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Fine-Tuning of Bitter Taste Receptors May Be Key to AnimalSurvival

One key to animal survival is bitter taste—the better to avoidingesting potentially harmful poisons or foods. The evolutionof bitter taste has been a hot topic amongst evolutionarybiologists, and with more and more DNA data available, arich area of exploration.

Now, Behrens et al. (2014) examined the genetic repertoireof bitter taste receptor genes in chickens and frogs, whichrepresent two extremes. Chickens only have three bitter tastereceptor genes (Tas2rs), whereas frogs have more than 50(humans are somewhere in the middle). They studied thedifferent molecular properties of cloned Tas2r genes andmeasured their responses when exposed to a panel of 46natural or synthetic bitter compounds.

First, they constructed a gene tree for a selection ofTas2r genes of various vertebrate species and showed thatall avian genes come from the same three ancestral genes.Frogs were found to have five ancestral genes, indicating thattheir expanded repertoire was due to later gene duplicationevents.

They showed that all the three chicken Tas2rs are “broadlytuned” for bitter taste, whereas six frog Tas2rs tested aremixed consisting of broadly as well as narrowly tunedreceptors. Interestingly, both chicken and frog receptorrepertoires responded to about half of the compounds, show-ing that the tuning range rather than the number of Tas2r

genes was a critical factor. In general, individual substancesactivated different receptors in clearly separated concentra-tion ranges, which may also provide a clue to the role of bittertaste diversity in enhancing the chance of survival.

The authors conclude that a low number of functionalTas2r genes found in chickens can be compensated by anincreased average tuning width. They speculate that the en-vironmental duality of amphibian life, living on both land andwater, may account for the increased Tas2r gene diversity infrogs. In mixed aquatic and terrestrial environments amphib-ians such as frogs may have encountered a larger number ofbitter compounds, causing the evolutionary pressure toprovide a larger taste receptor repertoire.

ReferenceBehrens M, Korsching SI, Meyerhof W. 2014. Tuning properties of avian

and frog bitter taste receptors dynamically fit gene repertoire sizes.Mol Biol Evol. 31:3216–3227.

Joseph Caspermeyer*,1

1MBE Press Office

*Corresponding author: E-mail: [email protected].

doi:10.1093/molbev/msu288

Advance Access publication October 27, 2014

Treasure Trove of Ancient Genomes Helps Recalibrate theHuman Evolutionary Clock

Just like adjusting a watch, the key to accurately telling evo-lutionary time is based upon periodically calibrating against agold standard.

Scientists have long used DNA data to develop molecularclocks that measure the rate at which DNA changes, that is,accumulates mutations, as a premiere tool to peer into thepast evolutionary timelines for the lineage of a given species.In human evolution, for example, molecular clocks, whencombined with fossil evidence, have helped trace thetime of the last common ancestor of chimpanzees andhumans to 5–7 Ma, and contributed to the recent “out ofAfrica” theory for a great human migration event 100,000years ago.

To improve the modeling and reading of the branches onthe human tree of life Rieux et al. (2014) compiled the mostcomprehensive DNA set to date, a new treasure trove of 146ancient (including Neanderthal and Denisovian) and modern

human full mitochondrial genomes (amongst a set of 320available worldwide). Mitochondrial DNA (mtDNA) is aprecious resource for evolutionary scientists, because theyhave a high mutation rate, and unlike genomic DNA, areonly maternally inherited.

Now, by using a variety of sophisticated calibrationtechniques, the authors have improved the accuracy ofusing mtDNA as a molecular clock by recalibrating thehuman evolutionary tree. They showed that a molecularclock calibrated with ancient sequences was far more accu-rate than the traditional ones based on archaeological evi-dence. With this new recalibration, scientists can now traceback, with greater accuracy than ever before, the first “Eves” ofthe many migrations leading to the colonization of the earthby anatomically modern humans. “The recent possibility togenerate high-quality genome sequences from ancientremains represents an amazing progress in our ability to

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� The Author 2014. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution. All rights reserved. For permissions, pleasee-mail: [email protected]

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accurately reconstruct the past history of many species,including our own,” said Rieux.

ReferenceRieux A, Eriksson A, Li M, Sobkowiak B, Weinert LA, Warmuth V,

Ruiz-Linares A, Manica A, Balloux F. Improved calibration of thehuman mitochondrial clock using ancient genomes. Mol Biol Evol.31:2780–2792.


1MBE Press Office




Study Determines How Bacterial Species Evolve AntibioticResistance

Given a critical change in the environment, how exactly, dospecies adapt?

Vogwill et al. (2014) wanted to get at the heart of thisevolutionary question by measuring the growth rates andDNA mutations of eight different species of Pseudomonasbacteria. They controlled a single but vital variable duringgrowth, the dose of the antibacterial drug rifampicin.

Overall, they challenged 480 populations from eightdifferent strains of Pseudomonas (3,840 total) with adaptingto the minimal concentration of rifampicin that is needed tocompletely inhibit the growth of the ancestral strain of eachspecies. They carried out the experiment over 30 generationsof bacteria. Next, the authors selected 75 randomly chosenrifampicin-resistant mutants from eight different clonal bac-terial strains and sequenced the rpoB gene in all 600 mutants,identifying 47 different mutations. They measured both thegrowth rates of the clones in the presence of rifampicin, andthe DNA mutations of a gene, rpoB, a known mediator ofdrug resistance.

They found that most of these rpoB mutations occurredonly once, some occurred multiple times in a single strain,and others occurred multiple times in multiple strains.However, in agreement with the prevailing hypothesis, pop-ulations of the same strain tended to evolve in parallel.Despite that fact the eight bacterial strains are geneticallyvery different from each other, they also found that thesame mutations have different effects on fitness in thedifferent strains, indicating that the genetic make-up isan important fitness factor. Finally, the authors

demonstrated that the growth rates varied more withinspecies than between species.

“Antibiotic resistance often evolves by mutations in genesthat are conserved across bacteria, raising the possibility thatresistance evolution might follow similar paths acrossbacteria,” said MacLean. “Our study provides good evidencethat the rest of the genome influences which resistancemutations are observed, and how these mutations influenceDarwinian fitness. These findings imply that we need to becautious when trying to extrapolate our understanding of thegenetics of antibiotic resistance between bacterial strains orspecies.”

The breadth of the study shows how the powerful newtool of experimental evolution can provide important insightsinto the relationships between DNA mutations, growth, andevolution.

ReferenceVogwill T, Kojadinovic M, Furio V, MacLean RC. 2014. Testing the role of

genetic background in parallel evolution using the comparativeexperimental evolution of antibiotic resistance. Mol Biol Evol. 31:3314–3323.


1MBE Press Office




Cellular Self-Destruct Program Has Deep Roots throughoutEvolution

In what seems like a counter-intuitive move against survival,within animals, some cells are fated to die from the triggeringof an elaborate cell death program, known as apoptosis. Now,

Sakamaki et al. (2014) have honed in on understanding theevolution of caspase-8, and a key cell death initiator moleculethat was first identified in humans.

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