A non-cell-autonomous mechanism for the control of plant architecture and epidermal differentiation involves intercellular trafficking of BREVIPEDICELLUS protein

2009 ◽  
Vol 36 (3) ◽  
pp. 280 ◽  
Author(s):  
Yeonggil Rim ◽  
Jin-Hee Jung ◽  
Hyosub Chu ◽  
Won Kyong Cho ◽  
Seon-Won Kim ◽  
...  
Keyword(s):  
Plant Architecture ◽  
Cortical Cell ◽  
Epidermal Differentiation ◽  
Intercellular Trafficking ◽  
Autonomous Function ◽  
In The Wild ◽  
Cell Layers ◽  
Function Expression ◽  
Knox Proteins ◽  
Mutant Phenotypes

Intercellular trafficking of maize KNOTTED1 and its homologous KNOTTED1-related homeobox (KNOX) proteins has been reported; however, little is known about the functional significance of KNOX trafficking in plant development. In this study, we showed that intercellular movement of BREVIPEDICELLUS (BP or KNAT1), the closest Arabidopsis homologue of KNOTTED1, is tissue-specific and takes place through a selective pathway. When BP was fused to a red fluorescent mCherry construct, it could move from the mesophyll to epidermal cells of leaves, although it could not move out from the cortex/endodermis of roots. Using a trichome rescue-trafficking assay, we also showed that BP fusion could confer gain-of-trafficking function to the cell-autonomous GLABROUS1 (GL1) protein. In the wild type, BP transcripts are expressed in the sub-epidermal cortical cell layers of the inflorescence stem and pedicel. However, bp mutant phenotypes include defects in epidermal cell differentiation suggesting a non-cell-autonomous function. Expression of a GFP:BP fusion under the control of a BP promoter specific to the stem cortex layers resulted in epidermal GFP fluorescence suggesting its movement from subepidermis to epidermis. Here, we provide evidence from complementation analyses using cell autonomous or non-cell-autonomous BP fusions that the intercellular trafficking of BP protein is important for plant architecture and epidermal differentiation.

scholarly journals Neural Activity in Frontal Cortical Cell Layers: Evidence for Columnar Sensorimotor Processing

2011 ◽  
Vol 23 (6) ◽  
pp. 1507-1521 ◽  
Author(s):  
Ioan Opris ◽  
Robert E. Hampson ◽  
Terrence R. Stanford ◽  
Greg A. Gerhardt ◽  
Sam A. Deadwyler
Keyword(s):  
Nonhuman Primates ◽  
Cortical Cell ◽  
Microelectrode Arrays ◽  
Sensory Information ◽  
Simultaneous Recording ◽  
Functional Interaction ◽  
Sensorimotor Processing ◽  
Differential Encoding ◽  
Layer 2 ◽  
Cell Layers

The mammalian frontal cortex (FCx) is at the top of the brain's sensorimotor hierarchy and includes cells in the supragranular Layer 2/3, which integrate convergent sensory information for transmission to infragranular Layer 5 cells to formulate motor system outputs that control behavioral responses. Functional interaction between these two layers of FCx was examined using custom-designed ceramic-based microelectrode arrays (MEAs) that allowed simultaneous recording of firing patterns of FCx neurons in Layer 2/3 and Layer 5 in nonhuman primates performing a simple go/no-go discrimination task. This unique recording arrangement showed differential encoding of task-related sensory events by cells in each layer with Layer 2/3 cells exhibiting larger firing peaks during presentation of go target and no-go target task images, whereas Layer 5 cells showed more activity during reward contingent motor responses in the task. Firing specificity to task-related events was further demonstrated by synchronized firing between pairs of cells in different layers that occupied the same vertically oriented “column” on the MEA. Pairs of cells in different layers recorded at adjacent “noncolumnar” orientations on the MEA did not show synchronized firing during the same task-related events. The results provide required evidence in support of previously suggested task-related sensorimotor processing in the FCx via functionally segregated minicolumns.

scholarly journals Modification of cell surface glycoprotein: addition of fucosyl residues during epidermal differentiation.

