scholarly journals AHK3-Mediated Cytokinin Signaling Is Required for the Delayed Leaf Senescence Induced by SSPP

2019 ◽  
Vol 20 (8) ◽  
pp. 2043
Author(s):  
Yanan Wang ◽  
Xiyu Zhang ◽  
Yanjiao Cui ◽  
Lei Li ◽  
Dan Wang ◽  
...  
Keyword(s):  
Leaf Senescence ◽  
Protein Phosphatase ◽  
Developmental Process ◽  
Loss Of Function ◽  
Cytokinin Signaling ◽  
Phenotypic Analysis ◽  
Exogenous Cytokinin ◽  
Cytokinin Treatment ◽  
Encoding Gene ◽  
Multiple Signaling

Leaf senescence is a highly-programmed developmental process regulated by an array of multiple signaling pathways. Our group previously reported that overexpression of the protein phosphatase-encoding gene SSPP led to delayed leaf senescence and significantly enhanced cytokinin responses. However, it is still unclear how the delayed leaf senescence phenotype is associated with the enhanced cytokinin responses. In this study, we introduced a cytokinin receptor AHK3 knockout into the 35S:SSPP background. The phenotypic analysis of double mutant revealed that AHK3 loss-of-function reversed the delayed leaf senescence induced by SSPP. Moreover, we found the hypersensitivity of 35S:SSPP to exogenous cytokinin treatment disappeared due to the introduction of AHK3 knockout. Collectively, our results demonstrated that AHK3-mediated cytokinin signaling is required for the delayed leaf senescence caused by SSPP overexpression and the detailed mechanism remains to be further elucidated.

scholarly journals Cytokinin Induction of Root Nodule Primordia in Lotus japonicus Is Regulated by a Mechanism Operating in the Root Cortex

2011 ◽  
Vol 24 (11) ◽  
pp. 1385-1395 ◽  
Author(s):  
Anne Birgitte Heckmann ◽  
Niels Sandal ◽  
Anita Søndergaard Bek ◽  
Lene Heegaard Madsen ◽  
Anna Jurkiewicz ◽  
...  
Keyword(s):  
Root Nodules ◽  
Lotus Japonicus ◽  
Underlying Mechanism ◽  
Loss Of Function ◽  
Cortical Cells ◽  
Root Cortex ◽  
Gus Reporter ◽  
Cortical Responses ◽  
Exogenous Cytokinin ◽  
Cytokinin Treatment

Cytokinin plays a central role in the formation of nitrogen-fixing root nodules following inoculation with rhizobia. We show that exogenous cytokinin induces formation of discrete and easily visible nodule primordia in Lotus japonicus roots. The expression of nodulin genes was up-regulated upon cytokinin treatment, suggesting that the genuine nodulation program was indeed activated. This offers a simple approach for dissecting the underlying mechanism. Cytokinin-induced nodule primordia formation was unperturbed in several loss-of-function mutants impaired in epidermal responses to either rhizobial infection, Nod factor application, or both. However, absence of primordia in nsp1, nsp2, and nin mutants showed the requirement for these transcriptional regulators in the cytokinin-mediated activation of the root cortex. Distinguishing the epidermal and cortical responses further, we found that external cytokinin application induced expression of the Nin::GUS reporter gene within the root cortex but not in the root epidermis. Using L. japonicus lhk1-1 and har1 mutants, we demonstrate that discrete activation of root cortical cells by cytokinin depends on the LHK1 cytokinin receptor and is subjected to HAR1-mediated autoregulation.

16. Physiological effects of IDH1 loss-of-function on Chondrocyte Differentiation through Hedgehog Pathway upregulation

2018 ◽  
Author(s):  
Cassie Tyson
Keyword(s):  
Developmental Stages ◽  
Hedgehog Pathway ◽  
Chondrocyte Differentiation ◽  
Loss Of Function ◽  
Wild Type ◽  
Phenotypic Analysis ◽  
Growth Plate Chondrocytes ◽  
Idh Mutations ◽  
Cartilage Tumors ◽  
Deficient Mice

