Avena fatua caryopsis dormancy release is associated with changes in KAR1 and ABA sensitivity as well as with ABA reduction in coleorhiza and radicle

Abstract Main conclusion The dormancy release in Avena fatua caryopses was associated with a reduction in the ABA content in embryos, coleorhiza and radicle. The coleorhiza proved more sensitive to KAR1 and less sensitive to ABA than the radicle. The inability of dormant caryopses and ABA-treated non-dormant caryopses to complete germination is related to inhibition and delayed of cell-cycle activation, respectively. Abstract As freshly harvested Avena fatua caryopses are dormant at 20 °C, they cannot complete germination; the radicle is not able to emerge. Both karrikin 1 (KAR1) and dry after-ripening release dormancy, enabling the emergence of, first, the coleorhiza and later the radicle. The after-ripening removes caryopse sensitivity to KAR1 and decreases the sensitivity to abscisic acid (ABA). The coleorhiza was found to be more sensitive to KAR1, and less sensitive to ABA, than radicles. Effects of KAR1 and after-ripening were associated with a reduction of the embryo’s ABA content during caryopsis germination. KAR1 was found to decrease the ABA content in the coleorhiza and radicles. Germination of after-ripened caryopses was associated with the progress of cell-cycle activation before coleorhiza emergence. Inhibition of the germination completion due to dormancy or treating the non-dormant caryopses with ABA was associated with a total and partial inhibition of cell-cycle activation, respectively.

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Gibberellin-like effects of KAR1 on dormancy release of Avena fatua caryopses include participation of non-enzymatic antioxidants and cell cycle activation in embryos

Planta ◽

10.1007/s00425-015-2422-1 ◽

2015 ◽

Vol 243 (2) ◽

pp. 531-548 ◽

Cited By ~ 17

Author(s):

Danuta Cembrowska-Lech ◽

Jan Kępczyński

Keyword(s):

Cell Cycle ◽

Avena Fatua ◽

Enzymatic Antioxidants ◽

Dormancy Release ◽

Cell Cycle Activation

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Reduced embryo sensitivity to abscisic acid in a sprouting-susceptible sorghum (Sorghum bicolor) variety is associated with altered ABA signalling

Seed Science Research ◽

10.1017/s0960258507708115 ◽

2007 ◽

Vol 17 (2) ◽

pp. 81-90 ◽

Cited By ~ 9

Author(s):

Nicolás Gualano ◽

Fernando Carrari ◽

María Verónica Rodríguez ◽

Laura Pérez-Flores ◽

Rodolfo Sánchez ◽

...

Keyword(s):

Abscisic Acid ◽

Sorghum Bicolor ◽

Developmental Stages ◽

Signal Transduction Pathway ◽

Transduction Pathway ◽

Aba Signal Transduction ◽

Aba Sensitivity ◽

Two Stages ◽

Aba Content ◽

Endogenous Aba

AbstractIn the work reported in this paper, we attempted to elucidate the nature of the different abscisic acid (ABA) sensitivities presented by developing embryos from sorghum [Sorghum bicolor (L.) Moench] lines with contrasting pre-harvest sprouting (PHS) behaviour (Redland B2, susceptible; IS 9530, resistant). We explored two different hypotheses for a possible mechanism: (1) a different functionality of the ABA signalling pathway, and (2) a different rate of ABA degradation/conjugation in the apoplast of embryos from these genotypes. To assess the first possibility, we used an ABA-responsive gene (Rab17) as a reporter of changes in endogenous ABA content, which were artificially induced in embryos from both genotypes by means of fluridone application immediately after anthesis, to reduce ABA content, and embryo incubation in the presence of ABA. A defect in ABA signalling should be seen as a level of Rab17 expression that is independent of endogenous ABA content. For testing the second possibility at two stages of development, embryos from both lines were isolated and incubated in water for different periods. ABA concentrations in embryos and the incubation media were quantified through radioimmunoassay. In contrast to our findings for the resistant IS 9530 line, Rab17 expression did not respond to changes in ABA levels in sensitive Redland B2 embryos. The ABA degradation/conjugation rates in embryos and incubation media did not show clear differences between sorghum lines for any of the developmental stages analysed. These results suggest that a disruption in the ABA signal transduction pathway in Redland B2 underlies the low ABA sensitivity shown by embryos from this line.