1982 ◽  
Vol 95 (2) ◽  
pp. 626-631 ◽  
Author(s):  
J D Zieske ◽  
I A Bernstein
Keyword(s):  
Cell Surface ◽  
Lectin Binding ◽  
Epidermal Cells ◽  
Epidermal Differentiation ◽  
Surface Glycoprotein ◽  
Basal Cells ◽  
Cell Surface Glycoprotein ◽  
Similar Treatment ◽  
Differentiated Cells ◽  
Cell Layers

When cutaneous sections from the newborn rat were treated with alpha-fucosidase, Ulex europeus agglutinin I (UEA) binding to the cell surface of the differentiated cells in the epidermis was diminished and there was an appearance in these cell layers of binding by Bandeiraea simplicifolia I-B4 lectin (BS I-B4), which normally is specific for the basal cells. A similar treatment with alpha-galactosidase resulted in a loss of BS I-B4 binding, but had no effect on UEA binding. Glycoproteins isolated from the membranes of epidermal cells showed a threefold increase in the ratio of binding to UEA versus BS I-B4 affinity columns as the proteins were derived from the more differentiated cell populations. These data suggest that alpha-fucosyl residues are added to the glycoproteins on the cell surfaces of differentiated cells, thus blocking alpha-galactosyl residues and changing the lectin binding specificity as epidermal cells move out of the basal cell layer.

scholarly journals A Cytochrome P450 Gene Is Differentially Expressed in Compatible and Incompatible Interactions Between Pepper (Capsicum annuum) and the Anthracnose Fungus, Colletotrichum gloeosporioides

1999 ◽  
Vol 12 (12) ◽  
pp. 1044-1052 ◽  
Author(s):  
Boung-Jun Oh ◽  
Moon Kyung Ko ◽  
Young Soon Kim ◽  
Kwang Sang Kim ◽  
Igor Kostenyuk ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Capsicum Annuum ◽  
Epidermal Cell ◽  
Colletotrichum Gloeosporioides ◽  
Defense Mechanism ◽  
Cortical Cell ◽  
Infection Process ◽  
Compatible Interaction ◽  
Incompatible Interaction ◽  
Cell Layers

The anthracnose fungus, Colletotrichum gloeosporioides, was previously shown to have an incompatible interaction with ripe-red fruit of pepper (Capsicum annuum). However, the fungus had a compatible interaction with unripe-mature-green fruit. Using mRNA differential display, we isolated and characterized a PepCYP gene expressed in the incompatible interaction. The PepCYP gene encodes a protein homologous to cytochrome P450 proteins containing a heme-binding domain. The expression level of PepCYP is higher in the incompatible interaction than in the compatible interaction, and then remains elevated in the incompatible interaction. In the compatible interaction, the expression of PepCYP is transient. The induction of Pep-CYP gene is up-regulated by wounding or jasmonic acid treatment during ripening. Analysis of PepCYP expression by in situ hybridization shows that the accumulation of PepCYP mRNA is localized in the epidermal cell layers, but not in the cortical cell layers. An examination of transverse sections of the fruits inoculated with the fungus shows that the fungus invades and colonizes the epidermal cell layers of the unripe fruit at 24 and 72 h after inoculation, respectively, but not those of the ripe fruit. These results suggest that the PepCYP gene product plays a role in the defense mechanism when the fungus invades and colonizes the epidermal cells of fruits in the incompatible interaction during the early fungal infection process.

Nature of Mutations Conferring Resistance to 8-Azaguanine in Mouse Cell Lines

1974 ◽  
Vol 14 (2) ◽  
pp. 235-251
Author(s):  
SEUNG-IL SHIN
Keyword(s):  
Rabbit Antiserum ◽  
Low Frequency ◽  
Mouse Cell ◽  
Parental Cell ◽  
Parental Cell Line ◽  
Wild Type ◽  
Mouse Tissues ◽  
In The Wild ◽  
Normal Enzyme ◽  
Mutant Phenotypes

