DOI: 10.1126/science.1153795
, 942 (2008);320Science
et al.José R. Dinneny
Stress
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Cell Identity Mediates the Response of
Arabidopsis Roots to Abiotic Stress
José R. Dinneny,1
*† Terri A. Long,1
* Jean Y. Wang,1
Jee W. Jung,1
Daniel Mace,2
Solomon Pointer,1
Christa Barron,3
Siobhan M. Brady,1
John Schiefelbein,3
Philip N. Benfey1,2
‡
Little is known about the way developmental cues affect how cells interpret their environment.
We characterized the transcriptional response to high salinity of different cell layers and
developmental stages of the Arabidopsis root and found that transcriptional responses are highly
constrained by developmental parameters. These transcriptional changes lead to the differential
regulation of specific biological functions in subsets of cell layers, several of which correspond to
observable physiological changes. We showed that known stress pathways primarily control
semiubiquitous responses and used mutants that disrupt epidermal patterning to reveal
cell-layer–specific and inter–cell-layer effects. By performing a similar analysis using iron
deprivation, we identified common cell-type–specific stress responses and revealed the crucial
role the environment plays in defining the transcriptional outcome of cell-fate decisions.
H
igh salinity is an important agricultural
contaminant (1) and has complex effects
on root physiology. Although a small set
of studies has begun to explore salt responses at
the cell-type–specific level (2, 3), it remains unclear
to what extent cell identity influences stress
responses and what mechanisms enable this regulation.
To directly address these issues, we generated
a genome-scale, high-resolution expression
map for roots grown under standard and highsalinity
conditions (4). We first performed a phenotypic
analysis using different concentrations of
salt and a time-course analysis [TC data set in the
supporting online material (SOM) text, Fig. 1, A
and F, fig. S1, and tables S1 and S2)] of the
response of whole roots to salt to select the
specific parameters (1 hour of exposure to 140
mM NaCl) for our spatial microarray analysis.
The root of Arabidopsis grows from stem
cells at the tip. We dissected roots into four longitudinal
zones (LZ data set in Fig. 1A and table
S1) for analysis, using the position of cells along
the longitudinal axis as a proxy for developmental
time (fig. S2) (5). Cell identity varies along the
radial axis; epidermal cells constitute the outermost
tissue, followed by the cortex, endodermis, and the
central stele (fig. S2). Cell-type–specific transcriptional
profiles were generated by fluorescenceactivated
cell sorting (FACS) of roots that express
green fluorescent protein (GFP) reporters in specific
cell types (6, 7) (RZ data set in Fig. 1A and
table S1). Six different GFP reporters were used
to profile all radial zones, including the columella
root cap and phloem vasculature (fig. S3 and
table S3). Intact roots rather than protoplasted or
isolated populations of cells were exposed to salt
to ensure that the observed transcriptional
response occurred in the context of the whole
organ. We performed control experiments to test
the effects of sorting on salt-responsive genes
(SOM text and tables S4 and S5) and used GFP
reporters (8) along with image analysis software
(9) to validate the accuracy of the RZ microarray
data (Fig. 1, B to D, and figs. S4 and S5).
With stringent statistical significance criteria,
we identified increasing numbers of differentially
expressed genes at higher spatial resolution:
238 (at 1 hour), 1173, and 3862 genes were identified
in our TC, LZ, and RZ experiments, respectively
(Fig. 1A and table S2). Genes regulated in
our TC experiment tended to respond to salt
stress in multiple radial or longitudinal zones,
whereas the majority of genes regulated in the
spatial data sets changed in only one zone (Fig. 1,
E, G, and H, and fig. S6).
One explanation for the prevalence of celltype–specific
responses may be that salt might
not have fully penetrated all root tissues, which
led to localized responses. We found, however,
that internal tissues tend to be highly responsive;
48% of salt-responsive genes were regulated in
1
Department of Biology, Duke University, Durham, NC 27708,
USA. 2
Institute for Genome Sciences and Policy Center for
Systems Biology, Duke University, Durham, NC 27708, USA.
