Apical-basal pattern formation in the Arabidopsis embryo: studies on the role of the gnom gene

Development ◽  
1993 ◽  
Vol 117 (1) ◽  
pp. 149-162 ◽  
Author(s):  
U. Mayer ◽  
G. Buttner ◽  
G. Jurgens
Keyword(s):  
Pattern Formation ◽  
Root Formation ◽  
Asymmetric Cell Division ◽  
Early Embryo ◽  
The Body ◽  
Wild Type ◽  
Early Effect ◽  
Normal Number ◽  
Mutant Seedling

gnom is one of several genes that make substantial contributions to pattern formation along the apical-basal axis of polarity in the Arabidopsis embryo as indicated by the mutant seedling phenotype. The apical and basal end regions of the body pattern, which include the meristems of the shoot and the root, fail to form, and a minority of mutant embryos lack morphological features of apical-basal polarity. We have investigated the developmental basis of the gnom mutant phenotype, taking advantage of a large number of EMS-induced mutant alleles. The seedling phenotype has been traced back to the early embryo in which the asymmetric division of the zygote is altered, now producing two nearly equal-sized cells. The apical daughter cell then undergoes abnormal divisions, resulting in an octant embryo with about twice the normal number of cells while the uppermost derivative of the basal cell fails to become the hypophysis, which normally contributes to root development. Consistent with this early effect, gnom appears to be epistatic to monopteros in doubly mutant embryos, suggesting that, without prior gnom activity, the monopteros gene cannot promote root and hypocotyl development. On the other hand, when root formation was induced in bisected seedlings, wild-type responded whereas gnom mutants failed to produce a root but formed callus instead. These results suggest that gnom activity promotes asymmetric cell division which we believe is necessary both for apical-basal pattern formation in the early embryo and for root formation in tissue culture.

Genetic analysis of pattern formation in the Arabidopsis embryo

Development ◽  
1991 ◽  
Vol 113 (Supplement_1) ◽  
pp. 27-38 ◽  
Author(s):  
Gerd Jürgens ◽  
Ulrike Mayer ◽  
Torres Ruiz Ramon A. ◽  
Thomas Berleth ◽  
Simon Miséra
Keyword(s):  
Pattern Formation ◽  
Large Scale ◽  
Early Embryo ◽  
Flowering Plant ◽  
Abnormal Development ◽  
Mutant Seedling ◽  
Basic Body ◽  
Plant Embryo ◽  
Embryonic Pattern Formation ◽  
Plant Arabidopsis Thaliana

Virtually nothing is known about the mechanisms that generate the basic body pattern in plant embryogenesis. As a first step towards the analysis of pattern formation, we have isolated and begun to characterise putative pattern mutants in the flowering plant, Arabidopsis thaliana. A large-scale screen for morphologically abnormal seedling mutants yielded about 250 lines for further study, and genetic evidence suggests saturation of the genome for this kind of mutation. The phenotypes of putative pattern mutants fall into distinct categories, classes and groups, which may reflect specific aspects of embryonic pattern formation. Mutant seedling phenotypes result from abnormal development in the early embryo. The implications of our findings are discussed with regard to the prospects for a mechanistic understanding of pattern formation in the plant embryo.

Touch insensitive foraging of Caenorhabditis elegans in a constrained structure

Nematology ◽  
2009 ◽  
Vol 11 (4) ◽  
pp. 551-554
Author(s):  
Jinu Eo ◽  
Kazunori Otobe
Keyword(s):  
Caenorhabditis Elegans ◽  
Natural Habitat ◽  
The Body ◽  
Wild Type ◽  
Agar Gel ◽  
Touch Sensor ◽  
Foraging Pattern

Abstract The objective of this study was to clarify the role of touch sensors in the foraging of Caenorhabditis elegans in a constrained structure. The strains tested included an array of mechanosensory mutants insensitive to touch in the body, tail or nose. The mutants and wild type nematodes repeated forward and backward movement in a micro-moulded substrate as on the surface of agar gel. Differences in the foraging pattern were not obvious among mutant groups having different touch sensor deficit in the substrate, and all strains of nematode successfully moved out of the T-shaped structure after searching the configuration of their environment. The results suggest that the touch sensor is a weak contributor to the performance of the worms when foraging, and the behaviour is governed by intrinsic spontaneous patterns in the absence of any stimuli in natural habitat.

