12.2018 | THE SCIENTIST 53© ISTOCK.COM, MARILYN NIEVES; YUANYUAN HUANG
MORE IS MORE: Multispecies forests generally outperform monocultures
in productivity and carbon accumulation.BAD ACTORS: Leukemic regenerating cells, rather than leukemia stem
cells, may be responsible for relapses after chemotherapy.ECOLOGY & ENVIRONMENTPatchwork Forests
THE PAPER
Y. Huang et al., “Impacts of species richness on productivity in a
large-scale subtropical forest experiment,” Science, 362:80–83, 2018.Plants can help mitigate climate change by removing and storing
carbon from the atmosphere. Bernhard Schmid, an ecologist
and environmental scientist at the University of Zurich, and
others have published observational research suggesting that, in
forests, higher species richness is associated with higher carbon
sequestration. But it wasn’t clear whether the relationship was
causal, Schmid says.
To explore the issue experimentally, Schmid and colleagues
in Germany and China enlisted the help of farmers in southeast
China’s Jiangxi Province to plant nearly 160,000 trees on small
plots such that each plot contained between 1 and 16 species.
After eight years, the 16-species plots had accumulated more
than twice the amount of carbon that the average single-species
plots had. Combined with previous findings, the results provide
“the most convincing evidence so far that forests that are more
diverse indeed are more productive and do store more carbon,”
Schmid says.
“It’s a nice paper,” says Martin Lukac, a forest ecologist at
the University of Reading in the UK who was not involved in the
work. “I wish we had more studies like this.” But he notes that
certain single-species plots—those planted with commercial
conifers—accumulated about as much carbon as 16-species plots
did. Although the authors acknowledge this result in their paper,
they could have explained more clearly that multispecies forests
have the added advantage of being more ecologically resilient to
climate change than monocultures, he says.
A longer-term study would help clarify the biodiversity-carbon
link, says Lukac, although as the trees grow larger, overcrowding
could contribute confounding effects. Schmid says his team would
like to continue the project. In the meantime, he hopes that land
managers and others in charge of reforestation will accept that “it
really makes sense to plant diverse forest.”
—Catherine OffordDISEASE & MEDICINEMoving Target
THE PAPER
A.L. Boyd et al., “Identification of chemotherapy-induced
leukemic-regenerating cells reveals a transient vulnerability of
human AML recurrence,” Cancer Cell, 34:P483–98.e5, 2018.Cancer researchers have long supposed that relapses of acute
myeloid leukemia (AML) arise from a population of leukemia stem
cells (LSC) that were dormant and therefore likely protected from
chemotherapies that target dividing cells.
But when Mickie Bhatia of McMaster University in Canada
and colleagues analyzed cancer cell populations from patient
samples as well as those obtained from AML cells grafted into
mice, they found that LSCs were depleted during chemotherapy.
“By kinetically profiling the cells, we got a better impression of what
was being killed during the chemotherapy, but also how it came
back,” says Bhatia.
His team then sampled patient bone marrow cells at multiple
time points post-chemotherapy, in parallel with samples from
xenografts grown from the patients’ tumors. In both, they identified
a small population of cells, dubbed leukemic regenerating cells
(LRCs), that had a gene expression profile distinctly different from
that of LSCs. “The leukemic regenerating cells are actually a product
of a response to chemotherapy,” says Bhatia. LRCs were present
in high numbers only transiently, with their numbers falling as
relapse occurred. One distinctive feature of these cells was
the production of several G-protein-coupled receptors (GPCRs),
and the researchers found that suppressing the expression of a
specific GPCR gene in LRCs prevented relapse in chemotherapy-
treated mice.
“Maybe there’s a short window after induction [of]
chemotherapy, where one could come in with a very specific
therapy directed against this small population of leukemia
regenerating cells,” says David Sykes, who studies AML at
Massachusetts General Hospital and was not involved with this
research. Sykes says the chances of finding similar target cell
populations in other cancers is high.
—Sukanya Charuchandra