scholarly journals phantastica: a gene required for dorsoventrality of leaves in Antirrhinum majus

Development ◽  
1995 ◽  
Vol 121 (7) ◽  
pp. 2143-2154 ◽  
Author(s):  
R. Waites ◽  
A. Hudson
Keyword(s):  
Cell Types ◽  
Antirrhinum Majus ◽  
Lateral Growth ◽  
Wild Type ◽  
Cell Identity ◽  
Lateral Organs ◽  
Floral Phenotype

To understand better the mechanisms that lead to dorsoventrality in the lateral organs of plants, mutants at the phantastica (phan) locus of Antirrhinum majus have been identified and characterised. The leaves, bracts and petal lobes of phan mutants show varying degrees of reduction in dorsal tissues, indicating that phan is required for establishing dorsal cell identity. Each phan mutant produces a variety of different leaf morphologies, but has a characteristic and relatively constant floral phenotype. In several different forms of phan mutant leaves and petal lobes, novel boundaries between dorsal and ventral cell types form ectopic axes of growth, suggesting that phan-dependent dorsal cell identity is required for lateral growth of the wild-type leaf and petal lobe. Comparisons between the development of wild-type and mutant petals or leaves reveal that phan acts early in development of these lateral organs. The possible role of the phan gene in evolution of different leaf forms is discussed.

scholarly journals Microtubule–microtubule sliding by kinesin-1 is essential for normal cytoplasmic streaming in Drosophila oocytes

2016 ◽  
Vol 113 (34) ◽  
pp. E4995-E5004 ◽  
Author(s):  
Wen Lu ◽  
Michael Winding ◽  
Margot Lakonishok ◽  
Jill Wildonger ◽  
Vladimir I. Gelfand
Keyword(s):  
Cytoplasmic Streaming ◽  
Cell Types ◽  
Nurse Cells ◽  
Wild Type ◽  
Actin Cortex ◽  
Microtubule Motor ◽  
Multiple Cell ◽  
Cytoplasmic Microtubules ◽  
Two Populations

Cytoplasmic streaming in Drosophila oocytes is a microtubule-based bulk cytoplasmic movement. Streaming efficiently circulates and localizes mRNAs and proteins deposited by the nurse cells across the oocyte. This movement is driven by kinesin-1, a major microtubule motor. Recently, we have shown that kinesin-1 heavy chain (KHC) can transport one microtubule on another microtubule, thus driving microtubule–microtubule sliding in multiple cell types. To study the role of microtubule sliding in oocyte cytoplasmic streaming, we used a Khc mutant that is deficient in microtubule sliding but able to transport a majority of cargoes. We demonstrated that streaming is reduced by genomic replacement of wild-type Khc with this sliding-deficient mutant. Streaming can be fully rescued by wild-type KHC and partially rescued by a chimeric motor that cannot move organelles but is active in microtubule sliding. Consistent with these data, we identified two populations of microtubules in fast-streaming oocytes: a network of stable microtubules anchored to the actin cortex and free cytoplasmic microtubules that moved in the ooplasm. We further demonstrated that the reduced streaming in sliding-deficient oocytes resulted in posterior determination defects. Together, we propose that kinesin-1 slides free cytoplasmic microtubules against cortically immobilized microtubules, generating forces that contribute to cytoplasmic streaming and are essential for the refinement of posterior determinants.

scholarly journals Platelet and Erythrocyte Extravasation across Inflamed Corneal Venules Depend on CD18, Neutrophils and Mast Cell Degranulation

2021 ◽  
Vol 22 (14) ◽  
pp. 7360
Author(s):  
Angie De La Cruz ◽  
Aubrey Hargrave ◽  
Sri Magadi ◽  
Justin A. Courson ◽  
Paul T. Landry ◽  
...  
Keyword(s):  
Mast Cell ◽  
Cell Types ◽  
Mast Cell Degranulation ◽  
Wild Type ◽  
Delayed Wound Healing ◽  
Corneal Epithelial ◽  
Corneal Abrasion ◽  
Low Levels ◽  
Endothelial Pores

