18 THE SCIENTIST | the-scientist.com
been emerging from diapause almost
three weeks earlier than usual—giving
them more time to harm corn plants
and potentially infest other crops, too.
“A t some spots, you have [corn bor-
ers] that are coming out of diapause
earlier,” says Dopman. “So early, in fact,
that they can squeeze in a second gen-
eration at the end of the year, whereas
the ones that wait around in diapause
only have a single generation.” Those
early-emerging larvae live mostly in
the southern US; in the northern states,
corn borers still don’t emerge until late
May or early June. But there’s no clear
geographical boundary between the
phenotypes, and in upstate New York
and Pennsylvania, where Dopman’s
lab has been collecting caterpillars, the
researchers found both early- and late-
emerging populations.
To find out how O. nubilalis might
be adjusting its emergence time, the
group recently scanned the genomes of
larvae in five populations—three early-
emerging and two late-emerging. The
team found that larval emergence time
was linked to variation in two genes
known to be involved in circadian
rhythms. One is period, or per, a gene
that regulates sleep-wake cycles in Dro-
sophila and has been linked to seasonal
timing in many other insect species. The
other gene, Pdfr, produces a receptor
that binds to a neurotransmitter called
pigment-dispersing factor, which in
Drosophila helps to regulate the activity
of clock neurons in the brain. Dopman
and his colleagues speculate that varia-
tion in the sequences of these two genes
could provide a way for corn borers, and
perhaps other insects as well, to adapt
to changes in season length (Curr Biol,
29:3501–509, 2019).
“This paper is incredibly interesting
and important because it sheds light on
the molecular basis of differences in sea-
sonal responses,” says Megan Meuti, an
entomologist at Ohio State University
who was not involved with the study. The
fact that the genes are already known
to be involved in circadian rhythms
suggests “that the differences in thesequences of the clock genes are not
only affecting seasonal responses, but
also daily responses as well.”
Daniel Hahn, an evolutionary physi-
ologist at the University of Florida, adds
that while previous research has focused
on how circadian clock gene polymor-
phisms are associated with the timing
of insects entering dormancy, this new
study shows that such variation is also
“associated with when animals are
going to come out of dormancy. That’s a
completely new facet that nobody’s been
able to do before.”Hahn, who was not involved with
the current study but has collaborated
with Dopman in the past, is planning to
work with the Dopman team to expand
on this research. In addition to uncover-
ing more about the basic biology of the
corn borer, the scientists hope that their
findings could inform genetic engineer-
ing approaches to disrupt the annual
cycle of these pests, says Dopman.
“One possibility that we’re looking into
is whether we can create an ecological
mismatch,” he says. “If an organism has
genes that cause it to enter diapause or
break diapause at inappropriate times,
then that population can crash.”
—Emily MakowskiAutism’s Cuffs
About four years ago, pathologist Mat-
thew Anderson was examining slices of
postmortem brain tissue from an indi-
vidual with autism under a microscope
when he noticed something extremely
odd: T cells swarming around a narrowspace between blood vessels and neural
tissue. The cells were somehow getting
through the blood-brain barrier, a wall
of cells that separates circulating blood
from extracellular fluid, neurons, and
other cell types in the central nervous
system, explains Anderson, who works at
Beth Israel Deaconess Medical Center in
Boston. “I just have seen so many brains
that I know that this is not normal.”
He soon identified more T-cell
swarms, called lymphocytic cuffs, in a
few other postmortem brains of people
who had been diagnosed with autism.
Not long after that, he started to detect
another oddity in the brain tissue—tiny
bubbles, or blebs. “I’d never seen them
in any other brain tissue that I’ve looked
at for many, many different diseases,” he
says. Anderson began to wonder whether
the neurological features he was observing
were specific to autism.
To test the idea, he and his colleagues
examined postmortem brain tissue sam-
ples from 25 people with autism spectrum
disorder (ASD) and 30 developmentally
normal controls. While the lymphocytic
cuffs only sporadically turned up in the
brains of neurotypical individuals, the
cuffs were abundant in a majority of the
brains from individuals who had had ASD.
Those same samples also had blebs that
appeared in the same spots as the cuffs.
Staining the brain tissue revealed that the
cuffs were filled with an array of different
types of T cells, while the blebs contained
fragments of astrocytes, non-neuronal
cells that support the physical structure of
the brain and help to maintain the blood-
brain barrier.
Reading the literature and drawing on
his experience as a pathologist, Anderson
started to think about blebs and what they
do when they show up in tissues beyond
the brain. For example, in cancer, “blebs
are generated when T cells attack a tumor
cell,” he explains. “The tumor cells will spit
out surface membrane pieces... as a way
to protect [themselves] from the attack,
but also possibly to deliver signals to other
cells around them.” In the brain samples
from individuals with ASD, the blebs visu-
ally resembled blebs created in response toNOTEBOOKIf an organism has genes
that cause it to enter dia-
pause or break diapause at
inappropriate times, then
that population can crash.
—Erik Dopman, Tufts University