3
Department of Molecular, Cellular, and Developmental Biology,
University of Michigan, Ann Arbor, MI 48109, USA.
*These authors contributed equally to this work.
†Present address: Temasek Lifesciences Laboratory, National
University of Singapore, Singapore 117604, Singapore.
‡To whom correspondence should be addressed. E-mail:
philip.benfey@duke.edu
Fig. 1. Salt-stress microarray data sets. (A) Venn diagram showing overlap between data sets (1-hour TC
comparisons in parentheses). (B to D) Salt-responsive GFP-reporter [(B) and (C)] for At3g49760 and
associated microarray data (D). EPI, epidermis and lateral root cap; COL, columella root cap; COR, cortex;
END, endodermis and quiescent center; STE, stele; PHL, protophloem. (E) Percentage of genes regulated
in one to six cell types identified in the TC and RZ data sets, respectively. (F to H) Ten most common
transcriptional changes in each data set and percent of responsive genes in each experiment (bottom
row). Yellow indicates up-regulated genes; blue indicates down-regulated genes. (I) Enriched GeneOntology
categories. (J) Expression patterns for cell-shape regulators in response to salt. (K and L) Cortex
cells (arrowheads) swell in response to salt. cob-1 mutants are hypersensitive to NaCl. Scale bars indicate
50 mm [(B) and (C)] and 30 mm [(K) and (L)].
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the cortex (Fig. 1H), and similar numbers were
regulated in the stele (28%) and in the epidermis
(31%). Along the longitudinal axis, an increase
in salt responsiveness correlates with the beginning
of the elongation zone, in which cells
begin to acquire their final shape and function
(Fig. 1G).
Testing our LZ and RZ data sets for enrichment
in Gene-Ontology (10) annotations (Fig. 1I,
fig. S7, and tables S6 and S7), we found 50 to
82%, respectively, of enriched categories are zonespecific
(fig. S8), indicating that salt stress regulates
distinct processes on the basis of developmental
context. Categories associated with stresses, including
abscisic acid (ABA) response, tend to be
enriched in multiple cell types, suggesting that
most previously characterized stress-response
genes are not cell-type–specific.
Salt stress results in radial swelling of the
outer tissue layers of roots (Fig. 1K and fig. S9)
(11), resembling plants with mutations in genes
important for cell-wall biogenesis or with reduced
tubulin expression. Several of these genes
are repressed in the cortex and epidermis, including
COBRA (COB) (12), RADIAL SWELLING3
(RSW3) (13), TUBULIN ALPHA-6 (TUA6) (14),
and KOBITO1 (KOB1) (15) (Fig. 1J). GeneOntology
categories associated with these
functions are also enriched (Fig. 1I). Consistent
with these findings, a hypomorphic allele of COB
enhances the salt-regulated radial swelling of the
cortex, indicating that the expression changes
facilitate the cell-shape changes (Fig. 1, K and L,
and fig. S9).
We compared cis-element enrichment in the
promoters of genes regulated in a zone-specific
manner with genes regulated in at least three
zones (semiubiquitous responders) for the LZ and
RZ data sets, respectively (Fig. 2A and table S8).
In the LZ data set, enrichment of many known cis
elements, such as drought-responsive element
(DRE) (16) and ABA-responsive element (ABRE)
(17, 18), was observed in both gene sets, whereas
enrichment was largely limited to the semiubiquitous
gene set in the RZ data set. Thus, although
canonical stress-response pathways appear to be
active in all cell layers, cell-type–specific responses
are distinguishable at the promoter level and probably
controlled by other cis elements. This suggests
that cell-type–specific salt responses are not simply
controlled by a combination of stress- and
developmental-regulatory elements in a single
promoter.
