SCIENCE sciencemag.org 4 JANUARY 2019 • VOL 363 ISSUE 6422 41-C
that is prone to double-stranded
DNA breakage owing to a high
thymine-guanine content. This
enhanced region of breakage
could lead to enhanced mutation
rates that facilitate repeated
adaptations to new environ-
ments. —SNV
Science, this issue p. 81
CONSERVATION
The distinctive sound of a
biodiverse forest
Assessing the state of
biodiversity in a forest is a time-
consuming task that typically
requires detailed on-the-ground
surveys. In a Perspective,
Burivalova et al. explain that
recordings of soundscapes
can provide an easier route to
this information. By record-
ing soundscapes from a forest
over time and comparing them
to a regional baseline, scien-
tists can determine whether a
forest’s ecosystem is healthy
or not. If the soundscape of
a forest spared from conver-
sion becomes impoverished
and altered, an on-the-ground
survey would be warranted. This
approach may be particularly
useful for companies interested
in sustainability certification
or zero-deforestation commit-
ments. —JFU
Science, this issue p. 28
TUBERCULOSIS
Faulty kinase purged by
tuberculosis?
Rare mutations in genes involved
in interferon-g–dependent
immunity underpin human
genetic susceptibility to severe
mycobacterial diseases,
including primary tuberculosis.
Boisson-Dupuis et al. investi-
gated whether two common
missense variants of the TYK2
Janus kinase that have impaired
catalytic activity conferred an
increased risk of tuberculosis.
Individuals homozygous for
the P1104A (proline to alanine
substitution at residue 1104)
variant of TYK2 are markedly
predisposed to developing
primary tuberculosis, defining
a common monogenic etiol-
ogy for the “white plague.” The
current frequency of the P1104A
allele in European popula-
tions is significantly decreased
compared with its frequency in
ancient European DNA samples.
These findings suggest that
negative selection against the
TYK2 P1104A allele by endemic
tuberculosis in Europe may have
contributed to a slow genetic
purge of this susceptibility allele
during recent millennia. —IW
Sci. Immunol. 3 , eaau8714 (2018).CANCER
Altering membrane
potential for cancer
Polymorphisms in the G pro-
tein–coupled receptor GPR35
are associated with increased
risk for certain inflammatory
diseases that can progress to
cancer. Schneditz et al. found
that GPR35 promoted the activ-
ity of Na+- and K+-dependent
adenosine triphosphatase
(Na+,K+-dependent ATPase),
a transmembrane pump that
sets the membrane potential in
cells. This effect was enhanced
by a disease-associated GPR35
variant. Stimulation of Na+,K+-
ATPase activity by GPR35
increased glycolysis and pro-
liferation in intestinal epithelial
cells. Na+,K+-ATPase deficiency
or treatment with a pepducin
targeting GPR35 decreased
tumor burden in mouse models
of intestinal cancer. —WW
Sci. Signal. 12 , eaau9048 (2019).Published by AAAS