Two stable mouse cell mutants A9 and RAG, which are resistant to 8-azaguanine and deficient in hypoxanthine-guanine phosphoribosyl transferase (HGPRT), have been studied in order to establish the nature of molecular changes conferring the mutant phenotypes. A specific precipitating rabbit antiserum was prepared against the normal HGPRT purified from mouse tissues, and used to test for cross-reacting material (CRM) in the mutant lysates. Neither mutants contained detectable cross-reacting material, as demonstrated by precipitation in-hibition tests. However, the L cell-derived mutant A9 was shown to have a low but significant level of HGPRT activity which was clearly different from that of the normal enzyme in the wild-type parental cell line. Compared to the wild-type enzyme, the HGPRT in A9 is extremely heat labile, and has an elevated substrate-binding constant in addition to distinct antigenic differences. Both A9 and RAG have been shown previously to revert to the normal phenotype with low frequency, thus ruling out gene deletions as a possible cause of the 8-azaguanine resistance. It is suggested that RAG could involve a recessive regulatory mutation, while A9 may contain a structurally altered HGPRT as a result of a missense mutation within the structural gene for this enzyme.

scholarly journals Identification of a Fourth Formate Dehydrogenase in Methylobacterium extorquens AM1 and Confirmation of the Essential Role of Formate Oxidation in Methylotrophy

2007 ◽  
Vol 189 (24) ◽  
pp. 9076-9081 ◽  
Author(s):  
Ludmila Chistoserdova ◽  
Gregory J. Crowther ◽  
Julia A. Vorholt ◽  
Elizabeth Skovran ◽  
Jean-Charles Portais ◽  
...  
Keyword(s):  
Formate Dehydrogenase ◽  
Wild Type ◽  
Methylobacterium Extorquens ◽  
Methanol Metabolism ◽  
Reading Frame ◽  
Formate Oxidation ◽  
In The Wild ◽  
Mutant Phenotypes ◽  
Small Open Reading Frame

ABSTRACT A mutant of Methylobacterium extorquens AM1 with lesions in genes for three formate dehydrogenase (FDH) enzymes was previously described by us (L. Chistoserdova, M. Laukel, J.-C. Portais, J. A. Vorholt, and M. E. Lidstrom, J. Bacteriol. 186:22-28, 2004). This mutant had lost its ability to grow on formate but still maintained the ability to grow on methanol. In this work, we further investigated the phenotype of this mutant. Nuclear magnetic resonance experiments with [13C]formate, as well as 14C-labeling experiments, demonstrated production of labeled CO2 in the mutant, pointing to the presence of an additional enzyme or a pathway for formate oxidation. The tungsten-sensitive phenotype of the mutant suggested the involvement of a molybdenum-dependent enzyme. Whole-genome array experiments were conducted to test for genes overexpressed in the triple-FDH mutant compared to the wild type, and a gene (fdh4A) was identified whose translated product carried similarity to an uncharacterized putative molybdopterin-binding oxidoreductase-like protein sharing relatively low similarity with known formate dehydrogenase alpha subunits. Mutation of this gene in the triple-FDH mutant background resulted in a methanol-negative phenotype. When the gene was deleted in the wild-type background, the mutant revealed diminished growth on methanol with accumulation of high levels of formate in the medium, pointing to an important role of FDH4 in methanol metabolism. The identity of FDH4 as a novel FDH was also confirmed by labeling experiments that revealed strongly reduced CO2 formation in growing cultures. Mutation of a small open reading frame (fdh4B) downstream of fdh4A resulted in mutant phenotypes similar to the phenotypes of fdh4A mutants, suggesting that fdh4B is also involved in formate oxidation.

scholarly journals Keratin alterations during embryonic epidermal differentiation: a presage of adult epidermal maturation.

1982 ◽  
Vol 93 (3) ◽  
pp. 551-559 ◽  
Author(s):  
S P Banks-Schlegel
Keyword(s):  
Molecular Weight ◽  
Stratum Corneum ◽  
Epidermal Differentiation ◽  
Molecular Weight Range ◽  
Cell Layers ◽  
Embryonic Skin ◽  
Thick Stratum ◽  
Keratin Proteins

