Spain’s Earth Scientists
and the Oil Spill
THE SPANISH COAST OF GALICIA IS CURRENT-
ly subject to an oil spill that, given its spatial
and temporal extent, could become one of
the worst spills ever. The Spanish and the
local Galician governments have been main-
taining for 30 days that, since 13 November,
when the tanker Prestige ran into problems,
every decision implemented throughout this
crisis, including the key resolution
of transporting the vessel offshore,
was guided by the technical advice
of Spanish experts. In our opinion,
the recurrence and indiscriminate
generalization implicit in such a
statement entail a serious threat to
the credibility of the Spanish Earth
sciences community as a whole.
Moreover, this crisis is revealing a
serious malfunctioning of the
national research system. This
moves us, as marine and atmos-
pheric scientists, and members of
the Spanish Institute of Oceanography
(IEO), National Research Council (CSIC),
universities, and other research centers, to
express the following:
1) Given the well-known winter clima-
tology of the area of the spill, dominated
by west-southwesterly winds and a south to
north slope current on the sea (1–11), the
decision to move the vessel from about
43°N, 9.5°W offshore to the southwest was
a consequence of poor communication
between the government officials dealing
with the spill and the scientific and tech-
nical communities, rather than a deficit of
knowledge. This move was responsible for
the spreading (spatial amplification) of the
spill, which now extends across about 900
km of shoreline. The position of the sunken
ship at about 42°N, 12°W, 145 nautical
miles off the south coast of Galicia will
probably cause successive oil waves
(temporal amplification) to arrive at the
Spanish, Portuguese, and/or French coasts.
Thirty days after the first spill (12), the
Galician coast now faces a third, and
possibly not the last, oil wave.
2) Once the oil spill had occurred, the
poor coordination of the Spanish authori-
ties has led to a very ineffective use of
scientific institutions, resources, and
knowledge, reflected in inexplicable delays
and overlapping actions. For example, the
first draft of a scientific action plan is
dated 13 December, 1 month after the
beginning of the crisis and 4 days after the
first scientific commission was convened.
3) We demand that the Spanish authori-
ties improve the mechanisms and logistics
for scientific and technical consultation
and refrain from making vague public
statements that are seriously, and unfairly,
damaging the image of Spanish marine and
PABLO SERRET,1XOSÉ ANTÓN ÁLVAREZ-SALGADO,2
ANTONIO BODE,3AND 419 OTHER SCIENTISTS FROM
32 UNIVERSITIES AND 6 RESEARCH INSTITUTIONS*
1Facultad de Ciencias, Universidad de Vigo, 36200
Vigo, Spain.2Instituto de Investigacions Mariñas,
Consejo Superior de Investigaciones Cientificas
(CSIC), Eduardo Cabello, 6, 36208 Vigo, Spain.
3Instituto Español de Oceanografía (IEO), Centro
Costero de A Coruña, Muelle de Ánimas s/n, A
5606/511/DC1 for a full list of all authors and
References and Notes
1. X.A. Álvarez-Salgado et al., Progr.Oceanogr., in press.
2. I. Álvarez, M. deCastro, R. Prego, M. Gómez Gesteira,
Estuarine Coastal Shelf Sci., in press.
3. J.M.Cabanas,A.Lavín,M.J.García,C.Pola,E.Tel Perez,
Mar.Sci.Symp., in press.
4. E. Fernández et al., J.Plankton Res. 15, 619 (1993).
5. R. Frouin,A. F. G. Fiuza, I.Ambar,T. J. Boyd, J.Geophys.
Res. 95, 679 (1990).
6. C.García-Soto,R.D.Pingree,L. Valdés,J.Geophys.Res.
107, 3118 (2002).
7. R. Haynes, E. D. Barton, J. Geophys. Res. 95, 11425
8. A. Lavin, G. Diaz, G. Casas, J. M. Cabanas, Inf.Téc.Inst.
Esp.Oceanogr. 15, 25 pp. (2000).