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Phytohormones, Isoprenoids, and Role of the Apicoplast in Recovery from Dihydroartemisinin-Induced Dormancy of Plasmodium falciparum

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.01771-17 ◽

2018 ◽

Vol 62 (3) ◽

Cited By ~ 7

Author(s):

Marvin Duvalsaint ◽

Dennis E. Kyle

Keyword(s):

Cell Cycle ◽

Plasmodium Falciparum ◽

Abscisic Acid ◽

Stress Response ◽

Regulatory Network ◽

Dormancy Release ◽

Content Type ◽

Cycle Arrest ◽

Aba Synthesis

ABSTRACT Many organisms undergo dormancy as a stress response to survive under unfavorable conditions that might impede development. This is observed in seeds and buds of plants and has been proposed as a mechanism of drug evasion and resistance formation in Plasmodium falciparum . We explored the effects of the phytohormones abscisic acid (ABA) and gibberellic acid (GA) on dihydroartemisinin (DHA)-induced dormant erythrocytic stages of P. falciparum parasites. Dormant ring stages exposed to ABA and GA recovered from dormancy up to 48 h earlier than parasites exposed to DHA alone. Conversely, fluridone, an herbicide inhibitor of ABA synthesis, blocked emergence from dormancy. Additionally, the role of the apicoplast was assessed in dormant parasite recovery. Apicoplast-deficient P. falciparum remained viable for up to 8 days without the organelle and recrudesced only when supplemented with isopentyl pyrophosphate (IPP). IPP was not required for survival in the dormant state. Fosmidomycin inhibition of isoprenoid biosynthesis did not prevent dormancy release from occurring in parasites with an intact apicoplast, but IPP or geranylgeranyl pyrophosphate was needed for complete recrudescence. In addition, the apicoplast and specifically the isoprenoids it produces are essential for recovery of dormant parasites. In summary, ABA and GA have significant effects on dormant parasites, and the phenotypes produced by these phytohormones and the herbicide fluridone also provide a means to explore the mechanism(s) underlying dormancy and the regulatory network that promotes cell cycle arrest in P. falciparum .

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Cell Cycle Activation of Peripheral Blood Stem and Progenitor Cells Expanded Ex Vivo with SCF, FLT-3 Ligand, TPO, and IL-3 Results in Accelerated Granulocyte Recovery in a Baboon Model of Autologous Transplantation but G0/G1and S/G2/M Graft Cell Content Does Not Correlate with Tranplantability

Stem Cells ◽

10.1634/stemcells.19-5-436 ◽

2001 ◽

Vol 19 (5) ◽

pp. 436-442 ◽

Cited By ~ 7

Author(s):

M. Drouet ◽

F. Herodin ◽

F. Norol ◽

F. Mourcin ◽

J. F. Mayol

Keyword(s):

Cell Cycle ◽

Progenitor Cells ◽

Peripheral Blood ◽

Ex Vivo ◽

Autologous Transplantation ◽

Cell Content ◽

Cell Cycle Activation ◽

Baboon Model ◽

Stem And Progenitor Cells

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Cell cycle‐dependent regulation of telomerase activity by auxin, abscisic acid and protein phosphorylation in tobacco BY‐2 suspension culture cells

The Plant Journal ◽

10.1046/j.0960-7412.2001.01244.x ◽

2002 ◽

Vol 29 (5) ◽

pp. 617-626 ◽

Cited By ~ 32

Author(s):

Seong Wook Yang ◽

EonSeon Jin ◽

In Kwon Chung ◽

Woo Taek Kim

Keyword(s):