Platelet extravasation during inflammation is under-appreciated. In wild-type (WT) mice, a central corneal epithelial abrasion initiates neutrophil (PMN) and platelet extravasation from peripheral limbal venules. The same injury in mice expressing low levels of the β2-integrin, CD18 (CD18hypo mice) shows reduced platelet extravasation with PMN extravasation apparently unaffected. To better define the role of CD18 on platelet extravasation, we focused on two relevant cell types expressing CD18: PMNs and mast cells. Following corneal abrasion in WT mice, we observed not only extravasated PMNs and platelets but also extravasated erythrocytes (RBCs). Ultrastructural observations of engorged limbal venules showed platelets and RBCs passing through endothelial pores. In contrast, injured CD18hypo mice showed significantly less venule engorgement and markedly reduced platelet and RBC extravasation; mast cell degranulation was also reduced compared to WT mice. Corneal abrasion in mast cell-deficient (KitW-sh/W-sh) mice showed less venule engorgement, delayed PMN extravasation, reduced platelet and RBC extravasation and delayed wound healing compared to WT mice. Finally, antibody-induced depletion of circulating PMNs prior to corneal abrasion reduced mast cell degranulation, venule engorgement, and extravasation of PMNs, platelets, and RBCs. In summary, in the injured cornea, platelet and RBC extravasation depends on CD18, PMNs, and mast cell degranulation.

scholarly journals A large panel of chicken cells are invaded in vivo by Salmonella Typhimurium even when depleted of all known invasion factors

Open Biology ◽  
2021 ◽  
Vol 11 (11) ◽  
Author(s):  
S. M. Roche ◽  
S. Holbert ◽  
Y. Le Vern ◽  
C. Rossignol ◽  
A. Rossignol ◽  
...  
Keyword(s):  
Gall Bladder ◽  
Cell Types ◽  
Human Infection ◽  
Cell Tropism ◽  
Wild Type ◽  
Phagocytic Cells ◽  
Bladder Cells ◽  
First Time

Poultry are the main source of human infection by Salmonella . As infected poultry are asymptomatic, identifying infected poultry farms is difficult, thus controlling animal infections is of primary importance. As cell tropism is known to govern disease, our aim was therefore to identify infected host–cell types in the organs of chicks known to be involved in Salmonella infection and investigate the role of the three known invasion factors in this process (T3SS-1, Rck and PagN). Chicks were inoculated with wild-type or isogenic fluorescent Salmonella Typhimurium mutants via the intracoelomic route. Our results show that liver, spleen, gall bladder and aortic vessels could be foci of infection, and that phagocytic and non-phagocytic cells, including immune, epithelial and endothelial cells, are invaded in vivo in each organ. Moreover, a mutant defective for the T3SS-1, Rck and PagN remained able to colonize organs like the wild-type strain and invaded non-phagocytic cells in each organ studied. As the infection of the gall bladder had not previously been described in chicks, invasion of gall bladder cells was confirmed by immunohistochemistry and infection was shown to last several weeks after inoculation. Altogether, for the first time these findings provide insights into cell tropism of Salmonella in relevant organs involved in Salmonella infection in chicks and also demonstrate that the known invasion factors are not required for entry into these cell types.

