Bacteria 'hotwire their genes' to fix a faulty motor

Bacteria ‘hotwire their genes’ to fix a faulty motor
Molecule NtrC - the protein used to ‘hotwire’ the bacteria

Researchers at the University of York are part of a team of scientist that has discovered how bacteria can restart their 'outboard motor' by hotwiring their own genes.

Unable to move and facing starvation, the evolved a new way to activate their flagellum – a rotating tail-like structure which acts like an outboard motor – by patching together a new genetic switch with borrowed parts.

The findings, published tomorrow (Friday 27 February 2015) in the journal Science, show that when an organism suffers a catastrophic mutation, it can rapidly rewire its . The remarkable speed with which old genes take on new tasks suggests that life has evolved unexpected levels of genetic flexibility and resilience.

The discovery was made by a team including Professor Michael Brockhurst, of the Department of Biology at York and scientists at the universities of Reading, Exeter and Massachusetts.

A chance observation by a researcher in Dr Rob Jackson's laboratory at Reading sparked the research project. The soil bacterium Pseudomonas fluorescens was engineered so that it could not make its 'propeller-like' flagellum rendering it unable to move. However, when a student accidentally left an agar plate with the immotile strain out on a bench over the weekend, the team discovered the bacteria evolved the ability to move again in just a few days. The bacteria had resurrected their flagella in the process.

Remarkably, this happened because the mutants had rewired a , which normally controls nitrogen levels in the cell, to activate the flagellum. This allowed the bacteria to move to new food sources and avoid starvation.

To understand how this had happened biologists at the University of York, compared which genes were being activated in bacteria before and after evolution. Professor Brockhurst said: "Bacteria use lots of genetic switches to turn their genes on and off. Each genetic switch controls a different set of genes.

"Amazingly, we found that just a single tiny change to one of these was enough to convert it from being a switch that would normally turn on the genes for using nitrogen into a switch that now turns on the genes to build the flagella. The result is that the bacterium had, in effect, evolved a way to hotwire its motor practically overnight."

Dr Tiffany Taylor, of the University of Reading and lead author of the study, added: "But the hotwiring comes at a cost. The replacement key is a molecule borrowed from a system which regulates nitrogen levels. The can now move, but it can't regulate nitrogen properly, which can build up and become toxic. Of course, it's an evolutionary price worth paying when the alternative is certain death."

These results suggest that new functions can evolve far quicker and much more easily than anyone previously expected. Dr Louise Johnson, an evolutionary biologist at the University of Reading, said: "Evolution has been described as a process of 'tinkering', but this work shows that evolution can be remarkably repeatable. When the situation is desperate, life finds a way."

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More information: Taylor T. B., Mulley, G., Dills A. H., Alsohim A. S., McGuffinL. J., StudholmeD. J., Silby  M. W., Brockhurst M. A., Johnson L. J., Jackson R. W. 2015. 'Evolutionary resurrection of flagellar motility via rewiring of the nitrogen regulation system' is published in Science. DOI: 10.1126/science.1259145
Journal information: Science

Provided by University of York
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Feb 27, 2015
The de novo creation of new structures and functions via nutrient-dependent RNA-directed DNA methylation and fixation of RNA-mediated amino acid substitutions via the physiology of reproduction, which is controlled by the metabolism of nutrients to species-specific pheromones, is reported in the context of mutations and rapid evolution (i.e., 4-days) and...

...two point mutations often recurring in independent lineages.

What this enables us to understand is how ecological variation leads to ecological adaptations manifested in nutrient-dependent metabolic networks linked to genetic networks and to morphological and to behavioral phenotypes.

It is tractable model of ecological adaptation that integrates everything currently known to serious scientists about physics, chemistry, and the conserved molecular mechanisms of cell type differentiation in all cells of all individuals of all species.

Feb 27, 2015
For extension of this tractable model across species via their life history transitions see: Nutrient-dependent/pheromone-controlled adaptive evolution: a model. http://www.ncbi.n...24693353

For comparison to the ridiculous claims made by evolutionary theorists in "Evolutionary Rewiring" http://www.the-sc...ewiring/ see the equally ridiculous textbook claim that "...genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world." (p. 199) Mutation-Driven Evolution

For an example of nutrient-dependent pheromone-controlled ecological adaptation in nematodes, see System-wide Rewiring Underlies Behavioral Differences in Predatory and Bacterial-Feeding Nematodes. http://linkinghub...12015000

Feb 28, 2015
This is a great summary of what is currently known about nutrient-dependent RNA-mediated pheromone-controlled cell type differentiation.