Differentiation of the epidermis during embryonic rabbit development was found to be accompanied by dramatic changes in keratin proteins. Immunofluorescent labeling with keratin antiserum revealed that the undifferentiated epithelium of 12-d embryos was already committed to making keratin proteins. At 18 d of embryogenesis, the epithelium contained keratin proteins in the molecular weight range of 40,000-59,000. The stratification of the epithelium into two cell layers at 20 d of development coincided with the appearance of a 65-kdalton keratin. When a thick stratum corneum developed at 29 d, several additional keratins became prominent, most notably the large keratins (61- and 64-kdalton) and a 54-kdalton keratin. In addition, the 40-kdalton keratin, which had been present in earlier embryonic epidermis, disappeared. Newborn epidermis resembled that of a 29-d embryonic epidermis, with the exception of the appearance or increase in concentration of two more keratin species (46- and 50-kdalton). In vitro culturing of keratinocytes from 12- and 14-d embryonic skin demonstrated that these cells contained essentially the same keratin profiles as the undifferentiated epithelium of 18-d embryos (40-59 kdalton). Keratinocytes grown from older embryos contained increased amounts of keratin, similar to the in vivo situation, but did not synthesize the high molecular weight keratins. The changes observed during embryonic epidermal differentiation appear to be recapitulated during the sequential maturation steps of adult epidermis.

scholarly journals A Novel Population of Inner Cortical Cells in the Adrenal Gland That Displays Sexually Dimorphic Expression of Thyroid Hormone Receptor-β1

Endocrinology ◽  
2015 ◽  
Vol 156 (6) ◽  
pp. 2338-2348 ◽  
Author(s):  
Chen-Che Jeff Huang ◽  
Cary Kraft ◽  
Nicole Moy ◽  
Lily Ng ◽  
Douglas Forrest
Keyword(s):  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Thyroid Hormone Receptor ◽  
Cortical Cell ◽  
Sexually Dimorphic ◽  
Cortical Cells ◽  
Receptor Isoforms ◽  
Sexually Dimorphic Expression ◽  
Cell Layers ◽  
Inner Cortex

Abstract The development of the adrenal cortex involves the formation and then subsequent regression of immature or fetal inner cell layers as the mature steroidogenic outer layers expand. However, controls over this remodeling, especially in the immature inner layer, are incompletely understood. Here we identify an inner cortical cell population that expresses thyroid hormone receptor-β1 (TRβ1), one of two receptor isoforms encoded by the Thrb gene. Using mice with a Thrbb1 reporter allele that expresses lacZ instead of TRβ1, β-galactosidase was detected in the inner cortex from early stages. Expression peaked at juvenile ages in an inner zone that included cells expressing 20-α-hydroxysteroid dehydrogenase, a marker of the transient, so-called X-zone in mice. The β-galactosidase-positive zone displayed sexually dimorphic regression in males after approximately 4 weeks of age but persisted in females into adulthood in either nulliparous or parous states. T3 treatment promoted hypertrophy of inner cortical cells, induced some markers of mature cortical cells, and, in males, delayed the regression of the TRβ1-positive zone, suggesting that TRβ1 could partly divert the differentiation fate and counteract male-specific regression of inner zone cells. TRβ1-deficient mice were resistant to these actions of T3, supporting a functional role for TRβ1 in the inner cortex.

Histological study of syncytia induced in cereals by the Mediterranean cereal cyst nematode Heterodera latipons

Nematology ◽  
2008 ◽  
Vol 10 (2) ◽  
pp. 279-287 ◽  
Author(s):  
Yuji Oka ◽  
Mishael Mor ◽  
Yitzhak Spiegel
Keyword(s):  
Cell Wall ◽  
Histological Study ◽  
Parenchymal Cell ◽  
Cortical Cell ◽  
Syncytium Formation ◽  
Wheat Root ◽  
Heterodera Avenae ◽  
Vascular Cylinder ◽  
Cell Layers ◽  
Heterodera Latipons

AbstractFeeding sites of Heterodera latipons in wheat, barley and Lolium rigidum were studied and compared with those of Heterodera avenae in wheat. Juveniles of H. latipons penetrated mainly differentiated roots and chose a root cortical cell as their initial syncytium cell (ISC) in wheat and barley, whilst H. avenae chose a vascular parenchymal cell as an ISC. The cell associated with females in wheat root underwent hypertrophy, and incorporated endodermis, pericycle and parenchyma cells of the vascular cylinder by cell wall dissolution. Syncytia of H. latipons contained a high number of organelles, including endoplasmic reticulum, mitochondria, plastids and amoeboid nuclei, whilst those of H. avenae were highly vacuolated. The syncytium partly occupied both the cortex and the vascular cylinder in contrast to those of H. avenae, which occupied most of the space within the vascular cylinder near the infection site. The cortical cell associated with H. latipons males did not undergo hypertrophy, but had dense cytoplasm, and incorporation of other cells by cell wall dissolution was rare. A similar syncytium formation process was observed with barley, but a cortical cell, several cell layers away from the endodermis, was chosen for the ISC. In resistant L. rigidum, H. latipons juveniles chose an endodermal cell or its neighbouring cortical cell as an ISC. Partial dissolution of cell wall was observed in neighbouring parenchymal cells, although the nematode did not develop into adults.