MiR-223 is dispensable for platelet production and function in mice

2013 ◽  
Vol 110 (12) ◽  
pp. 1207-1214 ◽  
Author(s):  
Xavier Loyer ◽  
Simon Leierseder ◽  
Tobias Petzold ◽  
Lin Zhang ◽  
Steffen Massberg ◽  
...  
Keyword(s):  
Platelet Adhesion ◽  
Cell Types ◽  
Surface Expression ◽  
Wild Type ◽  
Platelet Production ◽  
Multiple Cell ◽  
And Function ◽  
Deficient Mice ◽  
Platelet Depletion

SummaryMicroRNAs (miRNAs) are key physiological regulators in multiple cell types. Here, we assessed platelet production and function in mice deficient in miR-223, one of the most abundantly expressed miRNAs in platelets and megakaryocytes. We found platelet number, size, lifespan as well as surface expression of platelet adhesion receptors to be unchanged in miR-223-deficient mice. Likewise, loss of miR-223 did not affect platelet activation, adhesion and aggregation and also had no effect on bleeding times. Moreover, miR-223 null megakaryocytes developed normally and were capable to form pro-platelets. However, we detected a transient delay in the recovery of platelet numbers following antibody-induced platelet depletion in miR-223-deficient animals. This delay was not observed after transplantation of bone marrow from miR-223-deficient animals into wild-type recipients, indicating a non-cell-autonomous role of miR-223 for thrombopoiesis. Overall, our data indicate a surprisingly modest role of miR-223 in platelet production, while the function of platelets does not seem to depend on miR-223.

LAM1 is required for dorsoventrality and lateral growth of the leaf blade in Nicotiana

Development ◽  
1998 ◽  
Vol 125 (21) ◽  
pp. 4235-4243 ◽  
Author(s):  
N.A. McHale ◽  
M. Marcotrigiano
Keyword(s):  
Leaf Blade ◽  
Cell Types ◽  
Nicotiana Sylvestris ◽  
Lateral Growth ◽  
Lateral Plane ◽  
Cell Layers ◽  
Periclinal Chimeras ◽  
Autonomous Movement

The role of LAM1 in dorsoventrality and lateral growth of the leaf blade was investigated in the ‘bladeless’ lam1 mutant of Nicotiana sylvestris and in periclinal chimeras with lam1 and wild-type (N. glauca) cell layers. Mutant lam1 primordia show normal dorsoventrality at emergence, but produce blade tissue that lacks dorsal cell types and fails to expand in the lateral plane. In leaves of a lam1-glauca-glauca (L1-L2-L3) chimera, we observed restoration of dorsal identity in the lam1 upper epidermis, suggesting non-cell-autonomous movement of a dorsalizing factor between cell layers of the blade. A lam1-lam1-glauca chimera generated a leaf blade with lam1 cells in the L1-derived epidermis and the L2-derived upper and lower mesophyll. An in situ lineage analysis revealed that N. glauca cells in the L3-derived middle mesophyll restore palisade differentiation in the adjoining lam1 upper mesophyll. Movement of dorsalizing information appears short-range, however, having no effect on the upper lam1 epidermis in lam1-lam1-glauca. Clusters of lam1 mesophyll in distal or proximal positions show a localized default to radial growth, indicating that the LAM1 function is required for dorsoventrality and lateral growth throughout blade expansion.

Leafbladeless1 is required for dorsoventrality of lateral organs in maize

Development ◽  
1998 ◽  
Vol 125 (15) ◽  
pp. 2813-2823 ◽  
Author(s):  
M.C. Timmermans ◽  
N.P. Schultes ◽  
J.P. Jankovsky ◽  
T. Nelson
Keyword(s):  
Leaf Development ◽  
Homeobox Gene ◽  
Cell Types ◽  
Partial Loss ◽  
Cell Identity ◽  
Cell Recruitment ◽  
Lateral Organs ◽  
Lateral Organ ◽  
Complete Duplication ◽  
Lateral Propagation