scholarly journals Genetic analysis of the Arabidopsis TIR1/AFB auxin receptors reveals both overlapping and specialized functions

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Michael J Prigge ◽  
Matthieu Platre ◽  
Nikita Kadakia ◽  
Yi Zhang ◽  
Kathleen Greenham ◽  
...  
Keyword(s):  
Genetic Analysis ◽  
Early Embryo ◽  
Wild Type ◽  
The Family ◽  
Dependent Inhibition ◽  
Root Gravitropism ◽  
Specialized Function ◽  
Mutant Lines

The TIR1/AFB auxin co-receptors mediate diverse responses to the plant hormone auxin. The Arabidopsis genome encodes six TIR1/AFB proteins representing three of the four clades that were established prior to angiosperm radiation. To determine the role of these proteins in plant development we performed an extensive genetic analysis involving the generation and characterization of all possible multiply-mutant lines. We find that loss of all six TIR1/AFB proteins results in early embryo defects and eventually seed abortion, and yet a single wild-type allele of TIR1 or AFB2 is sufficient to support growth throughout development. Our analysis reveals extensive functional overlap between even the most distantly related TIR1/AFB genes except for AFB1. Surprisingly, AFB1 has a specialized function in rapid auxin-dependent inhibition of root growth and early phase of root gravitropism. This activity may be related to a difference in subcellular localization compared to the other members of the family.

The role of the monopteros gene in organising the basal body region of the Arabidopsis embryo

Development ◽  
1993 ◽  
Vol 118 (2) ◽  
pp. 575-587 ◽  
Author(s):  
T. Berleth ◽  
G. Jurgens
Keyword(s):  
Tissue Culture ◽  
Pattern Formation ◽  
Basal Body ◽  
Root Formation ◽  
Root Meristem ◽  
Body Region ◽  
Phenotypic Trait ◽  
Embryo Cells ◽  
Stage Embryo

The monopteros (mp) gene contributes to apical-basal pattern formation in the Arabidopsis embryo. mp mutant seedlings lack basal body structures such as hypocotyl, radicle and root meristem, and this pattern deletion has been traced back to alterations in the octant-stage embryo. Cells of the embryo proper and the uppermost cell of the suspensor fail to establish division patterns that would normally generate the basal body structures. The resulting absence of a morphological axis seems to be responsible for another phenotypic trait of mp seedlings, variable positioning of cotyledons. This relationship is suggested by weak mp seedling phenotypes in which the presence of a short hypocotyl is correlated with normal arrangement of cotyledons. Root formation has been induced in mp seedlings grown in tissue culture. This result supports the notion that the mp gene is required for organising the basal body region, rather than for making the root, in the developing embryo.

scholarly journals Loss of Dystrobrevin Causes Muscle Degeneration and a Short Lifespan in Caenorhabditis elegans

2017 ◽  
Vol 15 (9) ◽  
pp. 659-667
Author(s):  
Worawit SUPHAMUNGMEE ◽  
Prapaporn JATTUJAN ◽  
Krai MEEMON
Keyword(s):  
Protein Complexes ◽  
The Body ◽  
Muscle Degeneration ◽  
Cell Integrity ◽  
Wild Type ◽  
C Elegans ◽  
Short Lifespan ◽  
C Terminus ◽  
Cell Stability

