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| TB researcher Faramarz Valafar and his team have discovered what causes the TB bacterium to become resistant to antibiotics, which will help advance therapeutics and vaccine targets. |
The TB bacterium, Mycobacterium tuberculosis, is one of the malevolent designer's little triumphs (if you've been taken in by the intelligent [sic] design hoax).
Once a major killer in cities where crowded conditions made transmission easy for it, medical science had seemed on the point of eliminating it with antibiotics and vaccinations. However, it has now made a strong come-back due to developing antibiotic resistance and is now endemic in many third world and developing countries with some 10 million new cases and 1.8 million deaths a year in 2018.
Exactly how it did this so quickly for an organism that is slow-growing and which reproduces relatively slowly was something of a mystery to medical science because a slow generation time is not conducive to rapid evolution and yet antibiotic resistance can arise within weeks or months in an individual patient undergoing treatment.
Intelligent [sic] design advocates, of course, have what they think is a better explanation - it was redesigned by their putative designer as another escalation in its arms race against human medical science in its determination to make us sick and die in an especially nasty way.
However, scientists at San Diego State University think they have discovered that this was due to evolution after all, not to the intervention of a magician, malevolent or otherwise.
These discoveries always present a headache for intelligent [sic] design creationists because it makes them face a choice of either the malevolent intent of their favourite god whom they like to think of as kindly and loving, or accepting evolution as the only explanation that doesn't leave their god looking for all the world like a misanthropic, sadistic monster, which would violate their central dogma - that nothing in nature happens unless intentionally designed by their omniscient god in full knowledge of the consequences of its designs.
What the researchers at San Diego State University found is explained by Padma Nagappan in the university's News Center press release published today:
For a slow-growing microbe that multiplies infrequently, Mycobacterium tuberculosis, the pathogen that causes tuberculosis (TB) has long puzzled researchers as to how it develops resistance to antibiotics so quickly, in a matter of weeks to months.I explained in my popular book, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", how epigenetics is a strong argument against intelligent design:
Now, TB researchers at San Diego State University have uncovered a crucial clue to the mystery: the answer may lie in the epigenetic domain rather than the genetic domain where most scientists have concentrated their efforts.
Their discovery could help advance new diagnostics, therapeutics and vaccine targets.
Epigenetics is the study of inheritable changes in gene expression that do not involve a corresponding change to the underlying DNA sequence — meaning changes to the phenotype but no change in the genotype. This affects only the physical structure of the DNA, through a process called DNA methylation where a chemical ‘cap’ is added to the DNA molecule, preventing or facilitating the expression of certain genes.
The SDSU researchers describe the rapid response phenomenon they discovered as ‘intercellular mosaic methylation,’ a process by which Mycobacterium tuberculosis diversifies, creating multiple subpopulations each with its own phenotype. While antibiotics could kill many of these mutant subpopulations, at least a few do survive and develop drug resistance.
“We believe this also explains why diagnostic testing in some patients does not predict treatment failure, and why some patients come back months later with the disease reemerging in a far more resistant state,” said Faramarz Valafar, a TB expert with SDSU’s School of Public Health who studies the genetics and epigenetics of pulmonary diseases. “This is also why CT scans of the lungs of many “cured” patients show lesions with possible bacterial activity.”
But there is something else that the ID movement needs to explain and this brings me back to the point of this book in general and to this chapter in particular. Why is the whole complex process of epigenetics necessary in the first place?Now, it seems, if you accept the malevolent designer notion, that this incompetent designer has used this epigenetic work-around for its incompetence so solve the 'problem' of human medical science being on the verge of exterminating its special creation, the single-celled Mycobacterium tuberculosis.
Epigenetics is necessary because in multicellular organisms, any advantage of multicellularity is only realised by specialisation of cells and their arrangement into organs carrying out specialist functions. Many of these functions are only necessary in the first place because of multicellularity, of course. Mammals need digestive, respiratory and circulatory systems to get oxygen and nutrients and remove waste to the cells too far removed from the surface to do it the way single–celled organisms do it – by direct exchange with their environment.
Evolutionarily speaking, multicellularity gave some organisms an advantage over others, but it comes at a price. One of the prices is the complex system of epigenetics and the need to reset and start again with each new individual.
But why is this needed anyway? It is needed because, just like single–celled organisms, the cells of multicellular organisms inherit all the DNA of their parent cells regardless of their eventual function as specialised cells in specialised organs. Unless the unnecessary and unwanted genes are turned off there would be no specialisation and so no benefit from multicellularity. The last thing you want is your brain cells producing the digestive enzymes your pancreas secretes or your kidney cells producing the contractile proteins in your muscles. You want your cells to be specialised and be good at doing what they are specialised to do – and nothing else. When cells start becoming generalised and doing other things they are called cancer.
So what any ID model needs to explain is why any intelligent designer would arrange it so that all cells (with one or two limited exceptions) contain all the DNA of the entire organism when they only need a few special genes to function? Why is this complex system of epigenetics necessary in the first place? Why would an intelligent designer not design things so that as cells become specialised, they only get the DNA they need?
Instead, we have the ludicrous situation of prolific waste of resource in replicating all the DNA – with its attendant risk of going wrong – to have most of it permanently switched off in almost every one of our 70 trillion cells. Then we need a mechanism for resetting it and starting again in the newly–fertilised zygote.
Rubicondior, R. The Intelligent Design Hoax, pp. 133-134.
It treats a population of them more like a single, multicellular organism and produces clusters of 'specialised' cells using variations in epigenetic settings to evolve different sub-populations.
The research team's findings were published, open access, in eLife recently:
Abstract
This study assembles DNA adenine methylomes for 93 Mycobacterium tuberculosis complex (MTBC) isolates from seven lineages paired with fully-annotated, finished, de novo assembled genomes. Integrative analysis yielded four key results. First, methyltransferase allele-methylome mapping corrected methyltransferase variant effects previously obscured by reference-based variant calling. Second, heterogeneity analysis of partially active methyltransferase alleles revealed that intracellular stochastic methylation generates a mosaic of methylomes within isogenic cultures, which we formalize as ‘intercellular mosaic methylation’ (IMM). Mutation-driven IMM was nearly ubiquitous in the globally prominent Beijing sublineage. Third, promoter methylation is widespread and associated with differential expression in the ΔhsdM transcriptome, suggesting promoter HsdM-methylation directly influences transcription. Finally, comparative and functional analyses identified 351 sites hypervariable across isolates and numerous putative regulatory interactions. This multi-omic integration revealed features of methylomic variability in clinical isolates and provides a rational basis for hypothesizing the functions of DNA adenine methylation in MTBC physiology and adaptive evolution.
Samuel J Modlin, Derek Conkle-Gutierrez, Calvin Kim, Scott N Mitchell, Christopher Morrissey, Brian C Weinrick, William R Jacobs, Sarah M Ramirez-Busby, Sven E Hoffner, Faramarz Valafar
Drivers and sites of diversity in the DNA adenine methylomes of 93 Mycobacterium tuberculosis complex clinical isolates
eLife 2020;9:e58542 DOI: 10.7554/eLife.58542
Copyright: © The authors. Published byeLife Sciences Publications Ltd.
Reprinted under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
Curiously, I never seem to see a creationist say whether they prefer an explanation for these phenomenon that involves an unintelligent, amoral, undirected natural process like evolution by natural selection, or one that makes their favourite deity look like a loathsome monster, keen to spread pain and suffering throughout the world.
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