Excerpt: "During RNA editing, specific enzymes alter nucleotides in mRNA transcripts so that the resulting protein differs in amino acid sequence from what was encoded by the original DNA. Such RNA editing is a means to generate greater protein diversity..."

Mar 01, 2015
Nutrient-dependent/pheromone-controlled adaptive evolution: a model.
Funny... you seem to think that because a study says something was nutrient dependent, that it is also immediately pheromone controlled... where, EXACTLY in the study does it show support for your pheromone controlled or as causation for the MUTATIONS?
also note, they say
After 96 hours of incubation of AR2 and Pf0-2x at room temperature on SMM, two breakout mutations were visible, conferring first slow (AR2S and Pf0-2xS) and then fast (AR2F and Pf0-2xF) spreading over the agar surface
BUT thats not all, it also states
Our results demonstrate that natural selection can rapidly rewire regulatory networks in very few, repeatable mutational steps
Not the kohlslaw word salad BS crap you continually regurgitate here

Thus, the STUDY also supports Lenski, Extavour and ANON in their DEBUNKING of you and ME in my assertions that you can't comprehend SCIENCE/BIOLOGY

Mar 01, 2015
MORE support for my claims against you, as well as ANON, Real and more...
Genome resequencing revealed a single-nucleotide point mutation in ntrB in strain AR2S, causing an amino acid substitution within the PAS domain of the histidine kinase sensor NtrB [Thr97→Pro97 (T97P)]
that not enough?
The fast-spreading strain AR2F had acquired an additional point mutation in the σ54-dependent EBP gene ntrC, which alters an amino acid (R442C) within the DNA binding domain
how about this?
Mutations confirmed in slow-spreading motility variants are predicted to result in hyperphosphorylation of NtrC; mutations in fast-spreading variants lead to predicted switched specificity of NtrC-P toward FleQ targets. Slow- and fast-spreading variants share the same ancestry.
You mean... Lenski and Extavour are RIGHT?

the only person here talking out of their buttocks with their head stuffed in it is jk!

Mar 01, 2015
you like to make a claim that the studies support your stupidity and creationist/7th day adventist diatribe... it does NOT
it supports Evolution theory as well as supports former comments by ANON, Lenski and Dr. Extavour!
what that study you linked says
The ability to adapt to changes in the function of gene regulators, as opposed to structural genes, is a crucial aspect of evolutionary change. Taylor et al. mutated a central regulator for the formation of flagella in the bacterium Pseudomonas fluorescens. They then put the mutated flagella-free bacteria under strong selection pressure to regain mobility. The mutated bacteria regained the lost flagella, and motility, within 4 days. Two stereotypical mutations diverted an evolutionarily related regulator that normally controls nitrogen uptake to control flagella biosynthesis. The mutations increased the levels of the co-opted regulator, then altered its specificity for the flagella pathway.
[sic] ScienceMag

Mar 01, 2015
This is a great summary of what is currently known about nutrient-dependent RNA-mediated pheromone-controlled cell type differentiation.
i didn't see pheromones mentioned in that little article anywhere... but even that doesn't stop you from spreading your stupidity

tell you what... considering the science actually says something OTHER than what you tend to promote... why not go straight to the source? WHy can't you find out what it is really saying and why do you continually try to interpret it with your creationist stupidity?
perhaps because you are afraid of what it will tell you?

thank you for continuing to validate the linked study i just posted with every post you make
MORE support for my claims against you, as well as ANON, Real and more.
that means... ANON and all of OUR CLAIMS against you
not me against them

just you, jk

Mar 01, 2015
Quantum Criticality at the Origin of Life
Abstract excerpt: "Here we show that molecules taking part in biochemical processes from small molecules to proteins are critical quantum mechanically. ...biomolecules are tuned exactly to the critical point. ...we confirm that the energy level statistics of these biomolecules show the universal transitional distribution of the metal-insulator critical point and the wave functions are multifractals.... The findings point to the existence of a universal mechanism of charge transport in living matter. The revealed bio-conductor material is ... a new quantum critical material which can exist only in highly evolved systems and has unique material properties."

My comment: The findings appear to attest to the fact that amino acid substitutions link the communication required for life because the number of proteins grows exponentially with the number of amino acids. There's a model for that.