9. R. D. Pingree, B. Le Cann, J. Mar. Biol. Assoc. U.K. 70,
10. E. Teira, P. Serret, E. Fernández, Mar. Ecol. Prog. Ser.
219, 65 (2001).
11. W. S. Wooster, A. Bakun, D. R. Mclain, J. Mar. Res. 34,
12. This letter was written on 21 December 2002.
MICHAEL PHILLIPS’ CONTENTION THAT CO-
authors of fraudulent papers who signed
those papers in the belief that the data were
honest are themselves victims (“Should
coauthors share liability?” Letters, 22 Nov.,
p. 1554) is a disturbing proposition that one
would hope is not widely shared. It is unfor-
tunately saddening rather than shocking that
some would hew to such an idea. Certainly,
if the scientific community is to retain and
warrant the esteem of the public, then the
notion that coauthors do not have sufficient
knowledge of the details of the study they
purport to have participated in to vouch for
its integrity simply does not wash. As a
practical matter, mandating such responsi-
bility would service two useful purposes: (i)
to curb freeloading on papers by individuals
with only marginal involvement and (ii) to
provide a first line of defense against fraud.
For those whose do not wish or have the
time for this level of involvement, there is a
long-standing tradition of acknowledgment
short of authorship.
New York, NY, USA.
The Next Generation of
DONALD KENNEDY (“AFTERMATHS,” EDIT-
orial, 29 Nov., p. 1679) is wise to advocate
new means of encouraging science and tech-
nology training for future policy-makers in
the United States. The National Defense
Education Act is an informative model, not
least for its expansive view of the critical
skills the United States would require. By
focusing on educating the next generation of
public servants, however, Kennedy addresses
only a part of the United States’ intellectual
deficit and only part of our opportunity.
In an era of dazzling opportunities across
many scientific disciplines, our country has
been disinvesting (1). Federally supported
R&D shrank in 2000 to less than 0.7% of
the gross domestic product—a level last
seen before the Soviets launched Sputnik. A
laudable bipartisan effort to double the NIH
budget has nourished biomedical research
and training, but a steady attrition of invest-
ment has weakened the physical sciences
and engineering. The Department of
Energy’s funding for the physical sciences
has decreased by 20% since 1993. The
number of graduate students has dropped
A man walks along an oil-covered beach in Caion,
northern Spain, 18 November 2002.
Letters to the Editor
Letters (~300 words) discuss material published
in Science in the previous 6 months or issues
of general interest. They can be submitted by
e-mail (email@example.com), the Web
(www.letter2science.org), or regular mail
(1200 New York Ave., NW, Washington, DC
20005, USA). Letters are not acknowledged
upon receipt, nor are authors generally
consulted before publication.
published in full or in part, letters are subject
to editing for clarity and space.
www.sciencemag.org SCIENCEVOL 299 24 JANUARY 2003
CREDIT: CORBIS/REUTERS/PAUL HANNA
L E T T E R S
24 JANUARY 2003VOL 299SCIENCE www.sciencemag.org
proportionately, with U.S. students minori-
ties in many departments.
While continuing to welcome foreign
students and sustaining our enormously bene-
ficial position as graduate school to the world,
we must take new steps to encourage and
support the advanced graduate studies of U.S.
citizens in science and engineering. An ambi-
tious new program of graduate fellowships—
let us call them Benjamin Franklin fellow-
ships—would show students that our country
values science and technology and would spur
them toward creative public service. Graduate
students we attract during this decade will
help shape the world for half a century, so it
would be shortsighted to target a few special-
ties. It would be better by far to attract more of
our best students to the most interesting
sciences and to inspire them, like Benjamin
Franklin, to range over pure and applied
science, engineering, and even statecraft!
