New genes out of nothing

 

One key question in evolutionary biology is how novel genes arise and develop. Swedish researchers now show how new genes and functions that are advantageous to bacteria can be selected from random DNA sequences. The results are presented in the scientific journal mBio.

How do new genes and functional proteins arise and develop? This is one of the most fundamental issues in evolutionary biology. Two different types of mechanism have been proposed: (1) new genes with novel functions arise from existing genes, and (2) new genes and proteins evolve from random DNA sequences with no similarity to existing genes and proteins.

In the present study, the researchers explored the latter type of mechanism: evolution of new genes and proteins from randomised DNA sequences as its called as de novo evolution. It is fairly easy to understand that when a gene already exists, it can be modified and acquire a new function. But how does "nothing" turn into a function affording a small advantage that is favoured by natural selection?

The raw material for the experiment was an big library of some 500 million randomised gene sequences, from which peptide sequences with a biological function were identified. In the experiment, random gene sequences were placed on a plasmid and overexpressed. The scientists then investigated whether they could give bacteria a specific, defined property. Were they, for example, able to give the bacteria antibiotic resistance? They identified several short peptides (22-25 amino acids long) that could give the bacteria a high degree of resistance to aminoglycosides, an important class of antibiotics used for severe infections.

"When the project started, we had low expectations. We were amazed when we found peptides able to confer a resistance level 48 times higher," says Dr Michael Knopp, the study's lead author.

Through a combination of genetic and functional experiments, the scientists were able to demonstrate that the peptides cause resistance by attaching themselves to bacterial cell membranes and affecting the proton potential across the membrane. The disruption of the proton potential causes a decrease in antibiotic uptake, rendering the bacteria resistant.

"This study is important because it shows that completely random sequences of amino acids can give rise to new, advantageous functions, and that this process of de novo evolution can be studied experimentally in the laboratory," says Dan I. Andersson, Professor of Medical Bacteriology, who is chiefly responsible for the study.

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Source of the article: https://www.sciencedaily.com/releases/2019/06/190604131214.htm

New methods to identify AD drug candidates with anti-aging properties

Long thought to suppress cancer by slowing cellular metabolism, the protein complex AMPK also seemed to help some tumors grow, confounding researchers. Now, Salk Institute researchers have solved the long-standing mystery around why AMPK can both hinder and help cancer.

The lab of Salk Professor Reuben Shaw showed that late-stage cancers can trigger AMPK's cellular recycling signal to cannibalize pieces of the cell, supplying large lung tumors with the nutrients they need to grow. The work was published in  Cell Metabolism suggests that blocking AMPK in some conditions could stop the growth of advanced tumors in the most common type of lung cancer.

"Our study shows that the same dysfunction in a genetic circuit that causes non-small-cell lung cancer to begin with is necessary for more mature tumor cells to survive when they don't have enough nutrients," says Shaw, Director of the Salk Cancer Center. "It's exciting because not only does it solve a genetic 'whodunnit,' but it also points to a potential new therapeutic target for a cancer that is often diagnosed very late."

AMPK acts as a fuel gauge for the cell, overseeing energy input and output to keep the cell running smoothly. Similar to a car sensor flashing a low-gas signal or turning off a vehicle's AC to save energy, AMPK slows down cell growth and changes the cell's metabolism if the cell's fuel (nutrients) is low. Previously, Shaw discovered that AMPK could halt tumors' revved-up metabolism, as well as restore normal function to the liver and other tissues in diabetics.

"We found that tumors grew much more slowly when AMPK was not present," says Research Associate Lillian Eichner."That means that AMPK is not always functioning as a tumor suppressor, as we originally thought."

The team analyzed which genes in tumor cells from the same mouse models were being activated under various conditions. One gene that was particularly active was Tfe3, which is known to activate cellular recycling. It turned out that when tumors became large enough that cells in the middle were too far from easy access to nutrients, AMPK signaled Tfe3 to initiate recycling of cellular materials as nutrients--effectively cannibalizing pieces of the cell--for the tumor to use.

"Previously we were focused on how we could activate AMPK," says Eichner. "Now that we've identified this mechanism, we can shift to how to inhibit it in certain cancers."

Shaw, who holds the William R. Brody Chair, adds, "We're excited because more advanced tumors seem to rely on AMPK to survive, and understanding this mechanism means we may be able to treat them."

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