infested plants pass on a defense memory of pests and pathogens to help the next generation withstand invasions.

By | May 31, 2012

image: Seeds Inherit Memories of Enemies The Arabidopsis plant on the left received a priming treatment before infection with bacteria and shows no sign of disease. The plant on the right is an untreated control plant. Brigitte Mauch-Mani

The Arabidopsis plant on the left received a priming treatment before infection with bacteria and shows no sign of disease. The plant on the right is an untreated control plant. BRIGITTE MAUCH-MANI

After plants acquire resistance to pests and pathogens, their offspring shoot up through the soil with better defenses.  The findings, published in a recent series of papers in Plant Physiology, are the first to identify small interfering RNAs (siRNAs) as a possible mechanism of this inherited memory response, and suggest a new strategy for managing crop pests.

“It’s sort of like giving a vaccine to the parent and seeing immunity in the child,” said Andrei Alyokhin, who studies insect-plant interactions at the University of Maine and was not involved in the research. “It could help with the pest problem—induced resistance in plants is an extremely underutilized approach.”

Plants eventually come to know their enemies.  When a caterpillar first bites into a juicy leaf, plant cells release toxic chemicals that make the pest grow more slowly. This initial encounter with a hungry herbivore primes the plant—when caterpillars come back for a second invasion, the defense reaction is more aggressive.

This is why George Jander of the Boyce Thompson Institute for Plant Research in Ithaca, New York, and his colleagues intentionally expose their tomato plants to caterpillars. “The priming increases resistance, and we are now seeing inheritance in the next generation,” he said.

Jander and his colleagues placed a corn earworm on each of nearly one hundred tomato seedlings.  The researchers similarly exposed Arabidopsis weeds to white cabbage butterfly larvae.  They then planted a second generation of plants in a pest-free environment, and introduced the insects after several weeks. Sure enough, offspring of plants exposed to the pests sustained less leaf damaged, and the caterpillars grew to only 30 to 50 percent the size of the insects that plagued parent plants.  In Arabidopsis, this priming was even passed on to a third generation: the grandchildren of infested plants showed heightened resistance, even when their parents had not been exposed.

And the approach may be applicable to a wide range of pest species.  For example, after infesting parent plants with the diamond back moth, Jander found the white cabbage butterfly and beet armyworm were smaller and less abundant on progeny plants. Strangely, however, the diamond back moth devoured leaves as usual, raising the question of just how specific these defense responses are.

“I suspect there is specificity—it may be that plants distinguish between herbivores—but we don’t really know how these interactions work,” said Sergio Rasmann, a biologist at the University of Lausanne in Switzerland who collaborates with Jander. It could also be that the plants “turn on the same defense irrespective of what’s feeding on them,” said Jander.

Taking a closer look at the mechanisms of inheritance, Rasmann first turned to small interfering RNAs (siRNAs)—a class of molecules so small they can potentially diffuse through the plant from the leaves to a developing seed. When he grew mutants that lacked siRNAs, the second generation plants showed no sign of an inherited defense response.  “It seems you can’t prime the seeds without the siRNAs,” said Rasmann.

The findings are the first to demonstrate a role for siRNAs in next generation priming, wrote Ian Baldwin, of the Max Planck Institute in Jena, Germany, who was not involved in the research, in an email to The Scientist. But exactly how they work is unclear. “The actual siRNAs that are transmitted to the seeds, and their targets, still need to be identified.”

Jander questions whether the siRNAs serve as the vehicle of inheritance.  “[They could] also move to the seed and catalyze DNA methylation,” he said.  Indeed, after infesting Arabidopsis plants with virulent Pseudomonas syringae bacteria, researchers at the University of Sheffield found evidence for the combined regulation of methylation and histone modification.

The findings suggest a new way that farmers might protect future generations of crops—collect seeds from infested plants to grow stronger plants the following year.  “Farmers probably won’t want to rely on this alone, but when [next-generation priming] is incorporated into organic farming as one of many methods, it can help,” said Jander.

Seed farms might even employ benign bacteria, according to results published by Brigitte Mauch-Mani at the University of Neushâtel in Switzerland.  When the team exposed plants to a transformed strain of Pseudomonas syringae that triggered defenses but not disease, offspring were still more resistant to the virulent bacteria.

Although for industrial-scale applications, it might be easiest to use low-toxic chemicals to trigger the molecular defenses instigated by bacteria and herbivores, Jander said. He recently sprayed plants never exposed to caterpillars with the hormone methyl jasmonate, and found offspring were more resistant to disease than control groups. If chemical technology can be perfected, it might help researchers amplify the inherited defense response.

“The idea is very new, and there is a lot of work to be done,” Rasmann said.  “But if we can harness the next generation response, it might reduce the overwhelming loads of pesticides applied crop fields now days.”

E. Luna et al., “Next-generation systemic acquired resistance,” Plant Physiology, 158: 844-53, 2012.

S. Rasmann et al., “Herbivory in the previous generation primes plants for enhanced insect resistance,” Plant Physiology, 158: 854-63, 2012.

A. Slaughter et al., “Descendants of primed Arabidopsis plants exhibit resistance to biotic stress,” Plant Physiology, 158: 835-43, 2012.

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Anonymous

May 31, 2012

How refreshing it is to see evidence that biologists in SOME areas of research are aware of the fact that no form of "selection" is sufficient to explain anything about evolution.

As I've pointed out elsewhere, selection occurs post facto.  Nature cannot select what is not already there to select FROM.