Fermi National Accelerator Laboratory, Post Office
Box 500, Batavia, IL 60510, USA. E-mail:
1. “Federal Investment in R&D,” a project memorandum
prepared for the President’s Council of Advisors on
Science and Technology by the RAND Science and
Technology Policy Institute and the AAAS (see
Heat and Biodiversity
SINCETHETIME OFDARWIN,THE LATITUDINAL
gradient of increasing species diversity from
the poles to the equator has perplexed biolo-
gists and shaped ecological and evolutionary
theories. A. P. Allen et al. present a model
intended to explain this pattern (“Global
biodiversity, biochemical kinetics, and the
energetic-equivalence rule,” Reports, 30
Aug., p. 1545). Their model is a formaliza-
tion of the “species-energy hypothesis” and
predicts that “biodiversity is positively corre-
lated with productivity because more produc-
tive environments contain more individuals
and can therefore support more species popu-
lations above some minimum size required
for persistence” (p. 1547). The model predic-
tions are consistent with patterns of
increasing species number with increasing
mean air or water temperatures for trees,
amphibians, marine gastropods, fish, and
In spite of its intuitive appeal, this model
suffers from the two fundamental flaws of
the species-energy hypothesis. First, “envi-
ronmental energy” (in this model, mean
temperature) does not correspond to the
energy actually available to organisms,
which is the energy stored in carbon
compounds produced by photosynthesis.
Although it is true that the tropics tend to be
warmer than the temperate zone, higher
temperatures do not necessarily result in
higher productivity of plants or animals. The
most extensive data set on the net primary
productivity of plants compiled to date
reveals that the mean annual productivity of
tropical forests is the same as that of
temperate forests (1). Marine productivity is
much higher in the cold high-latitude
oceans, where the world’s great fisheries are
located, than in the warmer tropics (2).
Second, many of Earth’s highest diver-
sity areas have low productivity (3).
Examples include the mediterranean
climate shrublands of South Africa and
Australia, which occur on poor soils with
low primary productivity; the diversity of
bird species with small range sizes in Africa,
which is unrelated to net primary produc-
tivity (4); and the diversity of aquatic and
marine phytoplankton, which is higher in
unproductive, nutrient-poor environments
than in productive environments. All of
these patterns directly contradict the predic-
tions of species-energy theory. Thus, it does
not seem likely that a temperature-based
species-energy model is the explanation for
the latitudinal gradient of species diversity.
MICHAEL A. HUSTON
Environmental Sciences Division, Oak Ridge
National Laboratory,Oak Ridge,TN 37831,USA.E-
1. W. Cramer et al., in Terrestrial Global Productivity:
Past, Present, and Future, H. A. Mooney, J. Roy, B.
Saugier, Eds. (Academic Press, San Diego, CA, 2001),
2. M. J. Behrenfeld et al., Science 291, 2594 (2001).
3. M. A. Huston, Biological Diversity: The Coexistence of
Species on Changing Landscapes (Cambridge Univ.
Press, Cambridge, 1994).
4. E. Ravasz,A. L. Somera, D.A. Mongru, Z. N. Oltvai.A.-L.
Barabási, Science 297, 1551 (2002).
HUSTON SEEMS TO MISINTERPRET BOTH THE
substance and the intent of our Report. He
suggests that our model is some version of
the long-standing species-energy hypothesis
and then criticizes it for “suffer[ing] from the
two fundamental flaws” of this hypothesis.
Huston correctly points out that temperature
“does not correspond to the energy actually
available to organisms.” Indeed, temperature
indexes the average kinetic energy of mole-
cules, not the potential for photons, organic
compounds, and other energy and materials
to be used by, and fluxed through, organisms
and ecosystems. Temperature affects the rate
of metabolism, but it is not the fuel for
metabolism. Our paper argues that tempera-
ture affects biodiversity through its funda-
mental influence on the rates of biochemical
reactions, whole-organism metabolism, and
ecological interactions. The traditional
species-energy hypothesis attributes species
richness in large part to productivity, the rate
of flux of biologically usable potential
energy. Biodiversity is almost certainly
influenced by both kinetics and productivity,
but they are not the same thing.