The plant hormone ABA is known to mediate
stress responses, and ABA-response mutants are
partly resistant to high salinity (19). Strong enrichment
of ABRE cis elements in the promoters
of semiubiquitous responders suggested that
ABA activity is present throughout the root. To
test this, we examined the salt responsiveness of
hormone-marker genes (20). We find enrichment
of up-regulated ABA-marker genes in all cell
layers of the root (Fig. 2B and table S9) but not
for other hormones (fig. S10B). This apparent
widespread activity suggested that ABA might
primarily mediate semiubiquitous transcriptional
responses to salt. We therefore monitored the effects
of ABA deficiency on the expression of a
set of cell-type–specific, salt-stress–activated genes
(21, 22). We find that salt-induced expression is
diminished for many of these genes, similar to a
collection of semiubiquitous responders also
tested (Fig. 2, C and D). Together, these results
indicate that ABA regulates cell-type–specific
responses to salt stress in a manner independent
of characterized ABRE elements.
DRE and its derivatives are bound by a subclass
of APETALA2 (AP2)– and ethylene-responsive
element-binding protein–type transcription factors,
such as DREB2A (23, 24). Strong DRE enrichment
is detected in genes up-regulated in at least
three radial zones (Fig. 2A). Consistent with this,
DREB2A is expressed in all cell layers under saltstress
conditions (fig. S10C). Recently, potential
direct targets of DREB2A have been identified
(25). These targets tend to be up-regulated by
salt in at least three cell types at a higher frequency
than expected (P = 6.5 × 10−6
, Fig. 2E,
and table S10), supporting the hypothesis that the
DRE/DREB2A regulatory module primarily controls
semiubiquitous responses.
Fig. 2. Regulation of salt responses. (A) Enriched known cis-elements. Gene sets in red contain
fewer than 50 genes. Shading indicates increasing statistical significance from P = 1 × 10–3
to P =
1 × –10
; yellow box indicates cell-type–specific enriched cis elements. Figure S10A shows cis
elements enriched in salt-repressed gene sets. (B) ABA-marker genes are up-regulated and
enriched (asterisks, P < 1 × 10−4
) in all cell layers. (C and D) The aba-2 mutation significantly
affects semiubiquitous and cell-type–specific salt-responsive genes (asterisks, P < 0.05). (E)
DREB2A overexpression (OE) targets tend to be regulated in multiple cell types by salt. (F and G)
Gene sets regulated by epidermal patterning and salt stress. (H) Hair-cell regulators are
dynamically expressed in response to salt. (I and J) Hair-cell outgrowth is transiently suppressed
by salt stress. Scale bars, 100 mm [(I) and (J)].
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To understand how developmental pathways
regulate salt responses, we transcriptionally profiled
three mutants that alter cell-fate decisions in
the epidermis: werewolf myb23, caprice triptychon
(26), and scrambled (27) (fig. S11, A to D, and
table S11). By using less-stringent significance
criteria to aid in the identification of cell-type–
specific responses, we identified four sets of genes
whose activation or repression by salt is dependent
on correct epidermal patterning (Fig. 2, F and G,
fig. S11, F and G, and table S12). One gene set
whose expression is hair-identity–dependent and
repressed by salt shows enriched epidermal expression
in the RZ data set under standard conditions,
indicating that these genes are likely to be
hair-cell–specific and salt-responsive (Fig. 2F).
Root-hair elongation is inhibited by salt stress (28),
and we find that many of these repressed genes
encode structural components of the cell wall
(P = 1 × 10−8
) or are involved in trichoblast (haircell
precursor) differentiation (P = 1 × 10−4
).
Several of these genes, such as COBL9 (29) and
ROOT HAIR DEFECTIVE2 (RHD2) (30), show
fluctuating expression in the TC data set (Fig.
2H). By quantifying trichoblast cells that failed to
form hairs, we were able to track the effects of
salt stress on hair development. Hair outgrowth
was initially suppressed by salt stress, then
resumed after 8 hours of treatment (Fig. 2, I and
J, and fig. S11E). Thus, the response of roots is not
static but changes over time, potentially as a result
of adaptation.
Unexpectedly, 51% of the genes whose expression
is affected by salt and epidermal patterning
are exclusively regulated in nonepidermal
cell types, based on the RZ data set (table S12).
