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1 cell plate while the plate is stabilized by callose.
2 itive papillary accumulation of GFP-PEN1 and callose.
3 bably due to partial sieve tube occlusion by callose.
4 rolonged staining for the cell-plate polymer callose.
5 opic deposition of pectins, xyloglucans, and callose.
6 llulose synthase might be able to synthesize callose.
7 allose synthase activity and accumulate more callose.
8 colorized aniline blue, a stain specific for callose.
9 r material, with very little accumulation of callose.
10 by plants to fungal attack is deposition of callose, a (1,3)-beta-glucan polymer, in the form of cel
15 dition, both MAMPs also caused deposition of callose, a well-known marker of MAMP-elicited defense.
18 smonic acid-deficient plants caused enhanced callose accumulation and heightened resistance to CLA, s
19 anases (PdBGs) were identified that regulate callose accumulation and the number and distribution of
21 kob1-3, we did not detect drastic changes in callose accumulation at the neck regions of the plasmode
26 late-specific post-Golgi vesicle traffic and callose accumulation was analyzed using ES7, and it reve
27 uced genes in Sw-7 include those involved in callose accumulation, lignin deposition, proteolysis pro
28 c effects on membrane localization of SS and callose accumulation, whereas Ca(2+) addition reversed t
29 diates, deposition of phenolic compounds and callose, accumulation of phytoalexin, and expression of
30 veloped systemic priming of chitosan-induced callose after single inoculations with R. irregularis or
32 timely appearance of papillae, which contain callose and extracellular membrane material, as well as
33 atgpi8-1 mutants accumulate higher levels of callose and have reduced plasmodesmata permeability.
35 modesmata is important for the regulation of callose and LR development as part of the plant response
37 fications that include cell wall thickening, callose and phloem protein induction, and cellular plugg
38 efences dependent on signalling through ROS (callose and PR gene expression) were also modified or ab
39 se observations demonstrate that appropriate callose and sterol biosynthesis are required for maintai
40 res characterized by ectopic accumulation of callose and the occurrence of incomplete cell walls.
41 icles in cells containing elevated levels of callose and their reduction under ES7 treatment further
42 llular location to participate in cellulose, callose, and starch biosynthesis through its interaction
47 urity, and produce cell walls with excessive callose as revealed through staining with the aniline bl
48 ming of multiple immune responses, including callose-associated cell wall defenses that are under con
49 bidopsis but failed to elicit high levels of callose-associated defense in Arabidopsis plants blocked
51 ose synthase that mediates the deposition of callose at developing cell plates, root hairs, and plasm
53 n of the (1,3)-beta-glucan cell wall polymer callose at sites of attempted penetration is a common pl
55 rtly by the deposition of the glucan polymer callose at the cell wall at the site of pathogen contact
58 I3 However, als4 and als7 did not accumulate callose at this AlCl3 concentration even though root gro
59 4 (pmr4), a mutant lacking pathogen-induced callose, became resistant to pathogens, rather than more
64 idylinositol-anchored proteins Plasmodesmata Callose Binding 1 and the beta-1,3-glucanase PdBG2 and a
65 d-associated beta-1,3-glucanase (BG_pap) and CALLOSE BINDING PROTEIN1 (PDCB1) were identified as key
66 e suppression of the innate immunity-related callose biosynthesis and, hence, the progress of F. gram
72 ncluding radial swelling and accumulation of callose, can be mimicked with the inhibitor of N-glycosy
73 pe is dependent on the deposition of a thick callose-containing layer outside of the endosperm cell w
76 ed production of reactive oxygen species and callose depends on specific signaling events that lead t
77 se which is responsible for the synthesis of callose deposited at the primary cell wall of meiocytes,
78 e-specific conductivity and its reduction by callose deposition after injury was calculated for green
79 re is not an obligatory relationship between callose deposition and Al-induced inhibition of root gro
80 of the pathogenesis-related protein PR-1 and callose deposition and also plays a role in CRN2-induced
81 s also induced upon treatment with flg22 and callose deposition and cell death suppression assays in
83 ing gold labeling, modification of the CW by callose deposition and cellulose reduction was observabl
84 tance to pathogens and are required for both callose deposition and glucosinolate activation, suggest
86 alone increased aphid arrestment, suppressed callose deposition and increased the abundance of free a
87 on and downstream defence responses, such as callose deposition and pathogenesis-related (PR) gene ex
88 callose synthase PMR4 revealed that enhanced callose deposition and penetration resistance were PMR4-
90 nt of mlo2 mutant plants-exhibit spontaneous callose deposition and signs of early leaf senescence.