Huston is correct that in some cases,
high species diversity occurs in cold or
low-productivity environments. Temper-
ature and productivity are often, but by no
means always, correlated in nature, so it
will be a challenge to understand their
separate and interacting effects. Although
the rate of biological production is power-
fully constrained by temperature, it is also
affected by other environmental vari-
ables—most notably by the supply of water
and nutrients. The ability to predict the
kinetic effects of temperature from a basic
theoretical perspective should aid in under-
standing the other environmental factors
and ecological processes that also affect
biodiversity. Contrary to Huston’s asser-
tions, we do not claim that “a temperature-
based species-energy model is the explana-
tion for the latitudinal gradient of species
diversity.” We do claim that the funda-
mental effect of temperature on rates of
biological metabolism and ecological inter-
actions must be an important component of
any theory to explain the latitudinal and
other major patterns of species diversity.
JAMES H. BROWN,ANDREW P.ALLEN,
JAMES F. GILLOOLY
Department of Biology,University of New Mexico,
Albuquerque, NM 87131, USA.
Gluten Peptides and
IN THEIR REPORT “STRUCTURAL BASIS FOR
gluten intolerance in Celiac Sprue” (27 Sept.,
p. 2275), L. Shan et al. describe a 33-mer
gluten peptide that is resistant to degradation
in the gastrointestinal tract and contains
several T cell stimulatory epitopes. All
Celiac disease (CD) patients tested made T
cell responses to this 33-mer peptide.
Homologs of the peptide are present in
barley and rye, which are toxic to CD
patients, but not in oats, rice, and maize,
which are considered safe for patients. An
enzyme is described that eliminates the
T cell–stimulatory properties of the peptide.
Although we acknowledge that this is an
important step forward, we feel that it is an
oversimplification of the problem. There are
at least 15 T cell–stimulatory gluten peptides,
and most of these are not found in the 33-mer
peptide (1). In fact, in 50% of children with
CD, we find no responses to sequences in the
33-mer peptide, but we do find responses to
other gluten peptides (2). Also, the authors
ignore our description of a T cell–stimulatory
gluten peptide of which identical homologs
exist in barley and rye, but not in oats. This
peptide is also not found in the 33-mer
peptide (3). Evidently, responses to peptides
other than the 33-mer can be linked to
disease development and cereal toxicity.
Finally, we propose a word of caution
regarding the “therapy.” What is proposed is
enzymatic destruction of the peptide, which
may prove difficult because gluten is usually
present in a food matrix, together with many
other compounds. This severely complicates
gluten detection and quantification in food,
let alone enzymatic degradation and proof
that all relevant gluten peptides have been
degraded. Moreover, the authors incorrectly
state that all gluten peptides described by us
(2) will be destroyed by the enzyme.
Consequently, this enzyme treatment will
fail to remove toxicity completely.
FRITS KONING AND WILLEMIJN VADER
Department of Immunohematology and Blood
Transfusion, Leiden University Medical Center, PO
Box 9600, 2300 RC Leiden, Netherlands. E-mail:
1. M. F. Kagnoff, Gastroenterology 123, 939 (2002).
2. W.Vader et al., Gastroenterology 122, 1729 (2002).
3. W.Vader et al., J.Exp.Med. 195, 643 (2002).
WE THANK KONING AND VADER FOR THEIR
comments. The existence of T cell epitopes
outside the 33-mer peptide is explicitly
acknowledged by us in Table 2 and in cited
references, including a recent publication
by the authors. A key point, not mentioned
in their Letter, is the substantially enhanced
potency of the 33-mer in eliciting T cell
responses relative to individual epitopes
present in most short peptides (e.g., see
Fig. 3 and Table 2). Presumably, these
quantitative differences arise because of the
multivalency and proteolytic stability of the
33-mer. Therefore, it is inappropriate to
conclude that, just because individual
epitopes in the 33-mer do not stimulate
patient-derived T cells, the 33-mer will also
not do so. We are unaware of any published
results from the authors in which side-by-
side tests have been performed with the 33-
mer and other gliadin peptides on T cell
lines originally challenged with gluten.