Mar 01, 2015
My comment: The findings appear to attest to
well, since you are SPAMMING with copy/paste cross posts, then:
i didn't even bother to read any further... mostly because your track record for interpreting results of scientific studies is not only POOR, it is completely WRONG

you have YET to produce legitimate interpretations of ANY study, to date
case in point, your attempts to use Dr. Extavour to support your own fallacious model, until she completely debunked you and said you were WRONG
in that very same paper, we provide evidence that heritable differences in the genome sequences between Drosophila species, in other words, mutations, ALSO play a role in the evolution of the trait we are studying.

So Kohl is mistaken if he is claiming that my study (or Rich Lenski's work) provide evidence AGAINST the role of mutations in evolution

lets just see what the AUTHORS have to say about supporting your creationist views!

Mar 01, 2015
Epigenetic Landscape Models: The Post-Genomic Era

Abstract excerpt: "... a wealth of experimental data has accumulated, the general mechanisms of gene regulation have been uncovered, and the placement of specific molecular components within modular gene regulatory networks (GRN) has become a common practice."

Article excerpt: "Tissue-level patterning mechanisms such as cell-cell interactions; chemical signaling; cellular growth, proliferation, and senescence; inevitably impose physical limitations in terms of mechanical forces which in turn aect cellular behavior. This would thus imply non-homogenous GRNs with contrasting additional chemical and physical constraints."

Comparison to theory: "...genomic conservation and constraint-breaking mutation is the ultimate source of all biological innovations and the enormous amount of biodiversity in this world."

Mar 01, 2015

"In the 1980s, geneticists and molecular biologists such as Francis Crick, Leslie Orgel and Ford Doolittle used "selfish DNA" in a strict sense, to refer to DNA sequences that just accumulated in genomes by making copies – and which did not itself affect the phenotype (W. F. Doolittle & C. Sapienza, Nature 284, p601, and L. E. Orgel & F. H. C. Crick, p604, 1980). This stuff not only had no function, it messed things up if it got too rife: it could eventually be deleterious to the genome that it infected. Now that's what I call selfish! – something that acts in a way that is to its own benefit in the short term while benefitting nothing else, and which ultimately harms everything."

I look forward to hearing from either Extavour or Lenski without Captain Stumpy's involvement. However, I understand why they might want to let a science idiot speak for them.

Mar 01, 2015
Epigenetic Landscape Models: The Post-Genomic Era

This is not at odds with mutation and selection. Those same authors wrote this:


Mar 02, 2015
The merging of conceptually clear theories, computational/mathematical tools, and molecular/genomic data into coherent frameworks could be the basis for a much needed transformation of biological research from mainly a descriptive exercise into a truly mechanistic, explanatory and predictive endeavor - EL models associated with GRNs being a salient example.

What does "...not at odds with mutation and selection" mean without a salient example?

In my model the epigenetic landscape (EL) is linked to the physical landscape of DNA in the organized genomes of species from microbes to man via the conserved molecular mechanisms of biophysically constrained RNA-mediated amino acid substitutions and the chemistry of protein folding. Mutations perturb protein folding, which is why they can't be linked via natural selection to increasing organismal complexity.

What model of biologically-based cause and effect do you claim links mutation and selection to evolution?

Mar 02, 2015
This is not at odds with mutation and selection.

What kind of science idiot places mutations and selection into the context of a re-evolved flagellum?

Is this science idiot (aka Andrew Jones) claiming that mutations and selection to cause evolution of a new functional structure to occur in only 4 days? If not, what is he trying to tell us about mutations and selection?

Excerpted from above: "The remarkable speed with which old genes take on new tasks suggests that life has evolved unexpected levels of genetic flexibility and resilience."

That seems much more like Dobzhansky's "creationist" belief than his "evolutionist" belief since he reported that difference between primates as: "...the so-called alpha chains of hemoglobin have identical sequences of amino acids in man and the chimpanzee, but they differ in a single amino acid (out of 141) in the gorilla." http://www.jstor..../4444260

Mar 02, 2015
As you did with Lenski's example, you're misinterpreting this flagella example. There were no new genes created. If you read even just the abstract, which you linked to in your first post, you'd know what actually happened-


There was no new functional structure or gene created. There were merely two mutations altering existing regulatory elements:

We engineered immotile strains of the bacterium Pseudomonas fluorescens that lack flagella due to deletion of the regulatory gene fleQ. Under strong selection for motility, these bacteria consistently regained flagella within 96 hours via a two-step evolutionary pathway. Step 1 mutations increase intracellular levels of phosphorylated NtrC, a distant homolog of FleQ, which begins to commandeer control of the fleQ regulon at the cost of disrupting nitrogen uptake and assimilation. Step 2 is a switch-of-function mutation...

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