92 GAT1 thioredoxin in the redox regulation of callose deposition and symplastic permeability that is e
93 o activate cell wall-based responses such as callose deposition and that constitutive activation of B
94 luding induction of plant defence signalling callose deposition and the strengthening of plant cell w
95 eal that reactive oxygen species spiking and callose deposition are dispensable for the repression of
97 n to HDMBOA-Glc were associated with reduced callose deposition as an aphid defense response in vivo.
98 However, mlo3 genotypes display spontaneous callose deposition as well as signs of early senescence
99 Golovinomyces cichoracearum due to enhanced callose deposition at early time points of infection, wh
100 y upregulated by flg22 and facilitates rapid callose deposition at plasmodesmata following flg22 trea
101 SYNTHASE-LIKE 8 (GSL8), that is required for callose deposition at the cell plate, cell wall and plas
102 erea, production of reactive oxygen species, callose deposition at the cell wall, and enhanced PATHOG
105 tic model that highlights the differences in callose deposition between the resistant transgenic line
106 X-derived metabolites contribute to enhanced callose deposition by providing heightened resistance to
107 es an SA-independent pathway contributing to callose deposition by reducing accumulation of an indole
109 pression of HopAO1 in Arabidopsis suppresses callose deposition elicited by the Pst DC3000 hrpA mutan
110 hotoassimilate export in vte2 coincides with callose deposition exclusively in phloem parenchyma tran
113 allose synthase gene, and is responsible for callose deposition in developing sieve elements during p
114 r pattern (PAMP)-induced gene expression and callose deposition in host tissue, indicating that XopN
115 levated cytosolic Ca(2+) levels and enhanced callose deposition in hydathodes of seedlings treated wi
118 duction of reactive oxygen species (ROS) and callose deposition in pcrk1 mutant plants to determine t
120 n of PRX33 and PRX34 exhibit reduced ROS and callose deposition in response to microbe-associated mol
121 lent and avirulent Hpa, as well as decreased callose deposition in response to non-pathogenic Pseudom
124 the accumulation of reactive oxygen species, callose deposition in the cell wall, and the generation
125 t of host genes, compromised defense-related callose deposition in the host cell wall, and permitted
126 limitation, cell-specific apoplastic Fe and callose deposition in the meristem and elongation zone o
128 d genes PARG2 and NUDT7 and observed altered callose deposition in the presence of a chemical PARP in
132 The Delta CEL mutant activated SA-dependent callose deposition in wild-type Arabidopsis but failed t
133 PRR- and ACD6-dependent signaling to induce callose deposition independent of the presence of PAMPs.
135 ns in IBA-stimulated root growth modulation, callose deposition induced with a conserved peptide epit
141 , callose synthase gene RNAs accumulated and callose deposition was observed in SLWF-infested tissue.
145 ore, feeding by CLA on Mp708 plants enhanced callose deposition, a potential defense mechanism utiliz
146 one (oxo-C14-HSL) primed plants for enhanced callose deposition, accumulation of phenolic compounds,
147 nip mosaic virus (TuMV) infection suppresses callose deposition, an important plant defense induced i
149 splay a severe dwarf phenotype, constitutive callose deposition, and constitutive expression of patho
150 d upregulation of PTI marker genes, impaired callose deposition, and defective stomatal closure.
153 FLG22-INDUCED RECEPTOR-LIKE KINASE1, reduced callose deposition, and mitogen-activated protein kinase
154 ayed upregulation of PTI marker genes, lower callose deposition, and mitogen-activated protein kinase
155 responses including defense gene expression, callose deposition, and reactive oxygen species (ROS) an
156 ts have lower H(2)O(2) accumulation, reduced callose deposition, and reduced electrolyte leakage upon
157 ating bacterial colonization, suppression of callose deposition, and targeting the plant defense regu
158 does not affect hemicellulose strengthening, callose deposition, and the synthesis of structural defe
159 suppressed cell wall alterations, including callose deposition, characteristic of basal defence and
160 cies, mitogen-activated protein kinases, and callose deposition, corroborating a close link between t
161 r profile, abnormal Ubisch bodies, disrupted callose deposition, defective pollen wall formation such
162 ed with the monitoring of pathogen-triggered callose deposition, have identified major roles in patho
163 ygen species production but had no impact on callose deposition, indicating that CA-MPK4 allows discr
164 ecular patterns (flg22 and elf18), including callose deposition, lignin deposition, pigment accumulat
165 rides), which leads to premature cell death, callose deposition, or phloem protein accumulation, caus
166 due to constitutive defense-gene expression, callose deposition, reactive oxygen species (ROS) accumu
167 ecular pattern-triggered immunity, including callose deposition, reactive oxygen species burst and WR
168 n of the cell-growth phenotype and increased callose deposition, suggesting a role for SA in regulati
182 nthase activity was correlated with enlarged callose deposits and the focal accumulation of green flu
183 the pmr4 disruption mutant background, with callose deposits at the site of attempted fungal penetra
187 vary and the pollen tubes exhibited abnormal callose deposits throughout the tube and in the tips.