Moreover, in apparent contrast to the
authors’ findings, one of us (L.M.S.) has
observed T cell responses to one or more
epitopes found in the 33-mer in all adult
patients tested so far (n > 30).
Koning and Vader also draw attention to
the fact that other predictors of cereal toxi-
city have been proposed in the literature.
We do not state or imply that the 33-mer
sequence is the only known predictor of
cereal toxicity. Our observation that
homologs of the 33-mer are found in toxic
but not nontoxic cereals was simply
intended to rationalize its exceptional
L E T T E R S
www.sciencemag.orgSCIENCE VOL 29924 JANUARY 2003
Finally, Koning and Vader argue that, Download full-text
given the diversity of known immunogenic
epitopes in gluten and their assumptions
regarding the dynamics of gluten release
from food in the small intestine, the comple-
mentary action of endogenous proteases and
an exogenous prolyl endopeptidase (PEP)
“will fail” to detoxify gluten. To our knowl-
edge, every intestinal T cell epitope identi-
fied from gluten to date contains one or more
Pro residues. Bacterial PEPs have broad
tolerance for proline-containing peptides.
For example, although the F . meningoscep-
ticum PEP (used in our study) prefers
Pro-↓X-Pro motifs, it can also cleave other
Pro↓X-X motifs (1), especially in shorter
peptides, such as most gluten peptides gener-
ated by the action of gastric and pancreatic
proteases. Other homologous bacterial PEPs
will undoubtedly have varying S2, S1´, and
S2´ subsite preferences, some of which may
be even better suited for gluten detoxification
than the F . meningoscepticum enzyme. The
main conclusions from our study are that (i)
the mammalian digestive apparatus is inca-
pable of effective proteolytic cleavage on the
COOH-terminal side of internal Pro residues
in dietary proteins; (ii) PEPs from other
sources have this capability; and (iii) endoge-
nous proteases and an exogenous PEP act in
concert to dramatically accelerate the rate of
digestion (and consequent detoxification) of
Pro-rich dietary proteins such as gliadins. Of
course, only a carefully planned clinical
study will definitively answer the question of
whether such detoxification can provide a
Celiac Sprue patient some relief from the
severe burden of a strict, lifelong gluten-free
LU SHAN,1ØYVIND MOLBERG,5GARY M. GRAY,2
LUDVIG M. SOLLID,5CHAITAN KHOSLA1,3,4
1Department of Chemical
2Department of Medicine,
Chemistry, and 4Department of Biochemistry,
Stanford University, Stanford, CA 94305–5025,
University of Oslo, N-0027 Oslo, Norway.
5Institute of Immunology, Rikshospitalet,
1. F. Bordusa, H. D. Jakubke, Bioorg. Med. Chem. 6, 1775
L E T T E R S
www.sciencemag.orgSCIENCEVOL 29924 JANUARY 2003
CORRECTIONS AND CLARIFICATIONS
REVIEWS: “Molecular mecha-
nisms of axon guidance” by B. J.
Dixon (6 Dec., p. 1959). There
were several labeling errors in
Fig. 1A. The correct version of
the figure appears to the left.
hypoxic death in C. elegans by
the insulin/IGF receptor homolog
DAF-2” by B. A. Scott et al. (28
June, p. 2388). One of the daf-2
strains tested in the paper was
incorrectly called e979. The
strain referred to as daf-2(e979)
has subsequently been discov-
ered to be daf-2(m41). The
strain was obtained from the
Caenorhabditis Genetics Center
(CGC) as e979,but the error was
on the part of other investiga-
tors who originally submitted
the strain to the CGC. This
discovery does not change any
of the conclusions of the
authors’ work. In particular, the
lack of correlation of life-span
and hypoxic death is still main-
tained (r = 0.32, P = 0.36).
However, the Gly383to Glu
mutation assigned to the e979
mutant should in fact be
assigned to m41, as previously
reported [H. Yu, P. L. Larsen, J.
Mol.Biol. 314,1017 (2001)].