Thus, cell-fate decisions may have nonautonomous
effects on responses in other cell layers. We also
identified 47 genes that respond most dramatically
in hairless caprice triptychon mutants,
indicating that a component of the variation in
response is a direct outcome of changes in cell
identity and not solely the effects of enhanced salt
absorption in genetic backgrounds that develop
hairs (fig. S11, F and G, and table S12).
To determine whether the trends we observed
for salt stress hold for other environmental stimuli,
we generated TC, LZ, and RZ data sets for roots
exposed to iron-deficient media (–Fe, tables S1
and S2; control experiments described in SOM).
On the basis of the TC data, we performed the LZ
and RZ profiling at 24 hours. Iron is a necessary
micronutrient and is used in diverse processes
from photosynthesis to metabolism. Similar to
the salt stress data set, increasing numbers of
differentially expressed genes were detected with
increasing spatial resolution [at 24 hours: TC,
111 genes; LZ, 142 genes; and RZ, 1318 genes]
(Fig. 3A). Most genes are regulated in a zonespecific
manner (Fig. 3, B to D, and fig. S12, A
and B). Unlike salt stress, iron deprivation
elicited the strongest transcriptional response
after 24 hours of treatment in LZ 4 (85%) and
in the stele (36%), where iron is predominantly
stored in seeds and circulated in adult plants (31)
(Fig. 3, E to G, and fig. S12D). Putative and
known genes encoding iron transporter, chelator,
storage, metabolic, and regulatory proteins
responded in a cell-type–specific manner (Fig.
3H and table S18) (32, 33). The stele response
was enriched for generalized stress-responsive
genes and suggests that iron deficiency may be
sensed internally (Fig. 3I). Consistent with known
roles in nutrient absorption, genes activated in
the epidermis were enriched for metal-ion transport
and nicotianamine (metal chelator) biosynthesis
(Fig. 3I, fig. S12A, and table S7). Additionally,
cell-wall biogenesis and organization
genes, such as the proline-rich extensins associated
with root-hair morphogenesis (29), were downregulated
in epidermal cells and may explain
the observed changes in root-hair morphology
(Fig. 3, J and K) (34).
A comparison of the two RZ data sets revealed
that 20% of salt-responsive genes also
responded to iron deprivation (Fig. 4B and table
S15). Of these, about half are scored with similar
transcriptional changes across all five cell types
(Fig. 4A). We initially hypothesized that semiubiquitous
salt-responsive genes would be most
likely to encompass a general stress response;
Fig. 3. Iron-deficiency microarray data sets. (A) Venn diagram showing overlap between data sets
(1-hour TC comparisons in parentheses). (B) Iron-deficiency responsive GFP reporter (At1g08930)
and associated microarray data (C). (D) Percentage of genes regulated in one to six cell types
identified in the TC and RZ data sets, respectively. (E to G) Ten most common transcriptional changes
in each data set and percent of the total responsive genes in each experiment (bottom row). Yellow
indicates up-regulated genes; blue indicates down-regulated genes. (H) Regulation of putative and
known iron-deprivation response genes. Yellow indicates up-regulated genes; blue indicates downregulated
genes (At5g53550, FDR = 2.7 × 10−5
). (I) Enriched Gene-Ontology categories. miRNA,
microRNA; RNase, ribonuclease; GTPase, guanosine triphosphatase. (J) Expression patterns for cell-wall
biogenesis genes in response to iron deprivation (At3g49840, At3g54580, At4g08410, At5g06630, and
At5g06640). (K) Root hairs are shorter and misshapen (arrows) in response to iron deprivation. Scale bars,
50 mm [(B)and (K)].
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however, genes responsive to salt in all five
layers are the least likely to be coregulated by
iron deprivation, indicating greater environmental
specificity for these genes (Fig. 4B). This
suggests that cell-type–specific biological processes
are common targets for stress regulation,
whereas responses occurring in all cells must be
finely tuned for specific stimuli. To better understand
shared responses, we used the AffinityPropagation
clustering algorithm (35) to identify
gene sets that coclustered in the iron-deprivation
and salt-stress data sets (super clusters, table
S15). The largest set of coregulated genes displayed
concerted down-regulation in the epidermis
and encoded genes important for protein
biosynthesis (Fig. 4C and fig. S13A). Both
stresses result in reduced root length (figs. S1,
A to C, and S12C); this super cluster may represent
a common stress module associated with
growth suppression.
