scholarly journals Glutamate signalling via a MEKK1 kinase-dependent pathway induces changes in Arabidopsis root architecture

2013 ◽  
Vol 75 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Brian G. Forde ◽  
Sean R. Cutler ◽  
Najia Zaman ◽  
Patrick J. Krysan
Keyword(s):  
Root Architecture ◽  
Arabidopsis Root ◽  
Dependent Pathway

scholarly journals Capturing Arabidopsis Root Architecture Dynamics with ROOT-FIT Reveals Diversity in Responses to Salinity

2014 ◽  
Vol 166 (3) ◽  
pp. 1387-1402 ◽  
Author(s):  
M. M. Julkowska ◽  
H. C. J. Hoefsloot ◽  
S. Mol ◽  
R. Feron ◽  
G.-J. de Boer ◽  
...  
Keyword(s):  
Root Architecture ◽  
Arabidopsis Root

scholarly journals miR156-targeted SPL10 controls Arabidopsis root meristem activity and root-derived de novo shoot regeneration via cytokinin responses

2019 ◽  
Vol 71 (3) ◽  
pp. 934-950 ◽  
Author(s):  
Carlos Hernán Barrera-Rojas ◽  
Gabriel Henrique Braga Rocha ◽  
Laura Polverari ◽  
Diego Armando Pinheiro Brito ◽  
Diego Silva Batista ◽  
...  
Keyword(s):  
Shoot Regeneration ◽  
Root Meristem ◽  
De Novo ◽  
Expression Patterns ◽  
Primary Root ◽  
Loss Of Function ◽  
Arabidopsis Root ◽  
Squamosa Promoter Binding Protein ◽  
Spl Genes ◽  
Dependent Pathway

Abstract Root growth is modulated by different factors, including phytohormones, transcription factors, and microRNAs (miRNAs). MicroRNA156 and its targets, the SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) genes, define an age-dependent pathway that controls several developmental processes, including lateral root emergence. However, it remains unclear whether miR156-regulated SPLs control root meristem activity and root-derived de novo shoot regeneration. Here, we show that MIR156 and SPL genes have opposing expression patterns during the progression of primary root (PR) growth in Arabidopsis, suggesting that age cues may modulate root development. Plants with high miR156 levels display reduced meristem size, resulting in shorter primary root (PRs). Conversely, plants with reduced miR156 levels show higher meristem activity. Importantly, loss of function of SPL10 decreases meristem activity, while SPL10 de-repression increases it. Meristem activity is regulated by SPL10 probably through the reduction of cytokinin responses, via the modulation of type-B ARABIDOPSIS RESPONSE REGULATOR1(ARR1) expression. We also show that SPL10 de-repression in the PRs abolishes de novo shoot regenerative capacity by attenuating cytokinin responses. Our results reveal a cooperative regulation of root meristem activity and root-derived de novo shoot regeneration by integrating age cues with cytokinin responses via miR156-targeted SPL10.

scholarly journals IAA-Ala Resistant3, an Evolutionarily Conserved Target of miR167, Mediates Arabidopsis Root Architecture Changes during High Osmotic Stress

2012 ◽  
Vol 24 (9) ◽  
pp. 3590-3602 ◽  
Author(s):  
Natsuko Kinoshita ◽  
Huan Wang ◽  
Hiroyuki Kasahara ◽  
Jun Liu ◽  
Cameron MacPherson ◽  
...  
Keyword(s):  
Osmotic Stress ◽  
Root Architecture ◽  
Arabidopsis Root ◽  
Evolutionarily Conserved

scholarly journals Temporal responses of Arabidopsis root architecture to phosphate starvation: evidence for the involvement of auxin signalling

2003 ◽  
Vol 26 (7) ◽  
pp. 1053-1066 ◽  
Author(s):  
Y. AL-GHAZI ◽  
B. MULLER ◽  
S. PINLOCHE ◽  
T. J. TRANBARGER ◽  
P. NACRY ◽  
...  
Keyword(s):  
Root Architecture ◽  
Phosphate Starvation ◽  
Arabidopsis Root ◽  
Auxin Signalling

scholarly journals MEDIATOR18 influences Arabidopsis root architecture, represses auxin signaling and is a critical factor for cell viability in root meristems

2018 ◽  
Vol 96 (5) ◽  
pp. 895-909 ◽  
Author(s):  
Javier Raya-González ◽  
Araceli Oropeza-Aburto ◽  
Jesús S. López-Bucio ◽  
Ángel A. Guevara-García ◽  
Lieven de Veylder ◽  
...  
Keyword(s):  
Cell Viability ◽  
Root Architecture ◽  
Critical Factor ◽  
Auxin Signaling ◽  
Arabidopsis Root ◽  
Root Meristems

The Mechanism of Platelet Aggregation Induced by HLA-Related Antibodies

1996 ◽  
Vol 76 (05) ◽  
pp. 774-779 ◽  
Author(s):  
John T Brandt ◽  
Carmen J Julius ◽  
Jeanne M Osborne ◽  
Clark L Anderson
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Complement Activation ◽  
Thromboembolic Disease ◽  
Clinical Samples ◽  
Hla Antigen ◽  
Aggregation Response ◽  
Immune Mediated ◽  
Dependent Pathway

SummaryImmune-mediated platelet activation is emerging as an important pathogenic mechanism of thrombosis. In vitro studies have suggested two distinct pathways for immune-mediated platelet activation; one involving clustering of platelet FcyRIIa, the other involving platelet-associated complement activation. HLA-related antibodies have been shown to cause platelet aggregation, but the mechanism has not been clarified. We evaluated the mechanism of platelet aggregation induced by HLA-related antibodies from nine patients. Antibody to platelet FcyRIIa failed to block platelet aggregation with 8/9 samples, indicating that engagement of platelet FcyRIIa is not necessary for the platelet aggregation induced by HLA-related antibodies. In contrast, platelet aggregation was blocked by antibodies to human C8 (5/7) or C9 (7/7). F(ab’)2 fragments of patient IgG failed to induce platelet activation although they bound to HLA antigen on platelets. Intact patient IgG failed to aggregate washed platelets unless aged serum was added. The activating IgG could be adsorbed by incubation with lymphocytes and eluted from the lymphocytes. These results indicate that complement activation is involved in the aggregation response to HLA-related antibodies. This is the first demonstration of complement-mediated platelet aggregation by clinical samples. Five of the patients developed thrombocytopenia in relationship to blood transfusion and two patients developed acute thromboembolic disease, suggesting that these antibodies and the complement-dependent pathway of platelet aggregation may be of clinical significance.

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