Cartilage tumors are the most common and terminal primary neoplasms in bone. Physiologically, bones formed through endochondral ossification are regulated by the Hedgehog pathway and Parathyroid hormone-like hormone feedback loop. The upregulation of the infamous Hedgehog pathway has been demonstrated in several non-cartilaginous neoplasms. Recently, frequent mutational events of isocitrate dehydrogenase1 (IDH1) were identified in cartilage tumors. In other neoplasms, IDH mutations produces an oncometabolite that can promote HIF1a activation, contributing to tumorigenesis. Currently, the role of IDH1 mutations in cartilage tumors remain unknown. Investigating the physiological aspect of IDH1proves useful in identifying novel therapeutic targets for cartilage tumors. IDH1 deficient and wild-type littermates, were harvested for forelimbs and hindlimbs at various developmental stages for phenotypic analysis via hematoxylin and eosin staining. Histological analysis demonstrated IDH1 homozygous deficient mice at embryonic stages exhibited dwarfism and an elongated layer of hypertrophic chondrocytes. This was verified via immunohistochemistry Type 10 Collagen staining and Quantitative PCR (qPCR) using the chondrocyte terminal differentiation marker Col10a1. Whole skeletons of IDH1 deficient mice were subjected to skeletal double staining which demonstrated delayed mineralization of underdeveloped IDH1 deficient mice contrasted with wild-type littermates. qPCR was performed to examine the status of chondrocyte differentiation through the Hedgehog pathway in cultured primarymouse growth plate chondrocytes. Interestingly, IDH1 deficient non-neoplastic cells revealed significant upregulation of Hedgehog target molecules in IDH1 deficient chondrocytes. As a result, the loss-offunction of IDH1 was identified as a potential impairment of chondrocyte differentiation and a factor towards chondrocyte tumorgenisis.

scholarly journals N-acetylglucosaminyltransferase II Is Involved in Plant Growth and Development Under Stress Conditions

2021 ◽  
Vol 12 ◽  
Author(s):  
Jae Yong Yoo ◽  
Ki Seong Ko ◽  
Bich Ngoc Vu ◽  
Young Eun Lee ◽  
Seok Han Yoon ◽  
...  
Keyword(s):  
Plant Growth ◽  
Growth And Development ◽  
Stress Conditions ◽  
Root Growth Inhibition ◽  
Loss Of Function ◽  
Plant Growth And Development ◽  
Cytokinin Signaling ◽  
Mannose Residue ◽  
Glcnac Residue ◽  
Physiological Importance

Alpha-1,6-mannosyl-glycoprotein 2-β-N-acetylglucosaminyltransferase [EC 2.4.1.143, N-acetylglucosaminyltransferase II (GnTII)] catalyzes the transfer of N-acetylglucosamine (GlcNAc) residue from the nucleotide sugar donor UDP-GlcNAc to the α1,6-mannose residue of the di-antennary N-glycan acceptor GlcNAc(Xyl)Man3(Fuc)GlcNAc2 in the Golgi apparatus. Although the formation of the GlcNAc2(Xyl)Man3(Fuc)GlcNAc2 N-glycan is known to be associated with GnTII activity in Arabidopsis thaliana, its physiological significance is still not fully understood in plants. To address the physiological importance of the GlcNAc2(Xyl)Man3(Fuc)GlcNAc2 N-glycan, we examined the phenotypic effects of loss-of-function mutations in GnTII in the presence and absence of stress, and responsiveness to phytohormones. Prolonged stress induced by tunicamycin (TM) or sodium chloride (NaCl) treatment increased GnTII expression in wild-type Arabidopsis (ecotype Col-0) but caused severe developmental damage in GnTII loss-of-function mutants (gnt2-1 and gnt2-2). The absence of the 6-arm GlcNAc residue in the N-glycans in gnt2-1 facilitated the TM-induced unfolded protein response, accelerated dark-induced leaf senescence, and reduced cytokinin signaling, as well as susceptibility to cytokinin-induced root growth inhibition. Furthermore, gnt2-1 and gnt2-2 seedlings exhibited enhanced N-1-naphthylphthalamic acid-induced inhibition of tropic growth and development. Thus, GnTII’s promotion of the 6-arm GlcNAc addition to N-glycans is important for plant growth and development under stress conditions, possibly via affecting glycoprotein folding and/or distribution.