Previously we have shown that under standard
conditions, many biological functions are
regulated in a cell-type–specific manner (6, 36).
On comparison of expression under standard conditions
with these two stresses, we find that only
15% of cell-type–specific biological functions enriched
under standard conditions are conserved
(Fig. 4D, fig. S13, E and F, and table S16). Thus,
the majority of a cell type’s unique physiology is
environment-dependent. Although the percent of
genes that exhibited stable expression patterns between
standard conditions and each stress varied
for most cell types, the epidermis consistently
showed the least conservation (13 to 15%) (Fig.
4E). This trend holds despite the epidermis not
being the most responsive cell type for either
stress and suggests the functions that define this
layer are particularly dependent on environmental
constraints.
We identified 244 genes that are cell-type–
specific and whose expression pattern does not
substantially change with either stress (table S16).
Enriched Gene-Ontology categories are consistent
with known functions, and we discovered chloroplast
accumulation as a novel feature of the cortex
in light-grown roots (Fig. 4, Fand G). Additionally,
this gene set is enriched for many known regulators
of cell identity (table S17), suggesting that a small
set of core regulators maintain cell identity independent
of environmental fluctuations.
Our results reveal that the transcriptional state
of a cell is largely a reaction to environmental
conditions that are regulated by a smaller core set
of genes that stably determines cell identity. The
use of environmental stimuli combined with celland
developmental-stage–specific profiling will
enable the identification of high-confidence transcriptional
modules, an important first step in
modeling transcriptional networks in multicellular
organisms.
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supported by a Ruth Kirschstein National Research
Service Award postdoctoral fellowship, T.A.L. by an NSF
Minority Postdoctoral Research Fellowship, and S.M.B. by
a Natural Sciences and Engineering Research Council
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The authors have declared that no competing interests
exist. The National Center for Biotechnology Information
Gene Expression Omnibus accession numbers for new
microarray data discussed in this manuscript are
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Supporting Online Material
www.sciencemag.org/cgi/content/full/320/5878/942/DC1
Materials and Methods
SOM Text
Figs. S1 to S13
Tables S1 to S18
References
5 December 2007; accepted 19 March 2008
10.1126/science.1153795
Fig. 4. Comparison of
stresses. (A) Percent of irondeprivation–
and saltstress–coregulated
genes
that exhibit identical (region
5) or completely dissimilar
(region 0) regulation
in the RZ data set. (B) Percent
of salt-stress–responsive genes that are also iron-deprivation responsive and the number of cell
layers in which those genes respond under salt stress. Overall overlap is 20% (red line). (C) Super cluster
(no. 406). Figure S13 lists other super clusters. (D) Gene-Ontology categories enriched in gene sets with
environment-dependent cell-type–specific expression. (E) Percent conservation of cell-type–specific gene
sets comparing standard conditions with stress gene sets, respectively. (F) Gene-Ontology categories
enriched in gene sets with environment-independent cell-type–specific expression. (G) Chloroplast
enrichment in the cortex (c). Chloroplasts also accumulate in the pericycle, which was not specifically
profiled in these experiments. Scale bar, 50 mm.
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ERRATUM
www.sciencemag.org SCIENCE ERRATUM POST DATE 3 October 2008 1
CORRECTIONS&CLARIFICATIONS
Reports: “Cell identity mediates the response of Arabidopsis roots to abiotic stress” by J. R.
Dinneny et al. (16 May, p. 942). On page 945, the URL for the supporting online material was
incorrect. The correct URL is www.sciencemag.org/cgi/content/full/1153795/DC1.
Post date 3 October 2008
onSeptember18,2012www.sciencemag.orgDownloadedfrom