Duchene’s muscular dystrophy (DMD) is an inherited disorder in an X-linked recessive manner. Lack of dystrophin causes progressive muscle degeneration. Dystrophin structurally connects to actin filaments at the N-terminus while the C-terminus interacts with an integral domain of the dystroglycan complex. Among the associated molecules, dystrobrevin acts as a modulator protein exerting dystrophin's function for strengthening the cell stability. Previous data has reported the delayed muscle degeneration following an overexpression of the dystrobrevin (dyb) gene in the DMD-phenotype C. elegans, whose dystrophin (dys) gene was missing. This finding indicates the role of a modulator protein, rather than dystrophin, to maintain the cell integrity. The present study aims to investigate the phenotypes of C. elegans, due to dyb- or dys-deficiency. When compared with the wild-type, the dyb-deficient worms exhibited uncoordinated locomotion and lysis of the muscular layer in the body wall and internal organs as well as those observed in the dys-deficient worms. The ultrastructure of both mutant worms appeared severe muscle degeneration, decrease of the mitochondria, and replacement of fibrotic tissue, particularly the dys-mutant which was even more severe. Additionally, a shorter lifespan was observed with a 17 % reduction (p < 0.05) in dyb-deficient worms and 27 % reduction (p < 0.05) in dys-deficient worms when compared to wild-type. It is speculated that dystrobrevin may stabilize the cell through interaction with other protein complexes at the plasma membrane while it also binds to dystrophin. Therefore, the loss of dystrobrevin is also sufficient to disrupt the signaling pathway and causes muscle degeneration.

Mutations in the FASS gene uncouple pattern formation and morphogenesis in Arabidopsis development

Development ◽  
1994 ◽  
Vol 120 (10) ◽  
pp. 2967-2978 ◽  
Author(s):  
R.A. Torres-Ruiz ◽  
G. Jurgens
Keyword(s):  
Cell Division ◽  
Pattern Formation ◽  
Cell Polarity ◽  
Longitudinal Axis ◽  
Early Embryo ◽  
Cellular Level ◽  
The Body ◽  
Recessive Mutations ◽  
Morphological Criteria ◽  
Dependent Cell

The pattern of cell division is very regular in Arabidopsis embryogenesis, enabling seedling structures to be traced back to groups of cells in the early embryo. Recessive mutations in the FASS gene alter the pattern of cell division from the zygote, without interfering with embryonic pattern formation: although no primordia of seedling structures can be recognised by morphological criteria at the early-heart stage, all elements of the body pattern are differentiated in the seedling. fass seedlings are strongly compressed in the apical-basal axis and enlarged circumferentially, notably in the hypocotyl. Depending on the width of the hypocotyl, fass seedlings may have up to three supernumerary cotyledons. fass mutants can develop into tiny adult plants with all parts, including floral organs, strongly compressed in their longitudinal axis. At the cellular level, fass mutations affect cell elongation and orientation of cell walls but do not interfere with cell polarity as evidenced by the unequal division of the zygote. The results suggest that the FASS gene is required for morphogenesis, i.e., oriented cell divisions and position-dependent cell shape changes generating body shape, but not for cell polarity which seems essential for pattern formation.

The Role of VWF In BBB Permeability Associated with Hypoxia/Reoxygenation

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 2102-2102
Author(s):  
Georgette L. Suidan ◽  
Simon F. De Meyer ◽  
Alexander Brill ◽  
Stephen M. Cifuni ◽  
Denisa D. Wagner
Keyword(s):  
Endothelial Cells ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
The Body ◽  
Wild Type ◽  
Junction Protein ◽  
Bbb Permeability ◽  
Deficient Mice ◽  
Hypoxia Reoxygenation

