F Rosa Rubicondior: Unintelligent Design - Another Ludicrously Complex Arms Race, This Time Between Plants And A Predatory Fungus

Monday 1 January 2024

Unintelligent Design - Another Ludicrously Complex Arms Race, This Time Between Plants And A Predatory Fungus


Discovery: plants use “trojan horse” to fight mold invasions | News Running epigenetics a close second for the most obvious evidence on unintelligent design in nature is the ubiquitous arms race; Arms races are a major component of evolutionary biology, easily understandable in terms of evolution by natural selection. One organism (call it Organism A) predates on, or parasitises another (call it Organism B); this creates an advantage for Organism B in avoiding being eaten of serving as the host of Organism A, so any functional defense mechanism is selected for by natural selection. This in turn creates an advantage for Organism A to evolve a mechanism for overcoming Organism B's defences, and so on until a state of equilibrium is achieved in which either one or the other organism is no longer able to evolve further.

This can lead to some extreme adaptations such as the stupidly long neck and legs of the giraffe which is a response to acacia trees evolving longer trunks to place their leaves, flowers and seeds beyond the reach of giraffes. In the process, acacia trees need to produce masses of cellulose to build the trunk and pump water much higher against gravity than if they were low-growing bushes, and giraffes have to maintain a very high blood pressure to keep their brain supplied with oxygen while drinking water places them at risk of predation by lions because they can't stand up and raise their heads quickly or they will lose consciousness. And they need the additional complexity of special valves in their neck veins to maintain a high blood pressure to their brain.

Now, take away acacia trees (imagine a sudden virus that wipes them out) and the giraffe is no longer superbly adapted for its environment; instead, it is severely handicapped, and might even find feeding from an alternative source difficult.

Another arms race can be seen at the moment is where the SARS-CoV-2 virus is evolving new variants every few months in response to growing herd immunity in its hosts, the human population, due to vaccinations and sub-lethal infections. The virus is getting better at evading our antibodies for long enough for us to pass on the infection to someone else and is tending to be less lethal, so we survive to infect others, even being asymptomatic. Gradually the virus will evolve to become a relatively mild infection that most of us will catch as often as we catch the common cold, and only especially vulnerable people will be made seriously ill by it.

These are just two examples of hundreds of similar arms races in nature; there are even arms races between sexes of the same species as females evolve strategies to retain the ability to only mate with a male of her choice, while males evolve strategies to deprive her of that ability.

But how on Earth can this be explained in terms of design by a single designer, or, including the creationists fallback excuse for parasites, two designers - their supposedly omnipotent, omniscient god and 'Sin'? Would not an omnipotent, omniscient god know in advance what Sin's next response would be and create a design that it couldn't overcome, so an arms race never started in the first place? Or are we to believe that creationism’s god and this 'Sin' thing are equal in all things yet able to conceal their next move from something all-knowing, but powerless to stop its rival? In other words, neither omniscient nor omnipotent.

The notion of intelligent design is quite simply incompatible with the evidence of arms races, for which evolution provides a ready answer.

I have devoted the whole of chapter 3 to arms races in nature in my popular, illustrated book, The Unintelligent Designer: Refuting The Intelligent Design Hoax, but what it doesn't include is this recently discovered arms race between plants and a parasitic fungus, Botrytis cinerea, or gray mold.

It was discovered by a research team led by Professor Hailing Jin, professor of Microbiology & Plant Pathology at the University of California Riverside (UCR). The team have published their findings, open access, in the journal Cell Host & Microbe.

The team found that plants hit back at Botrytis cinerea by sending 'bubbles' of lipid containing mRNA to the fungal cells, which treat them as nutrients and ingest them. Once inside, these 'Trojan horse' packages unpack a whole lot of mRNA that suppresses the fungus. This arms race is not all one-sided either because the fungus uses the same method to send its mRNA into the plant tissues where they suppress the plant's immune responses.
How this was discovered, and its significance is explained in a UCR press release:
If you’ve ever seen a fuzzy piece of fruit in your fridge, you’ve seen gray mold. It is an aggressive fungus that infects more than 1,400 different plant species: almost all fruits, vegetables, and many flowers. It is the second most damaging fungus for food crops in the world, causing billions in annual crop losses.

