Professor Sokurenko and Assistant Professor Houra Merrikh
Professor Evgeni Sokurenko and assistant professor Houra Merrikh examine an organizational chart showing structural hotspot mutations in a gene. A study authored by the pair explained that bacteria arrange their genetic code to produce more frequent mutations
Professor Evgeni Sokurenko and assistant professor Houra Merrikh examine an organizational chart showing structural hotspot mutations in a gene. A study authored by the pair explained that bacteria arrange their genetic code to produce more frequent mutationsPhoto by Joshua Bessex
In introductory biology classes, professors teach their students that organisms take millions of years to evolve. But findings at the UW indicate that bacteria may speed up their evolution by arranging their genetic code to produce more frequent mutations.
In bacteria, complex protein structures duplicate genes in order to create new genetic code by unzipping, copying, and re-zipping the bacterial DNA strands.
Similarly, different proteins called transcription machinery move down strands of DNA and read the genetic code, which contains the instructions for the creation of new proteins.
However, the process isn’t so neat and orderly. Bacteria replicate and transcribe their DNA simultaneously. Therefore often machinery on the same strand or different strands collide, especially when the large protein structures move down adjacent strands at the same time.
UW assitant professor Houra Merrikh, Ph.D., and professor Evgeni Sokurenko, Ph.D., authored a study positing bacteria accelerate their evolution by placing specific genes at the site of these collisions.
“This could be a universal mechanism for controlling the rate of evolution,” Sokurenko said.
Random mutation to genetic code drive the evolution of species. And their research suggests that some bacteria intentionally orient certain genes in a DNA chain so they mutate more frequently.
Merrikh explained that they had observed the destructive nature of transcription and replication before, but scientists didn’t know if it caused mutations.
The various proteins involved in these two processes — replisomes, RNA polymerase (RNAP), and various other components — collide with each other, despite attempts by the bacteria to prevent the jams.
“The idea has generally been that the bias of the orientation is so most genes are positioned to avoid the worst,” Merrikh said. “There are still a significant number of genes that are subject to head-on conflict.”
The team’s data implies these collisions accelerate evolution, since genes that are head-on to replication mutate more frequently.
Scientists are still unsure how genes mutate under those circumstances, but the team observed an increased rate of evolution in the bacterial genes. They specifically chose Bacillus subtilis for the experiment because it had a high bias to orient genes to avoid conflict.
“We started with bacillus,” Merrikh said, “but we’re also seeing this accelerated evolution. Seeing if the differential bias of these genomes has anything to do is one prediction.”
Another prediction is that if this is a universal phenomenon, multiple organisms might position genes in this way to speed up evolution.
In general, DNA contains the code which instructs cells on how to create proteins, which perform necessary cellular functions.
In fact, genes in different bacteria can mutate in response to the similar environmental changes; scientists term such similar evolution in different organisms as convergent evolution. However, organisms that underwent convergent evolution manufactured the proteins slightly differently.
Sokurenko said that the analysis of DNA from different bacteria seemed to suggest that they were convergently evolving in the same way using the same mutation mechanism.
The finding also has implications regarding disease-causing bacteria.
According to Sokurenko’s colleague Sujay Chattopadhyay, Ph.D., E. coli can migrate to a place in the human body where they are not usually found, such as the urinary tract, then evolve via this mechanism to survive in the new environment. If they return to their original environment, like the gut, they may be outcompeted, but it’s still one possible method for bacterial pathogens to evolve.
“Until recently, there simply weren’t large enough collections of genetic strains from a single species,” Chattopadhyay said. “Now with several groups sequencing hundreds and thousands of genomes … we can identify naturally occurring mutants, and help clarify evolving genes.”
The impact of this not only helps scientists understand how genetic evolution works, but also figuring out how such mutant bacteria redesign themselves illuminates how bacteria evolve into deadlier and more infectious strains.
Different pathogenic E. coli have similar genetic variances generated by mutations.
Chattopadhyay stressed that medicine shouldn’t focus just on treating personalized pathogens, but also focus on the underlying mechanisms.
His lab group is also focused on developing clonal markers that highlight the transformed pathogens, while Merrikh will examine the actual biochemical mechanism of how the collisions mutate the genes.
“We truly hope to attract attention of students and other attention to the medical and evolutionary studies and apply the evolutionary thinking to understanding the basic fundamental molecular mechanisms of life,” Sokurenko said. “There’s a quote from Theodosius Dobhzansky, ‘Nothing in biology makes sense but in the light of evolution.’”
Reach reporter Garrett Black at firstname.lastname@example.org. Twitter: @garrettjblack
Several changes were made to the original article to make it more accurate. These include: changing the name of transcription factors to transcription machinery; indicating that DNA transcription and replication occur simultaneously; and stating the genes that are subject head-on to replication mutate more frequently. Furthermore, certain statements were removed for the sake of factual consistency. These include a statement about the ability of researchers to make a determination of the number of collisions in bacterial DNA and a claim about the lagging gene strand during DNA replication.
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