scholarly journals SAUR49 Can Positively Regulate Leaf Senescence by Suppressing SSPP in Arabidopsis

2019 ◽  
Vol 61 (3) ◽  
pp. 644-658 ◽  
Author(s):  
Zewen Wen ◽  
Yuanyuan Mei ◽  
Jie Zhou ◽  
Yanjiao Cui ◽  
Dan Wang ◽  
...  
Keyword(s):  
Leaf Senescence ◽  
Protein Phosphatase ◽  
Functional Characterization ◽  
Transcript Level ◽  
In Planta ◽  
Environmental Signals ◽  
Receptor Like Kinase ◽  
Premature Leaf Senescence ◽  
Natural Leaf ◽  
Two Hybrid

Abstract The involvement of SMALL AUXIN-UP RNA (SAUR) proteins in leaf senescence has been more and more acknowledged, but the detailed mechanisms remain unclear. In the present study, we performed yeast two-hybrid assays and identified SAUR49 as an interactor of SENESCENCE SUPPRESSED PROTEIN PHOSPHATASE (SSPP), which is a PP2C protein phosphatase that negatively regulates Arabidopsis leaf senescence by suppressing the leucine-rich repeat receptor-like protein kinase SENESCENCE-ASSOCIATED RECEPTOR-LIKE KINASE (SARK), as reported previously by our group. The interaction between SAUR49 and SSPP was further confirmed in planta. Functional characterization revealed that SAUR49 is a positive regulator of leaf senescence. The accumulation level of SAUR49 protein increased during natural leaf senescence in Arabidopsis. The transcript level of SAUR49 was upregulated during SARK-induced premature leaf senescence but downregulated during SSPP-mediated delayed leaf senescence. Overexpression of SAUR49 significantly accelerated both natural and dark-induced leaf senescence in Arabidopsis. More importantly, SAUR49 overexpression completely reversed SSPP-induced delayed leaf senescence. In addition, overexpression of SAUR49 reversed the decreased plasma membrane H+-ATPase activity mediated by SSPP. Taken together, the results showed that SAUR49 functions in accelerating the leaf senescence process via the activation of SARK-mediated leaf senescence signaling by suppressing SSPP. We further identified four other SSPP-interacting SAURs, SAUR30, SAUR39, SAUR41 and SAUR72, that may act redundantly with SAUR49 in regulating leaf senescence. All these observations indicated that certain members of the SAUR family may serve as an important hub that integrates various hormonal and environmental signals with senescence signals in Arabidopsis.

scholarly journals Leaf Senescence: The Chloroplast Connection Comes of Age

Plants ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 495 ◽  
Author(s):  
Martín L. Mayta ◽  
Mohammad-Reza Hajirezaei ◽  
Néstor Carrillo ◽  
Anabella F. Lodeyro
Keyword(s):  
Cell Death ◽  
Leaf Senescence ◽  
Developmental Process ◽  
Reproductive Organs ◽  
Common Thread ◽  
Dependent Cell ◽  
Redox Poise ◽  
Natural Leaf ◽  
As Stress ◽  
Stress Dependent

Leaf senescence is a developmental process critical for plant fitness, which involves genetically controlled cell death and ordered disassembly of macromolecules for reallocating nutrients to juvenile and reproductive organs. While natural leaf senescence is primarily associated with aging, it can also be induced by environmental and nutritional inputs including biotic and abiotic stresses, darkness, phytohormones and oxidants. Reactive oxygen species (ROS) are a common thread in stress-dependent cell death and also increase during leaf senescence. Involvement of chloroplast redox chemistry (including ROS propagation) in modulating cell death is well supported, with photosynthesis playing a crucial role in providing redox-based signals to this process. While chloroplast contribution to senescence received less attention, recent findings indicate that changes in the redox poise of these organelles strongly affect senescence timing and progress. In this review, the involvement of chloroplasts in leaf senescence execution is critically assessed in relation to available evidence and the role played by environmental and developmental cues such as stress and phytohormones. The collected results indicate that chloroplasts could cooperate with other redox sources (e.g., mitochondria) and signaling molecules to initiate the committed steps of leaf senescence for a best use of the recycled nutrients in plant reproduction.

