, 516 (2009);
et al. Anton Maximov,
Complexes to Membranes in Fusion
Complexin Controls the Force Transfer from SNARE
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the force generated by assembly of trans-SNARE
consistent with biochemical data (23). We postu-
late that after complexin binds to assembling
SNARE complexes, its N-terminal sequence ac-
complex assembly. The N terminus of complexin
might perform its activator function by pulling
the complex closer to the membrane, possibly
by binding to phospholipids, whereas the acces-
sory N-terminal a-helix might clamp the com-
plex by inserting into the space between the
v- and t-SNAREs or even substituting for one
of the SNAREs in the C-terminal segment of the
trans-SNARE complex (24). Once anchored on
the SNARE complex, the 40 N-terminal residues
of complexin both activate and clamp SNARE
complexes to control fast Ca2+-triggered neuro-
transmitter release in a process that is conserved
in all animals. Viewed in the broader picture,
complexin and synaptotagmin therefore operate
as interdependent clamp-activators of SNARE-
dependent fusion, with synaptotagmin exploiting
clamping function (11, 21, 22). In this molecular
pas-de-deux, the functions of both proteins are
intimately linked: Their phenotypes are identical
both as activators and as clamps, and one does
not operate without the other.
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H, His; I, Ile; K, Lys; L, Leu; M, Met; N, Asn; P, Pro; Q, Gln;
R, Arg; S, Ser; T, Thr; V, Val; W, Trp; and Y, Tyr.
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29 September 2008; accepted 5 December 2008
Widespread Increase of Tree Mortality
Rates in the Western United States
Phillip J. van Mantgem,1*†‡ Nathan L. Stephenson,1*† John C. Byrne,2Lori D. Daniels,3
Jerry F. Franklin,4Peter Z. Fulé,5Mark E. Harmon,6Andrew J. Larson,4
Jeremy M. Smith,7Alan H. Taylor,8Thomas T. Veblen7
Persistent changes in tree mortality rates can alter forest structure, composition, and ecosystem
services such as carbon sequestration. Our analyses of longitudinal data from unmanaged old
forests in the western United States showed that background (noncatastrophic) mortality rates have
increased rapidly in recent decades, with doubling periods ranging from 17 to 29 years among
regions. Increases were also pervasive across elevations, tree sizes, dominant genera, and past fire
histories. Forest density and basal area declined slightly, which suggests that increasing mortality
was not caused by endogenous increases in competition. Because mortality increased in small
trees, the overall increase in mortality rates cannot be attributed solely to aging of large trees.
Regional warming and consequent increases in water deficits are likely contributors to the
increases in tree mortality rates.
changes (1). Such feedbacks may already be un-
der way; for example, forest carbon storage may
in global patterns of tree growth and forest
productivity (2–4). Recent warming has been
implicated as contributing to episodes of forest
dieback (pulses of greatly elevated tree mortali-
ty), such as those mediated by bark beetle out-
breaks in western North America (5, 6). Yet little
effort has gone toward determining whether en-
vironmental changes are contributing to chronic,
tality and recruitment). Changes in demographic
rates, when compounded over time, can alter for-
est structure, composition, and function (7). For
tributing substantial feedbacks to global
example, a persistent doubling of background
mortality rate (such as from 1 to 2% year−1) ul-
timately would cause a >50% reduction in aver-
age tree age in a forest, and hence a potential
reduction in average tree size. Additionally,
changing demographic rates could indicate
forests approaching thresholds for abrupt die-
back. Yet spatially extensive analyses of long-
term changes in tree demographic rates have
been limited to tropical forests, where mortality
and recruitment rates both have increased over
the past several decades, perhaps in response to
rising atmospheric CO2concentrations, nutrient
Comparably extensive analyses have not been
conducted in temperate forests.
We sought to determine whether systematic
changes in tree demographic rates have occurred
recently in coniferous forests of the western
United States, and if so, to identify possible
causes of those changes. Although the western
United States has witnessed recent episodes of
forest dieback related to bark beetle outbreaks or
combinations of drought and outbreaks (5, 6),
most forested land continues to support seem-
ingly healthy forests that have not died back (9).
To minimize transient dynamics associated with
stand development and succession, we limited
our analyses to data from repeated censuses in
(10). Old forests contain trees of all ages and
demographic rates over a short period (such as a
few decades) are likely to be consequences of
exogenous environmental changes (2, 13). In
contrast, in young forests rapid demographic
changes can sometimes result largely from
endogenous processes (such as self-thinning
during stand development) (14), potentially
obscuring environmentally driven changes.
1U.S. Geological Survey, Western Ecological Research
Center, Three Rivers, CA 93271, USA.2USDA Forest Service,
Rocky Mountain Research Station, Moscow, ID 83843, USA.
3Department of Geography, University of British Columbia,
Vancouver, British Columbia V6T IZ2, Canada.4College of
Forest Resources, University of Washington, Seattle, WA
98195, USA.5School of Forestry and Ecological Restoration
Institute, Northern Arizona University, Flagstaff, AZ 86011,
versity, Corvallis, OR 97331, USA.7Department of Geog-
raphy, University of Colorado, Boulder, CO 80309, USA.
8Department of Geography, Pennsylvania State University,
University Park, PA 16802, USA.
*These authors contributed equally to this work.
†To whom correspondence should be addressed. E-mail:
email@example.com (P.J.V.); firstname.lastname@example.org
‡Present address: U.S. Geological Survey, Western Ecolog-
ical Research Center, Arcata, CA 95521, USA.
6Department of Forest Science, Oregon State Uni-
VOL 323 23 JANUARY 2009
on February 18, 2009