The maize leafbladeless1 (lbl1) mutant displays a variety of leaf and plant phenotypes. The most extreme manifestation in the leaf is the formation of radially symmetric, abaxialized leaves due to a complete loss of adaxial cell types. Less severe phenotypes, resulting from a partial loss of adaxial cell identity, include the formation of ectopic laminae at the boundary between abaxialized, mutant sectors on the adaxial leaf surface and the bifurcation of leaves. Ectopic laminae and bifurcations arise early in leaf development and result in an altered patterning of the leaf along the proximodistal axis, or in complete duplication of the developing organ. Leaf-like lateral organs of the inflorescences and flowers show similar phenotypes. These observations suggest that Lbl1 is required for the specification of adaxial cell identity within leaves and leaf-like lateral organs. Lbl1 is also required for the lateral propagation of leaf founder cell recruitment, and plays a direct or indirect role in the downregulation of the homeobox gene, knotted1, during leaf development. Our results suggest that adaxial/abaxial asymmetry of lateral organs is specified in the shoot apical meristem, and that formation of this axis is essential for marginal, lateral growth and for the specification of points of proximodistal growth. Parallels between early patterning events during lateral organ development in plants and animals are discussed.

Could lncRNAs contribute to β-cell identity and its loss in Type 2 diabetes?

2013 ◽  
Vol 41 (3) ◽  
pp. 797-801 ◽  
Author(s):  
Timothy J. Pullen ◽  
Guy A. Rutter
Keyword(s):  
Type 2 Diabetes ◽  
Cell Mass ◽  
Cell Types ◽  
Human Populations ◽  
Β Cell ◽  
Cell Identity ◽  
Genome Wide ◽  
And Function

The progression of Type 2 diabetes is accompanied by diminishing islet β-cell mass and function. It has been proposed that β-cells are lost not only through apoptosis, but also by dedifferentiating into progenitor-like cells. There is therefore much interest in the mechanisms which define and maintain β-cell identity. The advent of genome-wide analyses of chromatin modifications has highlighted the role of epigenetic factors in determining cell identity. There is also evidence from both human populations and animal models for an epigenetic component in susceptibility to Type 2 diabetes. The mechanisms responsible for defining the epigenetic landscape in individual cell types are poorly understood, but there is growing evidence of a role for lncRNAs (long non-coding RNAs) in this process. In the present paper, we discuss some of the mechanisms through which lncRNAs may contribute to β-cell identity and Type 2 diabetes risk.

scholarly journals Reduced allergic lung inflammation and airway responsiveness in mice lacking the cytoskeletal protein gelsolin

2020 ◽  
Vol 319 (5) ◽  
pp. L833-L842
Author(s):  
Maya Mikami ◽  
Gene T. Yocum ◽  
Nicola M. Heller ◽  
Charles W. Emala
Keyword(s):  
Airway Inflammation ◽  
Lung Inflammation ◽  
Ex Vivo ◽  
Cell Types ◽  
Asthma Severity ◽  
Wild Type ◽  
Allergic Lung Inflammation ◽  
Actin Capping

Airway smooth muscle hyperresponsiveness associated with chronic airway inflammation leads to the typical symptoms of asthma including bronchoconstriction and wheezing. Asthma severity is associated with airway inflammation; therefore, reducing airway inflammation is an important therapeutic target. Gelsolin is an actin capping and severing protein that has been reported to be involved in modulation of the inflammatory response. Using mice genetically lacking gelsolin, we evaluated the role of gelsolin in the establishment of house dust mite (HDM) antigen-induced allergic lung inflammation. The genetic absence of gelsolin was found to be protective against HDM sensitization, resulting in reduced lung inflammation, inflammatory cytokines, and Muc5AC protein in bronchoalveolar lavage (BAL) fluid. The number of eosinophils, lymphocytes, and interstitial macrophages in the BAL were increased after HDM sensitization in wild-type mice but were attenuated in gelsolin-null mice. The observed attenuation of inflammation may be partly due to delayed migration of immune cells, because the reduced eosinophils in the BALs from gelsolin-null mice compared with controls occurred despite similar amounts of the chemoattractant eotaxin. Splenic T cells demonstrated similar proliferation rates, but ex vivo alveolar macrophage migration was delayed in gelsolin-null mice. In vivo, the reduced lung inflammation after HDM sensitization in gelsolin-null mice was associated with significantly diminished airway resistance to inhaled methacholine compared with HDM-treated wild-type mice. Our results suggest that modulation of gelsolin expression or function in selective inflammatory cell types that modulate allergic lung inflammation could be a therapeutic approach for asthma.