Abstract Abstract 2102 Aberrant blood brain barrier (BBB) permeability is a hallmark pathology in many diseases of the central nervous system (CNS) including hypoxia, epilepsy, multiple sclerosis and ischemic stroke. Generalized hypoxia is a pathological condition in which the body as a whole is deprived of adequate oxygen supply. Hypoxia occurs in healthy people when they ascend to high altitudes, where it can cause altitude sickness, often manifested by headache, leading to potentially fatal complications such as high altitude cerebral edema (HACE). Hypoxia followed by reoxygenation (H/R) is also commonly used as a model to investigate pathology associated with ischemia/reperfusion as the latter condition is present in several disease states including stroke. In animal models, H/R has been shown to cause tight junction protein abnormalities, increased BBB paracellular permeability and edema. von Willebrand Factor (VWF) is a glycoprotein that is synthesized exclusively by endothelial cells and megakaryocytes. Endothelial cell-derived VWF is secreted constitutively and stored in Weibel-Palade bodies (WPB) from where it is released by regulated secretion into the plasma and subendothelium in response to endothelial activation. It has been demonstrated in vitro that exposure of cultured endothelial cells to hypoxia results in WPB exocytosis and VWF secretion. While it is known that VWF is expressed abundantly by cerebral endothelial cells, very little is known about the role of VWF in endothelial biology, particularly, in regulation of the BBB under stressful conditions. Several studies have shown that VWF protein is up regulated in plasma of patients with several neurological conditions involving BBB disruption such as stroke, severe head injury, cerebral malaria and cerebral venous sinus thrombosis. As it is known that C57BL/6 (wild-type) mice have increased BBB permeability induced by H/R, we investigated the status of BBB integrity in VWF-deficient mice (also on the C57BL/6 background). For these experiments, we used a mouse model of normobaric hypoxia (24 hours of 6% oxygen) followed by reoxygenation (1 hour ~21% oxygen). VWF antigen levels were measured by ELISA and BBB permeability was assessed by quantification of Evan's blue dye leakage into the brain. Our data indicate that plasma VWF levels in wild-type mice are significantly increased after hypoxia when compared to normoxic controls. Upon comparison with wild-type mice, we have determined that VWF-deficient mice have significantly less BBB permeability after H/R suggesting that VWF plays a role in BBB integrity under stressful conditions. We have previously reported that VWF-deficient mice have a defect in regulated P-selectin secretion (Denis et al., PNAS, 2001). To determine if the maintenance of BBB integrity found in VWF-deficient mice was due to lack of P-selectin we utilized an aptamer which inhibits P-selectin (Archemix). Inhibition of P-selectin in wild-type animals resulted in similar BBB permeability when compared to controls. Our findings suggest a critical role for VWF in BBB permeability after hypoxia/reoxygenation that is independent of P-selectin. Disclosures: No relevant conflicts of interest to declare.

ADAMTS13-/-zebrafish Model Created By Crispr/Cas Reveals a Novel Role of ADAMTS13 in Vascular Development and Prothrombotic Phenotype

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 1446-1446
Author(s):  
Liang Zheng ◽  
X. Long Zheng
Keyword(s):  
Vascular Development ◽  
Fluorescent Microscopy ◽  
Premature Stop Codon ◽  
The Body ◽  
Fluorescence Signal ◽  
Wild Type ◽  
Zebrafish Model ◽  
Growth Environment ◽  
Caudal Vein

Abstract Background: Deficiency of plasma ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13), a von Willebrand factor (VWF)-cleaving enzyme, in humans results in thrombotic thrombocytopenic purpura (TTP), a potentially fatal syndrome. Previous studies have demonstrated that ADAMTS13, particularly the C-terminal domains of ADAMTS13 may stimulate or inhibit angiogenesis, depending on the growth environment. However, the role of ADAMTS13 in vascular development in vivo is not known. Objective: To identify the novel function of ADAMTS13 beyond the proteolysis of VWF, we generated ADAMTS13 knockdown and knockout zebrafish to determine the vascular development and propensity for development of thrombosis. Methods: Morpholino anti-sense RNA was microinjected to the embryos of a double transgenic Tg (gata1:dsRed; fli1:eGFP)zebrafish to transiently block ADAMTS13 translation. Also, CRSIPR/Cas9 system was employed to generate ADAMTS13 knockout zebrafish. The vascular development and thrombus formation were determined by fluorescent microscopy. Results: Approximately 30% of ADAMTS13 knockdown zebrafish exhibited vascular abnormalities in the dwarf intersegmental vessels and narrow caudal vein plexus (Fig. 1A and B). To confirm the phenotype, ADAMTS13 knockout using CRSIPR/Cas system was performed. Approximately 85% of the F0 fish carried insertion or deletion mutations in the targeted region. The founder fish were outcrossed to wild type fish to generate heterozygous F1 fish. Fourteen different mutation sequences with germ line transmission were identified in 33 F1 mutants. The siblings carrying an 8-bp deletion mutation, which created a premature stop codon in the signal peptide region of ADAMTS13, were then crossed to produce F2 progeny. The genotypes and protein expression were further confirmed by sequencing and by Western blot, respectively. As shown, a significant higher rate of vascular development defects, particularly in intersegmental vessels and caudal vein, was observed in homozygous ADAMTS13 knockout fish compared to the heterozygous and wild type fish (Fig. 1C). Thrombosis was triggered by incubation of larvae with various low concentrations (0.06%-0.25%) of FeCl3 and determined by the real-time change of fluorescence intensity within 10 min in the head region of larvae under a fluorescent microscope. When compared with wild type fish, ADAMTS13-/- fish demonstrated dramatically decreased fluorescence signal (Fig.1D), indicative of the cessation of blood flow elsewhere in the body after FeCl3injury. Conclusion: Our results demonstrate that severe deficiency of ADAMTS13 in zebrafish results in abnormalities of vascular development and increases the propensity of thrombosis after oxidative injury in fish larvae. These results suggest that ADAMTS13 may have other substrates than VWF. The zebrafish model may turn out to be a powerful tool for identifying a novel pro-angiogenic or anti-thrombotic agent. Disclosures Zheng: Alexion: Research Funding; Ablynx: Consultancy.