scholarly journals Desmoglein 1–dependent suppression of EGFR signaling promotes epidermal differentiation and morphogenesis

2009 ◽  
Vol 185 (7) ◽  
pp. 1243-1258 ◽  
Author(s):  
Spiro Getsios ◽  
Cory L. Simpson ◽  
Shin-ichiro Kojima ◽  
Robert Harmon ◽  
Linda J. Sheu ◽  
...  
Keyword(s):  
Basal Layer ◽  
Growth Factor Receptor ◽  
Epidermal Differentiation ◽  
Keratinocyte Differentiation ◽  
Desmosomal Cadherins ◽  
Tissue Integrity ◽  
Extracellular Signal ◽  
Signaling Axis ◽  
Cell Layers ◽  
Dependent Cell

Dsg1 (desmoglein 1) is a member of the cadherin family of Ca2+-dependent cell adhesion molecules that is first expressed in the epidermis as keratinocytes transit out of the basal layer and becomes concentrated in the uppermost cell layers of this stratified epithelium. In this study, we show that Dsg1 is not only required for maintaining epidermal tissue integrity in the superficial layers but also supports keratinocyte differentiation and suprabasal morphogenesis. Dsg1 lacking N-terminal ectodomain residues required for adhesion remained capable of promoting keratinocyte differentiation. Moreover, this capability did not depend on cytodomain interactions with the armadillo protein plakoglobin or coexpression of its companion suprabasal cadherin, Dsc1 (desmocollin 1). Instead, Dsg1 was required for suppression of epidermal growth factor receptor–Erk1/2 (extracellular signal-regulated kinase 1/2) signaling, thereby facilitating keratinocyte progression through a terminal differentiation program. In addition to serving as a rigid anchor between adjacent cells, this study implicates desmosomal cadherins as key components of a signaling axis governing epithelial morphogenesis.

scholarly journals The Autotransporter Esterase EstA of Pseudomonas aeruginosa Is Required for Rhamnolipid Production, Cell Motility, and Biofilm Formation

2007 ◽  
Vol 189 (18) ◽  
pp. 6695-6703 ◽  
Author(s):  
Susanne Wilhelm ◽  
Aneta Gdynia ◽  
Petra Tielen ◽  
Frank Rosenau ◽  
Karl-Erich Jaeger
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Cell Motility ◽  
Outer Membrane ◽  
Biofilm Formation ◽  
Cellular Motility ◽  
Membrane Composition ◽  
Rhamnolipid Production ◽  
Catalytically Active ◽  
In The Wild ◽  
Mutant Phenotypes

ABSTRACT Pseudomonas aeruginosa PAO1 produces the biodetergent rhamnolipid and secretes it into the extracellular environment. The role of rhamnolipids in the life cycle and pathogenicity of P. aeruginosa has not been completely understood, but they are known to affect outer membrane composition, cell motility, and biofilm formation. This report is focused on the influence of the outer membrane-bound esterase EstA of P. aeruginosa PAO1 on rhamnolipid production. EstA is an autotransporter protein which exposes its catalytically active esterase domain on the cell surface. Here we report that the overexpression of EstA in the wild-type background of P. aeruginosa PAO1 results in an increased production of rhamnolipids whereas an estA deletion mutant produced only marginal amounts of rhamnolipids. Also the known rhamnolipid-dependent cellular motility and biofilm formation were affected. Although only a dependence of swarming motility on rhamnolipids has been known so far, the other kinds of motility displayed by P. aeruginosa PAO1, swimming and twitching, were also affected by an estA mutation. In order to demonstrate that EstA enzyme activity is responsible for these effects, inactive variant EstA* was constructed by replacement of the active serine by alanine. None of the mutant phenotypes could be complemented by expression of EstA*, demonstrating that the phenotypes affected by the estA mutation depend on the enzymatically active protein.

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