188 f directly inoculated spikelets, while these callose deposits were not observed in infections by the
189 sporocytes are abnormal in appearance and in callose distribution and they fail to proceed through me
191 ether, these data show the essential role of callose during the late stages of cell plate maturation
192 s of developing sieve elements revealed that callose failed to accumulate in the plasmodesmata of inc
195 ol primary root growth via meristem-specific callose formation, likely triggered by LPR1-dependent re
199 egulates the level of plasmodesmal-localized callose in order to locally downregulate symplasmic perm
203 d the accumulation of the cdiGRP protein and callose in vasculature-associated cells with or without
204 er EXO70B1 or EXO70E2 inhibited secretion of callose induced by the bacterial flagellin-derived pepti
209 ccharide biosynthesis is that cellulose (and callose) is synthesized at the plasma membrane (PM), whe
216 mber and position using aniline blue-stained callose, mCitrine-labeled material was used to calculate
219 nd maintaining the positional specificity of callose-modifying glycosylphosphatidylinositol proteins
220 protein (GFP) and aniline blue (a stain for callose normally observed at plasmodesmata) and found th
223 se responses, which induced the formation of callose papillae, hydrogen peroxide accumulation and the
224 strongly induced the deposition of spot-like callose patches in vascular bundles of directly inoculat
225 nt cell walls, does not contain cellulose or callose, pectin methylesterases (PMEs) likely play a cen
226 minal fucose residues on the side chain, and callose persists in the cell walls after the cell plates
229 erm pollen tubes all have callosic walls and callose plugs (in contrast, no gymnosperms have these fe
230 ines the sites of Fe accumulation as well as callose production, which interferes with symplastic com
233 not release the microspores, suggesting that callose removal is not sufficient to disperse the micros
234 tion, suggesting that the pathogen-triggered callose response is required for resistance to microbial
236 mpatibility showed a synergistic increase in callose responsiveness following co-inoculation with bot
237 cell wall layer, highly autofluorescent and callose rich, deposited only in the upper part of the tr
238 and the basal parts of mature trichome by a callose ring that is also deposited in an EXO70H4-depend
245 t cells over-expressing CalS1 display higher callose synthase activity and accumulate more callose.
246 small molecule endosidin 7 (ES7) inhibiting callose synthase activity and arresting late cytokinesis
249 es were separated from the majority (80%) of callose synthase activity, a marker for the plasma membr
250 fer UDP-glucose from sucrose synthase to the callose synthase and thus help form a substrate channel
251 gene encoding a putative cell plate-specific callose synthase catalytic subunit (CalS1) was recently
255 tdy2 mutants provides evidence that the Tdy2 callose synthase functions in vascular maturation and th
257 demonstrate that CalS7 is a phloem-specific callose synthase gene, and is responsible for callose de
259 und configuration, suggesting that the plant callose synthase may be regulated by Rop1 through the in
261 disruption mutant lacking the stress-induced callose synthase PMR4 revealed that enhanced callose dep
262 ET2 encodes GLUCAN SYNTHASE-LIKE8 (GSL8), a callose synthase that mediates the deposition of callose
263 ta suggest that UGT1 may act as a subunit of callose synthase that uses UDP-glucose to synthesize cal
264 te that one of these genes, CalS5, encodes a callose synthase which is responsible for the synthesis
267 This resistance was due to mutation of a callose synthase, resulting in a loss of the induced cal
268 TANT4 (PMR4), which encodes a stress-induced callose synthase, under the control of the constitutive
272 past five years, identification of genes for callose synthases has proven difficult because cognate g
276 The induction of cell wall apposition and callose synthesis led us to hypothesize that Yariv bindi
277 f CalS1 in transgenic tobacco cells enhanced callose synthesis on the forming cell plate, and that th
288 hey are responsible for the formation of the callose wall that separates the microspores of the tetra
289 eeping specific membrane domains next to the callose wall to prevent formation of exine at these site
290 etween the plasma membrane and the overlying callose wall, and requires the normal callose wall forma
292 lete meiosis I, but they do not have a thick callose wall; they often fail to complete meiotic cytoki
299 e may be the plant cell wall polysaccharide, callose, which is a polymer of beta-1,3-linked glucose.
301 small sieve plate pores might be occluded by callose within minutes, but plants containing sieve tube