Also, as I've pointed out elsewhere, the overwhelming number of random mutations -- especially the more advanced and complex the species -- are DELETERIOUS.  A general assumption seems to be rampant that gametic cells are unaffected by anything that happens to somatic cells.  Denial of heritability of "acquired characteristics,"  (Lamarckism) leaves evolutionary biology with nothing to theorize around than fortunate accidents of mutation versus unfortunate accidents of mutation.  Yet random mutations that are BOTH beneficial AND need-appropriate are unlikely in exponential proportion to deleterious mutations (those that reduce fitness rather than increase it).

It has been less than a decade ago that, for many both inside and outside biological research, "selfish genes" were credited with being the veritable architects of beneficial species change (and, by extension of that, the architects of origins of species).  Anyone who (as I did then, and do now) said there was something drastically WRONG with that simplistic picture often was accused of being unwilling or unable to accept the obvious. Yet it was not then obvious and is not now obvious, and FINALLY research like that cited in this article, recognizes and accepts that it was not and is not obvious.

Less than a decade ago, DNA other than genes was labeled "junk DNA."  Now perhaps even evolutionary biologists may be beginning to catch on to the fact that SOME mechanism or mechanisms has to/have to be in play, whereby an increase in fitness from one generation to the next can never make sense on basis of random mutations, and consequent conservation of the lucky ones, while the unlucky ones cause cancers, birth defects and other kinds of deleterious inheritance.

Consider how vague it would be to say that EPIGENETICS accounts for the ability of gametes to produce offspring with characteristics that are all of these:
1)  New to the species;
2)  Iteratively heritable by subsequent generations;
3)  Beneficial; AND,
4)  Provides a solution to an environmental enemy or threat.

Such a statement would not be false.  It merely would be vague?

What would make enormous sense to me is that evolutionary biologists would join molecular biologists in seeking the specific mechanisms which account for the fact that species come up with offspring which have characteristics meeting the above cited four essential criteria for SPECIFIC NEED-DRIVEN fitness changes to increase over  successive generations. 

ONLY  THAT would explain anything about evolution.

If the only mechanisms were random chance mutations and selective factors that operate on those mutations, a species would be at the mercy of chance in a game in which the odds are exponentially in favor of deleterious results, and exponentially counter to coming up with anything both useful and appropriate to a specific need.

Now, that said, the next issue is for ANY research findings to also do the following:

RULE  OUT CONCLUSIVELY that a fortuitous (need-appropriate) heritable change in offspring is not merely a selection of epigenetic propensities ALREADY  THERE.

Unless it can be absolutely ruled out that there is anything NEW that has occurred, then selection may only have operated upon PRE-EXISTING choices.  This would NOT be evolutionary.

MUCH confusion seems to exist between two distinct categories -- one of which is evolutionary in essence, and one which is in NO WAY evolutionary:

A.  For selection to occur between one EXISTING potential genotype and another EXISTING genotype would not be, in any sense, evolutionary; however,

B.  For the gametes to come up with a new to the species, iteratively heritable, beneficial and specific need-meeting characteristic -- following exposure to a new environmental enemy, now THAT would be evolutionary.

Can it be that the time has come for a NEW  TERM in molecular biology:  "epigenotype"?  (: > )

The current state of evolutionary theory encompasses a glossing over of what (for me, at least) amounts to a glaring need for defining specific mechanisms that would account for how species COME  UP  WITH  changes meeting the four criteria cited above, in order that selection (natural, artificial or otherwise) would have an opportunity to act upon.

Nothing said here is intended to support any hypothesis other than the hypothesis that some of the hypotheses of bio-evolutionary theory -- in its current state -- fall far short of what some individuals -- both inside and outside the sciences -- seem to realize.

Avatar of: reese66

reese66

Posts: 4

June 2, 2012

This shows biotech can be used for good not evil, even in the ag industry. I guess the idea is that we can somehow control methylation via the siRNAs?

Avatar of: Dov Henis

Dov Henis

Posts: 1457

June 2, 2012

Seeds Inherit Memories of Enemies
http://the-scientist.com/2012/...
 
Houses do not inherit. Seeds do not inherit.
RNAs,  RNA nucleotide genes, are ORGANISMS.  RNA and DNA genomes are ORGANISMS, evolved as templates by and for the RNAs natural selection
 
The evolution and development of these primal organisms are the basis of our evolution and development.
Life is just another mass format…
 
Dov Henis (comments from 22nd century)
http://universe-life.com/

Avatar of: spittlebugs

spittlebugs

Posts: 1

June 3, 2012

As an organic farmer, I am excited about the prospects of this discovery. I would like to see testing done on the next generation defense response on more plants such as corn, sunflowers, soybeans, etc.

Avatar of: dovhenis

dovhenis

Posts: 97

June 8, 2012

Seeds Inherit Memories of Enemies
http://the-scientist.com/2012/...
 
Houses do not inherit. Seeds do not inherit.
Organisms inherit.
RNAs,  RNA nucleotide genes, are ORGANISMS.  RNA and DNA genomes are ORGANISMS, evolved as templates by and for the RNAs natural selection
 
The evolution and development of these primal organisms are the basis of our evolution and development.
Life is just another mass format…
 
Dov Henis (comments from 22nd century)
http://universe-life.com/

Avatar of: Edward R. Mikol

Edward R. Mikol

Posts: 1457

June 9, 2012

Lamarck laughs with a siRNA smile.

Avatar of: RichardPatrock

RichardPatrock

Posts: 52

June 14, 2012

 But haven't you heard about giraffes?

Avatar of: RichardPatrock

RichardPatrock

Posts: 52

June 14, 2012

This factor may be an influence on population cycles of insects on trees.

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