A new paper in the journal Cell Host & Microbe describes how plants send tiny, innocuous-seeming lipid “bubbles” filled with RNA across enemy lines, into the cells of the aggressive mold. Once inside, different types of RNA come out to suppress the infectious cells that sucked them in.

“Plants are not just sitting there doing nothing. They are trying to protect themselves from the mold, and now we have a better idea how they’re doing that,” said Hailing Jin, Microbiology & Plant Pathology Department professor at UCR and lead author of the new paper.

Previously, Jin’s team discovered that plants are using the bubbles, technically called extracellular vesicles, to send small RNA molecules able to silence genes that make the mold virulent. Now, the team has learned these bubbles can also contain messenger RNA, or mRNA, molecules that attack important cellular processes, including the functions of organelles in mold cells.

“These mRNAs can encode some proteins that end up in the mitochondria of the mold cells. Those are the powerhouses of any cells because they generate energy,” Jin explained. “Once inside, they mess up the structure and function of the fungal mitochondria, which inhibits the growth and virulence of the fungus.”

It isn’t entirely clear why the fungus accepts the lipid bubbles. Jin theorizes they might just be hungry. “The fungus likely takes up the vesicles because they just want nutrients. They don’t know those RNAs are hidden in the vesicles,” she said.

The strategy is an efficient one for the plants, because one mRNA molecule can have an outsized effect on the fungus. “The beauty of delivering mRNA, instead of other forms of molecular weapons, is that one RNA can be translated into many copies of proteins. This amplifies the effect of the mRNA weapon,” Jin said.

Mold also uses these same lipid bubbles to deliver small, damaging RNAs into the plants they are infecting to suppress host immunity, an ability developed as part of a co-evolutionary arms race. Because RNAs are easily degraded, the bubbles provide excellent protection for transporting vulnerable cargo, for both plants and fungi.

“During infections, there are always a lot of communications and molecule exchanges where plants and fungi try to fight against each other,” Jin said. “Previously people looked at proteins being exchanged. Now, modern technology has enabled us to discover another important group of players in this battle.”

Going forward, the scientists are hoping to use this discovery to create innovative, eco-friendly fungicides. “RNA-based fungicides would not leave toxic residue in the environment and would not affect humans or animals. RNA is present in most food, and it is easily digested,” Jin said.

“There is a never-ending battle to control pests and pathogens. If we can deliver mRNA that interferes with mold cellular functions, we may be able to help plants more effectively fight in this battle.”
Technical detail appears in the team's published paper in Cell Host & Microbe:
Graphical abstract
Highlights
  • Arabidopsis delivers mRNAs via extracellular vesicles into fungal pathogen cells
  • Delivered host mRNAs are translated within fungal cells
  • Proteins translated from delivered host mRNAs reduce fungal infection
  • Knockouts in host genes corresponding to delivered mRNAs are more susceptible
Summary

Cross-kingdom small RNA trafficking between hosts and microbes modulates gene expression in the interacting partners during infection. However, whether other RNAs are also transferred is unclear. Here, we discover that host plant Arabidopsis thaliana delivers mRNAs via extracellular vesicles (EVs) into the fungal pathogen Botrytis cinerea. A fluorescent RNA aptamer reporter Broccoli system reveals host mRNAs in EVs and recipient fungal cells. Using translating ribosome affinity purification profiling and polysome analysis, we observe that delivered host mRNAs are translated in fungal cells. Ectopic expression of two transferred host mRNAs in B. cinerea shows that their proteins are detrimental to infection. Arabidopsis knockout mutants of the genes corresponding to these transferred mRNAs are more susceptible. Thus, plants have a strategy to reduce infection by transporting mRNAs into fungal cells. mRNAs transferred from plants to pathogenic fungi are translated to compromise infection, providing knowledge that helps combat crop diseases.

