Science 14Feb2020

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(see the Perspective by Nayak
and Twardowski). Fragmentation
is thus perhaps the most
important process controlling
the remineralization of sinking
organic carbon. —HJS
Science, this issue p. 791;
see also p. 738


CIRCADIAN RHYTHMS


Redundancy


in circadian clocks?


The transcription factor BMAL1
is a core component of the
mammalian circadian clock;
without it, circadian behaviors
are abolished. However, Ray et
al. found that in animals lack-
ing BMAL1, peripheral tissues
synchronized with a brief pulse
of the glucocorticoid hormone
dexamethasone appear to retain
a 24-hour pacemaker that sus-
tains rhythmic gene expression,
protein abundance, and protein
phosphorylation in excised liver
cells and fibroblasts (see the
Perspective by Brown and Sato).
These oscillations persisted
in the absence of cues from
changes in light or temperature.
The results raise intriguing ques-
tions about the possible nature
of the oscillator that maintains
the observed rhythms. —LBR
Science, this issue p. 800;
see also p. 740


BIODIVERSITY LOSS


Cascading impacts


of prey loss


The global pandemic caused by
the amphibian fungal pathogen
Batrachochytrium dendrobatidis
has decimated frog populations
around the world. This decline
has been called out as a poten-
tial catastrophe for amphibian
species. What has been less
explored are the impacts of
amphibian declines on other
members of their ecological
communities. Using survey data
collected over 13 years, Zipkin et
al. looked at diversity and body
condition of a tropical snake
community heavily affected by
chytridiomycosis. They found
that affected snake communi-
ties were less diverse and most


species were in decline, except
for a few “winning” species.
—SNV
Science, this issue p. 814

NEONATAL JAUNDICE
Targeting acidity
in jaundice
Neonatal hyperbilirubinemia,
also called jaundice, is a pedi-
atric condition caused by high
bilirubin levels. When associ-
ated with acidosis, jaundice can
trigger neurotoxicity and lead to
neurological impairments. Lai et
al. investigated the link between
acidosis and jaundice in human
samples and animal models. In
samples from children with con-
comitant acidosis and jaundice,
neuronal injury was increased
compared with children with
jaundice and no acidosis. In
mice, bilirubin potentiated the
activity of acid-sensing ion
channels (ASICs) in neurons,
increased firing, and caused cell
death. Hyperbilirubinemia and
acidosis also promoted cognitive
impairments in mice, but these
were prevented by ASIC dele-
tion. Targeting ASICs could be a
promising way to prevent neuro-
logical impairments associated
with jaundice. —MM
Sci. Transl. Med. 12 , eaax1337 (2020).

14 FEBRUARY 2020 • VOL 367 ISSUE 6479 754-C
Published by AAAS
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