scholarly journals Arabidopsis ABIG1 Functions in Laminar Growth and Polarity Formation through Regulation by REVOLUTA and KANADI

2021 ◽  
Author(s):  
Jesus Preciado ◽  
Kevin Begcy ◽  
Tie Liu
Keyword(s):  
Leucine Zipper ◽  
Genetic Interaction ◽  
Interaction Analysis ◽  
Cell Types ◽  
Physical Interaction ◽  
Loss Of Function ◽  
Lateral Organs ◽  
Aba Insensitive ◽  
New Evidence

Leaf laminar growth and adaxial-abaxial boundary formation are fundamental outcomes of plant development. Boundary and laminar growth coordinate the further patterning and growth of the leaf, directing the differentiation of cell types within the top and bottom domains and promoting initiation of lateral organs along their adaxial/abaxial axis. Leaf adaxial-abaxial polarity specification and laminar out-growth are regulated by two transcription factors, REVOLUTA (REV) and KANADI (KAN). ABA INSENSITIVE TO GROWTH 1 (ABIG1) is a HOMEODOMAIN-LEUCINE ZIPPER (HD-ZIP) Class II transcription factor and is a direct target of the adaxial-abaxial regulators REV and KAN. To investigate the role of ABIG1 in the leaf development and establishment of polarity, we examined the phenotypes of both gain-of-function and loss-of-function mutants. Through genetic interaction analysis with REV and KAN mutants, we have determined that ABIG1 plays a role in leaf laminar-growth as well as in adaxial-abaxial polarity establishment. Genetic and physical interaction assays showed that ABIG1 interacts with the transcriptional corepressor TOPLESS (TPL). This study provides new evidence that another HD-ZIP II gene, ABIG1, facilitates growth through the corepressor TPL.

scholarly journals Inflammatory Monocytes but Not Neutrophils Are Necessary To Control Infection with Toxoplasma gondii in Mice

2010 ◽  
Vol 78 (4) ◽  
pp. 1564-1570 ◽  
Author(s):  
Ildiko R. Dunay ◽  
Anja Fuchs ◽  
L. David Sibley
Keyword(s):  
Acute Infection ◽  
Critical Role ◽  
Cell Types ◽  
Wild Type ◽  
Inflammatory Monocytes ◽  
Intestinal Pathology ◽  
Parasite Replication ◽  
Acute Toxoplasmosis ◽  
Acute Ileitis

ABSTRACT Previous studies have suggested that both inflammatory monocytes and neutrophils are important for controlling acute toxoplasmosis in the mouse model. To test the role of these cell types, we used monoclonal antibody (MAb) RB6-8C5 to deplete both subsets of cells or MAb 1A8 to selectively remove neutrophils. RB6-8C5 MAb-treated mice succumbed to oral infection with T oxoplasma gondii, similar to Ccr2−/− mice, which are deficient in monocyte recruitment but have normal neutrophils. In contrast, mice treated with MAb 1A8 controlled parasite replication and survived acute infection. Ccr2−/− mice suffered from acute ileitis and inflammation in the spleen that was associated with a lack of inflammatory monocytes and elevated numbers of neutrophils. RB6-8C5 MAb-treated C57BL/6 mice also suffered from intestinal pathology and splenic damage, although this was less extensive due to the reduced numbers of neutrophils. Neutrophil-depleted infected wild-type mice displayed no pathological changes, compared to untreated infected controls. Collectively, these observations demonstrate the critical role of inflammatory monocytes during the acute infection with the parasite T. gondii and reveal that neutrophils are not protective but rather contribute to the pathology.

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