evolution in a test tube
Experimental evolution studies reveal drug targets
and resistance mechanisms
is song in Darwin’s finches, hybrid speciation may be more likely. Furthermore, when
hybrids can exploit a different ecological
niche, hybrid speciation is more likely (5, 7).
With high-resolution genomic data available for Darwin’s finches (2, 8) and for
many other species that have undergone
adaptive radiation, such as cichlid fishes
and Heliconius butterflies [for example,
(9, 10)], we are poised to learn more about
whether the origin of Big Birds by means of
homoploid hybrid speciation is anomalous
or common and whether this mechanism
might frequently explain cases of rapid
speciation. However, challenges remain
in distinguishing genetic signals of homoploid hybrid speciation from other situations where hybridization has occurred in
the history of a lineage, but was not the
causal mechanism of speciation. Hybridization can act to infuse genetic variation into
a lineage, facilitating adaptive diversification, before speciation or adaptive radiation (11) or as diversification proceeds (12).
These signals can be difficult to disentangle
using genomic data alone (4), particularly
in cases in which the species involved are
closely related. These challenges underscore
the incredible value that longitudinal field-based observational studies can add to DNA
sequencing data, as in Lamichhaney et al.
It is also important to establish whether
species produced through homoploid hybrid
speciation can persist over long time scales
(thousands to millions of years), and how
their persistence compares to species produced through other speciation mechanisms,
such as species formed during long periods
of geographic isolation. It is possible that
species formed through homoploid hybrid
speciation disappear just as rapidly as they
arise. This has important implications for
understanding whether this process contributes to the buildup of biodiversity. Watching
the fate of the Big Birds will provide one answer. Although long-term evolutionary analyses are difficult, this study illustrates that
the tremendous effort of collecting such data
sets has equally tremendous value. j
1. D. Schluter, The Ecology of Adaptive Radiation (Oxford
Univ. Press, 2000).
2. S. Lamichhaney et al. , Science359, 224 (2018).
3. J. R. Meyer et al., Science 354, 1301 (2016).
4. M. Schumer etal .,Evolution 68, 1553 (2014).
5. C. A. Buerkle et al ., Heredity 84, 441 (2000).
6. P. R. Grant, B. R. Grant, 40 Years of Evolution: Darwin’s
Finches on Daphne Major Island (Princeton Univ. Press,
7. B. L. Gross, L. H. Rieseberg, J. Hered. 96, 241 (2005).
8. S. Lamichhaney et al., Nature 518, 371 (2015).
9. Heliconius Genome Consortium, Nature 487, 94 (2012).
10. D. Brawand et al. , Nature 513, 375 (2014).
11. J. I. Meieretal. , Nat.Commun.8, 14363 (2017).
12. O.Seehausen, Trends Ecol.Evol. 19, 198(2004).
By Jane M. Carlton
Malaria is an infectious disease caused by the Plasmodium para- site, and transmitted by Anopheles mosquitoes. In 2016, a staggering 216 million cases of malaria and 445,000 deaths were recorded,
mostly in Africa, although half of the
world’s population in 91 countries is at
risk of the disease (1). Malaria prevention
methods include control of the mosquito
with insecticide-treated bed nets and in-
door residual spraying of insecticides.
Prompt diagnosis through the use of rapid
diagnostic tests is also key. Although there
is a malaria vaccine, RTS,S/AS01, it shows
limited efficacy and has yet to be used
widely. However, the frontline against ma-
laria is antimalarial drugs, in particular
artemisinin-based combination therapies
(ACTs), which are mixtures of artemis-
inin and its derivatives from the Chinese
sweet wormwood herb, with drugs such
as piperaquine. Alarmingly, the parasite is
now resistant to most drugs that have been
developed (see the figure). It is imperative
that we identify new inhibitors if progress
in reducing malaria is to be sustained. On
page 191 of this issue, Cowell et al. (2) pres-
ent a major step forward, revealing new
antimalarial drug targets and their pos-
sible resistance mechanisms.
The Plasmodium parasite is a formidable
eukaryotic microbe, an ancient organism
that has shaped the history, politics, and
evolution of its human host. Almost 500
species have been identified that infect
mammals, birds, and reptiles; however,
only five routinely infect humans, including
Plasmodium falciparum, the deadliest, and
Plasmodium vivax, the most geographically
widespread (3). Because of its virulence and
ease of in vitro culture, research has focused on P. falciparum, and molecular and
cell biology techniques have been developed
for its interrogation, such as genome editing (4, 5), and high-throughput analyses,
such as metabolomics (6).
These are worrisome times for the battle
against malaria. In addition to the parasite
being resistant to almost every single-drug
CQ Pyrimethamine PfPailin
Spread of resistance
ACT resistance CQ resistance Endemic
Malaria endemicity and drug resistance
12 JANUARY 2018 • VOL 359 ISSUE 6372 159
P. falciparum endemicity and the spread of drug resistance
Malaria is endemic in the countries highlighted in light blue. Resistance to antimalarial drugs such as
chloroquine (CQ) and pyrimethamine is widespread (darker blue), while resistance to artemisinin-based combination therapies (ACTs) is spreading. A new P. falciparum strain, PfPailin, that is resistant to
artemisinin plus piperaquine, has been found. Data presented in the map are adapted from (7, 8).