Introduction

Host-microbe interactions represent a molecular battleground involving exchanges of diverse classes of biomolecules.1,2,3 Although toxins, metabolites, and proteins are transferred between hosts and microbes during infection,2,3 transfer of RNAs is less well understood. Small RNAs (sRNAs) are a class of short non-coding RNAs that can induce silencing of target genes with sequence complementarity.4 Recent discoveries show that some microbes deliver sRNAs into host cells and hijack host Argonaute (AGO) proteins to silence host genes for successful infection, a process named “cross-kingdom RNAi.”5,6,7,8,9 During the co-evolutionary arms race between hosts and microbes, hosts also transfer sRNAs into interacting microbes to silence virulence-related genes in pathogens.1,10,11,12 However, it is unknown whether other classes of RNA molecules, such as messenger RNAs (mRNAs), can also move from hosts to interacting microbes.

Extracellular vesicles (EVs) are a diverse group of cell-derived membranous structures that are released into the extracellular environment. EVs contain a cargo of various biomolecules, including proteins, lipids, nucleic acids (such as RNA and DNA), and metabolites.13 They serve as important mediators of intercellular communication by transferring biological molecules, thereby influencing various physiological and pathological processes in diverse organisms.14 In animals, EVs have gained significant attention in the scientific and medical communities due to their potential as diagnostic and therapeutic tools.14 In plants, EVs play an important role in protecting sRNA during trafficking from hosts to interacting microbes to the detriment of pathogen infection.10,15 Strikingly, fungal pathogen Botrytis cinerea, which causes gray mold disease on more than 1,400 plant species,16 uses a similar strategy as its plant host to also deploy EVs to protect and transport sRNA effectors into host cells for cross-kingdom RNAi.17

mRNA conveys genetic information within cells that are usually translated into proteins to fulfill its biological function. Intercellular and systemic mRNA trafficking within an organism has been reported in animals and plants.18,19,20,21 In animals, EVs are important for intercellular and systemic sRNA and mRNA trafficking within an organism.18,22,23,24 Recently, the fungal pathogen of maize, Ustilago maydis, was shown to secrete EVs containing mRNAs, which may participate in regulating plant-pathogen interactions.25 However, it is currently unclear whether plant EVs can transport mRNAs and other classes of RNA molecules aside from sRNAs. Critically, if mRNAs can move from plants to interacting microbes, are they translated in the microbes and what is the potential consequence to pathogen fitness and infectivity?

Here, our findings demonstrate that EVs transport plant mRNAs to interacting pathogenic fungal cells. Importantly, we observed that these transferred host mRNAs are associated with fungal polysomes for translation, with the potential to compromise infection. These discoveries inform potential future strategies for effectively controlling plant diseases.


The amusing thing about this daft example of 'intelligent [sic] design' is that the solution the designer came up with to the problem for plants it designed when it designed gray mold to parasitise plants, was the same solution it designed for gray mold because its solution for plants was now a problem for gray mold to be solved.

Arms races simply add to the complexity of organisms and increase waste for no ultimate long-term benefit. These are the antithesis of good, intelligent design, which is minimally complex, minimally wasteful and always designed for a specific purpose.

If anyone can produce a reasonable context in which the same designer repeatedly designing solutions to problems it creates as solutions to problems it creates, can be regarded as the act of a supreme intelligence, then I'd love to read it. About the best we ever get from creationists is the ludicrously circular reasoning which goes, "It must be intelligently designed because it was designed by an intelligent designer", which passes for logic in the creationist cult.

Similarly, I’d love to hear an explanation of why an arms race between two supposedly omniscient, omnipotent intelligent designers doesn’t leave both of them looking powerless and ignorant. It would probably as amusing as the explanation for how creationism’s god is the only entity capable of designing complex living organisms, but ‘Sin’ also designed complex living organisms.

Thank you for sharing!









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