F Rosa Rubicondior: Malevolent Designer News - How Creationism's Favourite Sadist is Making a Fungus Better at Harming Us.

Thursday 4 August 2022

Malevolent Designer News - How Creationism's Favourite Sadist is Making a Fungus Better at Harming Us.

Scanning electron micrograph of infectious yeast spores (purple) on the surface of the structure where they are produced following sexual reproduction (in blue, the basidium)

© Chaoyang Xue, Kasey Carroll, and Joseph Heitman (Duke University Department of Molecular Genetics and Microbiology); and Valerie Knowlton (North Carolina State University, Center for Electron Microscopy)
This is how highly resistant strains of fungi emerge - Newsportal - Ruhr-Universität Bochum

Creationist mode:


Something you can almost bet your house on is that, if there is a way to make sick people sicker or suffer more, Creationism's intelligent [sic] designer will find a way to do it. It will then take on the challenge of making sure it's design can continue to do its work despite the efforts of medical science to combat it with drugs to cure us of infections or to prevent us getting them.

An obvious case in point is the way it keeps redesigning the SARS-CoV-2 virus that causes COVID-19 to make it more infectious and/or help it evade any immunity we may have got from previous infections or medical science's vaccines. Another example is the growing number of dangerous bacterial pathogens that are becoming antibiotic resistant.

Yet another example is the subject of this paper by scientists from Duke University in the USA and Ruhr-Universität Bochum (RUB), Germany who have shown how a pathogenic fungus, Cryptococcus neoformans has developed resistance to the antibiotics of choice used to treat patients infected with it.

The news release from RUB explains the problem:

The results are highly relevant for combating fungal infections in clinical practice, veterinary medicine and agriculture.

In the western hemisphere, the number of people with a lowered immune defence is increasing, because life expectancies are rising rapidly and treatment with immunosuppressants after organ transplants is becoming more common. This is associated with an increase in fungal infections.

Professor Ulrich Kück, co-author
Senior Professor in General and Molecular Botany
Ruhr-Universität Bochum, Bocum, Germany
Cryptococcus neoformans is a yeast-like fungus that can infect humans. It is one of the most significant human pathogenic fungi responsible for so-called cryptococcosis. It triggers acute infections in immunocompromised patients; and the mortality rate may be as high as 70 per cent. Specific drugs, named antifungals, are available for treatment, but they don’t always work – a phenomenon similar to antibiotic resistance. This is because fungal strains that are resistant to the drugs often evolve in hospitals, which makes treatment more difficult. So far, it was unclear which cellular and genetic mechanisms lead to this resistance.
So-called transposons, however, were known to play a role in the resistances. Transposons are jumping genes, i.e., DNA segments that can change their position in the genome and thus affect the function of genes. If a transposon jumps into a gene that’s critical for susceptibility to a drug, it’s possible for resistance to emerge. The mobility of the transposons is controlled by regulatory RNAs, so-called small interfering RNA, or siRNA for short.

RNA mechanism causes resistance.

In their current study, the researchers discovered gene mutations in resistant isolates that led to siRNA control being switched off. By introducing an intact copy of the gene, it was possible to restore siRNA control; as a result, the researchers were able to prevent the transposons from jumping and shed light on the cause of resistance. Due to their small size, the gene segments that code for siRNAs are not easy to find in the genome. Tim Dahlmann managed to locate them with special bioinformatic analyses. By identifying the resistance mechanisms, it will be possible to use them for the treatment of mycoses in humans in the future.

Creationist mode:


Sadly, the team's published paper in Nature Microbiology is behind a paywall, but the abstract can be read here. In it they say:
… Whole-genome sequencing revealed both hypermutator genomes harbour a nonsense mutation in the RNA-interference component ZNF3 and hundreds of Cnl1 elements organized into massive subtelomeric arrays on each of the fourteen chromosomes. Quantitative trait locus mapping in 28 progeny derived from a cross between a hypermutator and wild-type identified a locus associated with hypermutation that included znf3. CRISPR editing of the znf3 nonsense mutation abolished hypermutation and restored small-interfering-RNA production. We conclude that hypermutation and drug resistance in these clinical isolates result from RNA-interference loss and accumulation of Cnl1 elements.
Creationists might like to note that, what the reserchers refer to as a 'nonsense mutation', in other words, a mutation that doesn't code for anything and which simply breaks a gene, is beneficial to the fungus in that the broken gene is one that made it susceptible to the antifungal drug, so it is able to live and reproduce in the presence of the drug. This refutes any claim that a mutation is always detrimental and deleterious. Clearly, this one isn't, from the point of view of the fungus.

We know from a study of biology that DNA replication, and the mechanism for transcribing DNA into RNA to use as templates for making proteins, is a far from perfect mechanism, hence the mutations that create the variations on which natural selection can act to give rise to evolution. This illustrates the utilitarian, sub-optimal nature of what evolution has produced and is the basis for understanding how biodiversity arose and why all living things can be traced back ultimately to a common ancestor, or at least a small set of common ancestors that shared genetic information via plasmids - transposable sections of DNA or transposons - so the current situation is a legacy from the way living organisms evolved.

It makes no sense as the product of intelligent design by an omniscient designer, who would not have included imperfections and would not have ended up with something that looks just like the sub-optimal product of a mindless utilitarian process with no plan and no objectives.

But rather than understand that perfectly straightforward mechanism, Creationist frauds would rather have people believe that the designer of this problem the scientists have discovered, designed it deliberately, that is, with the intention of producing exactly this problem and making sick people even sicker and that it then designed a work-around for the 'problem' scientists created by making an antifungal drug to combat it.

Clearly, these frauds have no desire to extol the virtues of a loving god who wishes to minimise suffering and create a maximally good world since they are happy to portray it as a malevolent, sadistic monster – which calls into question whether they really do believe in it, if they aren’t worried about the consequences of this negative portrayal of it.

Their objective is to exploit people's superstitious fear of a vengeful and irascible, omnipresent, mind-reading, invisible deity in order to control them politically and ensure they continue to try to buy safety and security, by stuffing money into their bank accounts.


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