A fire salamander.
Credit: Jaime Bosch.
Creationist mode: 
Embarrassingly for Creationists, when their divine malevolence wanted to improve the ability of one of its pathogens to kill salamanders, it used a method that Creationists deny exists. It increased the amount of genetic information, not by magic like creationists believe genetic information gets created, but by using one of the methods evolutionary biologists know creates new genetic information naturally, without magic or supernatural entities - so-called 'jumping genes'.
'Jumping genes' or transposons, are pieces of DNA that have the ability to copy and paste themselves into new parts of the DNA, often carrying genes with them. In so doing they add new information into the genome and replicate any genes they carry with them. These copies of genes can them mutate without loss of function because the originals still exist, or as in the case of this fungal pathogen, they can augment the activity (and the virulence) of the original gene.
The fungal pathogen is Batrachochytrium salamandrivorans (Bsal) which infects the skin of salamanders, killing them. This is of course an example of beneficial mutations (from Bsal’s point of view), since Bsal produces more copies of itself the more salamanders it can infect.
Creationist mode: 
The discovery of these jumping genes and their role in increasing the virulence of Bsal was made by a team of scientists led by the MRC Centre for Medical Mycology at Exeter University, Devon, UK. Their findings as published, open access, in Proceeding of the National Academy of Science (PNAS).
The Exeter University news release gives the details:
A fungus that infects salamanders contains multiple copies of the same “jumping genes”, scientists have discovered.
Jumping genes, called transposons, can “copy and paste” themselves and impact the organism.
Most organisms have some repeated parts of their DNA, some of which are jumping genes, but this can be harmful – and mechanisms exist to prevent or limit this.
However, the new study – led by the MRC Centre for Medical Mycology at the University of Exeter – finds a possible evolutionary advantage of these jumping genes in a fungus called Batrachochytrium salamandrivorans (Bsal).
Not only did they find different versions of these jumping genes repeated multiple times in Bsal’s genome – but the gene in question appears to have duplicated another group of genes that play a role in how severely it affects infected fire salamanders.
Bsal and related fungal species infect amphibians worldwide, and have been responsible for more than 90 extinctions. Bsal infects the skin of salamanders and newts and causes severe wounds.
It emerged in Asia, where many newts and salamanders have some tolerance, but it has spread to Europe and is causing European salamander populations to decline.
Using new sequencing technologies, we found that Bsal has undergone a genome expansion compared to related species – that is to say, it now has a bigger genome with more genes and also more of these ‘jumping gene’ transposons.
If you think of an organism’s genome as a blueprint, transposons are like having many identical pages, and sometimes, during the process of copying and pasting, other parts of the book are also copied.
It appears that this copying and pasting caused by repetitive jumping gene transposons has also amplified some skin-destroying genes. Having more of these skin-destruction genes allow the fungus to destroy the skin of salamanders more quickly, making it more deadly.
Theresa Wacker, first author.
Medical Research Council Centre for Medical Mycology
University of Exeter, Exeter, UK.The new study found the ability of jumping gene transposons to copy and paste themselves contributed significantly to this expansion. The team are now doing further research.Most organisms have a few jumping gene transposons. In humans, they typically make up less than 1% of the genome, and we have controlling mechanisms to prevent this from rising.
In Bsal, repeated jumping genes make up about 19% of the genome. Transposon jumping genes can interfere with regular gene function and cause problems for the organism – but for Bsal this seems to be outweighed by the advantages.
This kind of gene repetition is probably more widespread in nature than we currently realise.
If, as appears to be the case, it confers an evolutionary advantage for the pathogen by making it more virulent, it’s not clear why this isn’t much more common.
Dr. Rhys A Farrer, lead author.
Medical Research Council Centre for Medical Mycology
University of Exeter, Exeter, UK
Senior author Dr Rhys Farrer said repetitive DNA, including jumping genes, is sometimes referred to as “junk” DNA.
The study’s finding shed new light on the evolution of a major amphibian disease, and Dr Farrer called it a “paradigm shift” in terms of identifying repetitive genome content as a driving force behind its pathobiology.
The team's findings can be read in the journal PNAS:
SignificanceOf special note for Creationists:
Batrachochytrium salamandrivorans (Bsal) and its closest relative B. dendrobatidis (Bd) are fungal pathogens that threaten amphibians globally. Pathogenicity in vertebrates by species of Batrachochytrium is thought to have emerged from nonpathogenic and saprobic relatives over millions of years through gene expansions of secreted proteolytic enzymes families. Using deep nanopore sequencing and comparative genomics, we discover that Batrachochytrium genomes have undergone a repeat-driven expansion characterized by flanking repetitive elements enriched around pathogenicity genes, genes with signatures of positive selection, and genes upregulated during infection. These genomic features are the hallmarks of two-speed genomes that have to date only been described in plant pathogens. These discoveries shed new light on the evolution of fungal pathogens of vertebrates driving global declines and extinctions.
Abstract
The origins and evolution of virulence in amphibian-infecting chytrids Batrachochytrium dendrobatidis (Bd) and Batrachochytrium salamandrivorans (Bsal) are largely unknown. Here, we use deep nanopore sequencing of Bsal and comparative genomics against 21 high-quality genome assemblies that span the fungal Chytridiomycota. We discover that Bsal has the most repeat-rich genome of the Chytridiomycota, comprising 40.9% repetitive elements; this genome has expanded to more than 3× the length of its conspecific Bd, with autonomous and fully functional LTR/Gypsy elements contributing significantly to the expansion. The M36 metalloprotease virulence factors are highly expanded (n = 177) in Bsal, most of which (53%) are flanked by transposable elements, suggesting they have a repeat-associated expansion. We find enrichment upstream of M36 metalloprotease genes of three novel repeat families belonging to the repeat superfamily of LINEs that are implicated with gene copy number variations. Additionally, Bsal has a highly compartmentalized genome architecture, with virulence factors enriched in gene-sparse/repeat-rich compartments, while core conserved genes are enriched in gene-rich/repeat-poor compartments. Genes upregulated during infection are primarily found in the gene-sparse/repeat-rich compartment in both Bd and Bsal. Furthermore, genes with signatures of positive selection in Bd are enriched in repeat-rich regions, suggesting these regions are a cradle for the evolution of chytrid pathogenicity. These are the hallmarks of two-speed genome evolution, and this study provides evidence of two-speed genomes in an animal pathogen, shedding light on the evolution of fungal pathogens of vertebrates driving global declines and extinctions.
Wacker, Theresa; Helmstetter, Nicolas; Wilson, Duncan; Fisher, Matthew C.; Studholme, David J.; Farrer, Rhys A. Two-speed genome evolution drives pathogenicity in fungal pathogens of animals
Proceedings of the National Academy of Sciences (PNAS) (2023); 120(2), e2212633120. DOI: 10.1073/pnas.2212633120
Copyright: © 2023 The authors.
Published by PNAS. Open access
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
- If this is intelligent design, the designer can't be regarded as benevolent, since the purpose of the fungus, and then of the modifications the team found, appears to be to make salamanders suffer and die.
- The mechanism of the mutations is one which biologists already recognise as one of the methods by which information can increase in a genome.
- This is an example of a beneficial (to the fungus) mutation since, by increasing its virulence, it is increasing the number of copies of the duplicated genes in the genome of the next generation compared to the normal compliment of genes.
- The scientists are entirely dependent on the Theory of Evolution to explain why this mutation has increased and spread in the species genome. There is no suggestion in their findings that magic creation is a better explanation.
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