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Fragile DNA key to evolutionary leaps, say Stanford scientists

Fragile DNA key to evolutionary leaps, say Stanford scientists

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It’s 2019 and time is flying by. Like many parents, for me the passage of time is marked most dramatically by watching my children as they (somehow, miraculously) morph into smart, capable teens and young adults. The inevitable, dramatic changes that occur during this transition got me thinking about a recent discussion I had with developmental and evolutionary biologist David Kingsley, PhD.

Kingsley, together with graduate student Kathleen Xie, recently cracked a longstanding evolutionary mystery to reveal how organisms play a high-stakes game of DNA chicken as they struggle to adapt to changing conditions. Regions of fragile DNA, prone to breakage, can lead to major changes in body structure or metabolism that could confer a survival advantage and big evolutionary payoffs. The researchers published their findings recently in Science.

As I described in our release:

The researchers, who studied a tiny fish called the threespine stickleback, found that such ‘fragile’ DNA regions create genetic hot spots that mutate much more rapidly, and dramatically, than neighboring sequences. The resulting changes can help an organism vault far ahead of its peers in the evolutionary arms race.

Although similar findings have been described in bacteria, this is one of the first studies to show that the same process has occurred in vertebrates to create dramatic changes in body structure. It also addresses a long-standing mystery in evolutionary biology.

The mystery is why instances of parallel evolution (a term that describes how different species often independently acquire similar advantageous traits in response to similar evolutionary pressures) often rely on changes in the same regions of DNA.

As Kingsley described:

There is a lot of evidence that the same genes across different populations or species are often responsible for similar evolutionary changes. What hasn’t been clear is why this is happening. This study describes at a biochemical level, down to the atoms and sequences in DNA, how a particular type of mutation can arise repeatedly, which then contributes to a complex skeletal trait evolving over and over again in wild fish species.

Kingsley and Xie were studying how many freshwater stickleback populations have lost a bony pelvic structure called a hind fin that is prevalent in their saltwater cousins. Losing this fin appears to help the tiny fish conserve calcium and avoid predators that might latch onto the structure. Previous research in the Kingsley lab had pinpointed a change in a region of DNA that drives the expression of a protein necessary for hind fin development. Xie found that this region is particularly prone to breakage and is likely to be unstable during DNA replication.

The researchers believe that these DNA features may have allowed various populations of freshwater sticklebacks to repeatedly lose the hind fin in the face of environmental pressure and that similar fragile DNA regions may be responsible for the evolution of advantageous traits in other organisms.

“Many vertebrates, including early humans, are dealing with a small population size and relatively long generation times,” Kingsley said. “There aren’t that many generations available in which to evolve new, potentially advantageous traits. Under these conditions, it may be particularly important for mutations to occur at elevated rates, and to have sweeping effects.”

Illustration by Kathleen Xie, provided by David Kingsley

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