scholarly journals SUN-590 27-Hydroxycholesterol Triggers the Whitening of Brown Adipose Tissue

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Arvand Asghari ◽  
Linh Bui ◽  
Robert Stephen ◽  
Michihisa Umetani
Keyword(s):  
Estrogen Receptor ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
White Adipose Tissue ◽  
Vehicle Control ◽  
The Body ◽  
Wild Type ◽  
Brown Adipose

Abstract 27-Hydroxycholesterol (27HC) is the most abundant oxysterol in circulation and metabolized by a P450 enzyme CYP7B1. Its levels closely correspond to those of cholesterol in the body. In addition, previously it was found that 27HC is an endogenous selective estrogen receptor modulator (SERM), which links cholesterol metabolism to estrogen receptor actions (1). Brown adipose tissue (BAT) is the primary source of energy expenditure and energy homeostasis, as well as body temperature maintenance. While previously it was believed that BAT activity is limited to neonates and young children, it is now recognized that BAT is also active in adult humans and its function is impaired by metabolic diseases such as obesity. BAT is also a secretory organ and produces brown adipokines, although the exact function of BAT and adipokines from this tissue in obesity has not been completely understood. Recently, it was reported that 27HC plays an important role in obesity and augments body weight gain in response to a high fat, high cholesterol (HFHC) diet by increasing pre-adipocyte population in the white adipose tissue. 27HC mimics the effects by HFHC diet-feeding on white adipose tissue, such as promoting the inflammation and macrophage infiltration (2). In this study, we explored the effect of 27HC on BAT morphology and function. First, we compared the morphology of BAT from wild-type mice and Cyp7b1-/- mice that have elevated levels of 27HC using H&E staining. Interestingly, brown adipocytes from Cyp7b1-/- mice were larger in cell size than those from wild-type mice, and the cells were mostly unilocular compared to the multilocular cells from wild-type mice, indicating the transition toward a “whitening” phenotype. Next, We treated mice fed a normal chow or a HFHC diet with 27HC or vehicle control for 8 weeks to examine the direct effect by 27HC on BAT. Similar to the phenotype in Cyp7b1-/-mice, 27HC increased the “whitening” of BAT regardless of the diet. We also determined the gene expression of brown adipocyte markers such as UCP1, PGC1a, and DIO2, and found that 27HC significantly decreased the expression of the BAT markers regardless of the diet, confirming the “whitening” observed in the morphology. Moreover, the energy expenditure in mice treated with 27HC was decreased compared to the vehicle control on a HFHC diet, suggesting that 27HC also alters BAT function. These results show that 27HC causes the whitening of BAT, and shed light on the important role of 27HC in brown adipose tissue function. Future experiments will be warranted toward further understanding of the role of 27HC in BAT function. Reference:(1) Umetani, Michihisa, et al. Nature medicine 13.10 (2007): 1185. (2) Asghari, Arvand, et al. Endocrinology 160.10 (2019): 2485-2494.

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