scholarly journals Distinct Requirements for Zebrafish Angiogenesis Revealed by aVEGF-AMorphant

Yeast ◽  
2000 ◽  
Vol 1 (4) ◽  
pp. 294-301 ◽  
Author(s):  
Aidas Nasevicius ◽  
Jon Larson ◽  
Stephen C. Ekker
Keyword(s):  
Normal Development ◽  
Developmental Process ◽  
Vascular Endothelial ◽  
Vascular Structure ◽  
Loss Of Function ◽  
Quality Model ◽  
Tissue Remodelling ◽  
Structure Specification ◽  
Endothelial Growth Factor

Angiogenesis is a fundamental vertebrate developmental process that requires signalling by the secreted protein vascular endothelial growth factor-A (VEGF-A).VEGF-Afunctions in the development of embryonic structures, during tissue remodelling and for the growth of tumour-induced vasculature. The study of the role ofVEGF-Aduring normal development has been significantly complicated by the dominant, haplo-insufficient nature ofVEGF-A-targeted mutations in mice. We have used morpholino-based targeted gene knock-down technology to generate a zebrafishVEGF-Amorphant loss of function model. ZebrafishVEGF-Amorphant embryos develop with an enlarged pericardium and with major blood vessel deficiencies. Morphological assessment at 2 days of development indicates a nearly complete absence of both axial and intersegmental vasculature, with no or reduced numbers of circulating red blood cells. Molecular analysis using the endothelial markersfli-1andflk-1at 1 day of development demonstrates a fundamental distinction betweenVEGF-Arequirements for axial and intersegmental vascular structure specification.VEGF-Ais not required for the initial establishment of axial vasculature patterning, whereas all development of intersegmental vasculature is dependent onVEGF-Asignalling. The zebrafish thus serves as a quality model for the study of conserved vertebrate angiogenesis processes during embryonic development.

scholarly journals An ABA-regulated and Golgi-localized protein phosphatase controls water loss during leaf senescence in Arabidopsis

2011 ◽  
Vol 69 (4) ◽  
pp. 667-678 ◽  
Author(s):  
Kewei Zhang ◽  
Xiuying Xia ◽  
Yanyan Zhang ◽  
Su-Sheng Gan
Keyword(s):  
Leaf Senescence ◽  
Water Loss ◽  
Protein Phosphatase

scholarly journals Sex-Specific Social Behavior and Amygdala Proteomic Deficits in Foxp2+/− Mutant Mice

2021 ◽  
Vol 15 ◽  
Author(s):  
Maria Jesus Herrero ◽  
Li Wang ◽  
David Hernandez-Pineda ◽  
Payal Banerjee ◽  
Heidi Y. Matos ◽  
...  
Keyword(s):  
Social Behavior ◽  
Social Interactions ◽  
Social Behaviors ◽  
Autism Spectrum ◽  
Loss Of Function ◽  
Neuronal Communication ◽  
Males And Females ◽  
Spectrum Disorders ◽  
Encoding Gene ◽  
Dopamine Signaling

In humans, mutations in the transcription factor encoding gene, FOXP2, are associated with language and Autism Spectrum Disorders (ASD), the latter characterized by deficits in social interactions. However, little is known regarding the function of Foxp2 in male or female social behavior. Our previous studies in mice revealed high expression of Foxp2 within the medial subnucleus of the amygdala (MeA), a limbic brain region highly implicated in innate social behaviors such as mating, aggression, and parental care. Here, using a comprehensive panel of behavioral tests in male and female Foxp2+/– heterozygous mice, we investigated the role Foxp2 plays in MeA-linked innate social behaviors. We reveal significant deficits in olfactory processing, social interaction, mating, aggressive, and parental behaviors. Interestingly, some of these deficits are displayed in a sex-specific manner. To examine the consequences of Foxp2 loss of function specifically in the MeA, we conducted a proteomic analysis of microdissected MeA tissue. This analyses revealed putative sex differences expression of a host of proteins implicated in neuronal communication, connectivity, and dopamine signaling. Consistent with this, we discovered that MeA Foxp2-lineage cells were responsive to dopamine with differences between males and females. Thus, our findings reveal a central and sex-specific role for Foxp2 in social behavior and MeA function.

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