A newly discovered protein helps the fungus that causes white mould stem rot in sunflowers and more than 600 other plant species bypass the plants' defences.
Scientists working for the Agricultural Research Service (ARS) of the US Department of Agriculture (USDA) have discovered how a fungus can invading and kill plants, despite the fact that plants have defences in place supposedly for preventing exactly that sort of attack by parasitic fungi.
And, of course, being an observation of reality, their finding utterly refutes the childish notion of intelligent design creationism.
First consider this:
If you were intelligent and tasked to design living organisms, would you design an organism (say Organism B) that lived parasitically on other organisms that you had designed earlier (say, Organism A)? If you did, would you then treat Organism B as a problem and give Organism A a system for resisting Organism B, making it harder for Organism B to live?
And, if you did something that idiotic, would you then treat your protection for Organism A as another problem and modify Organism B so it could still parasitise Organism A by evading the defences you gave it?
Well, if you are Creationism's supposedly intelligent [sic] designer, that it exactly what you would do.
If you've fallen for the creationist notion that there is just a single intelligent [sic] designer of all living things, that is exactly what you think an intelligent designer would do. If you're also a fundamentalist Christian or Moslem (which almost all creationists are) you also think this putative intelligent designer is one and the same as the god you worship and think of as omni-benevolent in addition to being omnipotent and omniscient.
This, of course, tells us more about the gullibility and ignorance of fundamentalist creationists than it does about any putative designer, and what they regard as intelligence, especially since there is a perfectly good scientific explanation, backed up by over a century and a half of research and meticulous observation, that explains how the situation described above came about, and even predicts that it will develop as a mindless, unplanned but inevitable evolutionary arms race.
The fungus in question is the fungus, Sclerotinia sclerotiorum which causes white mould stem rot in a number of plants, many of which are important food crops, such as potatoes, soybeans, sunflowers, peas, lentils, canola, and many other broad leaf crops. It can cause loses of billions of dollars in a bad year.
From the ARS news release accompanying the open access paper in Nature Communications:
This is explained more technically in the abstract to the team's paper:A protein that allows the fungus that causes white mold stem rot in more than 600 plant species to overcome plant defenses has been identified by a team of U.S. Department of Agriculture Agricultural Research Service and Washington State University scientists.What you have is essentially a continuous arms race between fungal pathogens and their plant hosts, an intense battle of attack, counterattack and counter-counterattack in which each is constantly developing and shifting its chemical tactics in order to bypass or overcome the other's defenses.
We found it by looking at the materials excreted by the fungus, and there it was. When we found this protein, SsPINE1, which interacted with PGIP, it made sense.
Weidong Chen, study leader
USDA Agricultural Research Service
Grain Legume Genetics and Physiology Research Unit
Pullman, WA, USA
Knowledge of this protein, called SsPINE1, could help researchers develop new, more precise system of control measures for the Sclerotinia sclerotiorum fungus, which attacks potatoes, soybeans, sunflowers, peas, lentils, canola, and many other broad leaf crops. The damage can add up to billions of dollars in a year of bad outbreaks.
S. sclerotiorum fungi cause plants to rot and die by secreting chemicals called polygalacturonases (PG), which break down the plant's cell walls. Plants evolved a way to protect themselves by producing a protein that stops or inhibits the fungus' PG, labeled PGIP, which was discovered in 1971. Since then, scientists have known that some fungal pathogens have a way to overcome plant's PGIP. But they had not been able to identify it.
The key to identifying SsPINE1 was looking outside the fungi cells, according to Chen.I got goosebumps when we found this protein. It answered all these questions scientists have had for the last 50 years: Why these fungi always overcome plant defenses? Why do they have such a broad host range, and why are they so successful?
Associate professor Kiwamu Tanaka, co-author
Department of Plant Pathology
Washington State University, Pullman, WA, USA
Then to prove that the protein SsPINE1 was what allowed Sclerotinia to bypass plants' PGIP, Chen and his colleagues deleted the protein in the fungus in the lab, which dramatically reduced its impact.
AbstractAs I point out in my book, The Malevolent Designer: Why Nature's God is not Good, parasites and the inevitable arms races between parasite and host, are entirely inconsistent with the notion of a single, benevolent intelligent designer, since parasites cannot be regarded as the creation of a benevolent being and having what amounts to an arms race with itself, cannot be regarded as the act of an intelligent entity of any sort, benevolent, malevolent or indifferent.
Plant pathogens degrade cell wall through secreted polygalacturonases (PGs) during infection. Plants counteract the PGs by producing PG-inhibiting proteins (PGIPs) for protection, reversibly binding fungal PGs, and mitigating their hydrolytic activities. To date, how fungal pathogens specifically overcome PGIP inhibition is unknown. Here, we report an effector, Sclerotinia sclerotiorum PGIP-INactivating Effector 1 (SsPINE1), which directly interacts with and functionally inactivates PGIP. S. sclerotiorum is a necrotrophic fungus that causes stem rot diseases on more than 600 plant species with tissue maceration being the most prominent symptom. SsPINE1 enhances S. sclerotiorum necrotrophic virulence by specifically interacting with host PGIPs to negate their polygalacturonase-inhibiting function via enhanced dissociation of PGIPs from PGs. Targeted deletion of SsPINE1 reduces the fungal virulence. Ectopic expression of SsPINE1 in plant reduces its resistance against S. sclerotiorum. Functional and genomic analyses reveal a conserved virulence mechanism of cognate PINE1 proteins in broad host range necrotrophic fungal pathogens.
Wei, Wei; Xu, Liangsheng; Peng, Hao; Zhu, Wenjun; Tanaka, Kiwamu; Cheng, Jiasen; Sanguinet, Karen A.; Vandemark, George; Chen, Weidong
A fungal extracellular effector inactivates plant polygalacturonase-inhibiting protein
Nature Communications 13, 2213 (2022). DOI: 10.1038/s41467-022-29788-2
Copyright: © 2022 The authors. Published by Springer Nature Ltd.
Open access
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
The inescapable conclusion from findings such as these about the natural world is that there is no intelligence involved; that whatever process produces these host-parasite relationships is mindless, amoral, unintelligent, utilitarian and lacking any discernible plan - exactly like the process that biologists call "evolution by natural selection".
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