Cell Cycle ◽

Abscisic Acid ◽

Suspension Culture ◽

Protein Phosphorylation ◽

Telomerase Activity ◽

Culture Cells ◽

Cycle Dependent

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Differential Effect of Jasmonic Acid and Abscisic Acid on Cell Cycle Progression in Tobacco BY-2 Cells

PLANT PHYSIOLOGY ◽

10.1104/pp.010592 ◽

2002 ◽

Vol 128 (1) ◽

pp. 201-211 ◽

Cited By ~ 110

Author(s):

Agnieszka Świa̧tek ◽

Marc Lenjou ◽

Dirk Van Bockstaele ◽

Dirk Inzé ◽

Harry Van Onckelen

Keyword(s):

Cell Cycle ◽

Abscisic Acid ◽

Jasmonic Acid ◽

Differential Effect ◽

Cell Cycle Progression ◽

Cycle Progression

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Histone H3 transcription in Saccharomyces cerevisiae is controlled by multiple cell cycle activation sites and a constitutive negative regulatory element

Molecular and Cellular Biology ◽

10.1128/mcb.12.12.5455-5463.1992 ◽

1992 ◽

Vol 12 (12) ◽

pp. 5455-5463 ◽

Cited By ~ 1

Author(s):

K B Freeman ◽

L R Karns ◽

K A Lutz ◽

M M Smith

Keyword(s):

Saccharomyces Cerevisiae ◽

Cell Cycle ◽

Cell Division ◽

Transcriptional Activation ◽

Regulatory Element ◽

Histone H3 ◽

Regulatory Elements ◽

Cell Division Cycle ◽

Cell Cycle Activation ◽

Multiple Cell

The promoters of the Saccharomyces cerevisiae histone H3 and H4 genes were examined for cis-acting DNA sequence elements regulating transcription and cell division cycle control. Deletion and linker disruption mutations identified two classes of regulatory elements: multiple cell cycle activation (CCA) sites and a negative regulatory site (NRS). Duplicate 19-bp CCA sites are present in both the copy I and copy II histone H3-H4 promoters arranged as inverted repeats separated by 45 and 68 bp. The CCA sites are both necessary and sufficient to activate transcription under cell division cycle control. A single CCA site provides cell cycle control but is a weak transcriptional activator, while an inverted repeat comprising two CCA sites provides both strong transcriptional activation and cell division cycle control. The NRS was identified in the copy I histone H3-H4 promoter. Deletion or disruption of the NRS increased the level of the histone H3 promoter activity but did not alter the cell division cycle periodicity of transcription. When the CCA sites were deleted from the histone promoter, the NRS element was unable to confer cell division cycle control on the remaining basal level of transcription. When the NRS element was inserted into the promoter of a foreign reporter gene, transcription was constitutively repressed and did not acquire cell cycle regulation.

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Connecting cell-cycle activation to neurodegeneration in Drosophila

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease ◽

10.1016/j.bbadis.2006.10.007 ◽

2007 ◽

Vol 1772 (4) ◽

pp. 446-456 ◽

Cited By ~ 11

Author(s):

Vikram Khurana ◽

Mel B. Feany

Keyword(s):

Cell Cycle ◽

Cell Cycle Activation

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Pathogenic tau disrupts the cellular program that maintains neuronal identity

10.1101/2021.03.05.434166 ◽

2021 ◽

Author(s):

Adrian Beckmann ◽

Paulino Ramirez ◽

Maria Gamez ◽

William J. Ray ◽

Bess Frost

Keyword(s):

Alzheimer’S Disease ◽

Cell Cycle ◽

Alzheimer's Disease ◽

Epithelial Mesenchymal Transition ◽

Tumor Formation ◽

Therapeutic Approaches ◽

Nuclear Pleomorphism ◽

Mesenchymal Transition ◽

Neuronal Identity ◽

Cell Cycle Activation

AbstractNeurons in human Alzheimer’s disease acquire phenotypes that are also present in various cancers, including over-stabilization of the cytoskeleton, nuclear pleomorphism, decondensation of constitutive heterochromatin, and aberrant activation of the cell cycle. Unlike in cancer, in which cell cycle activation drives tumor formation, activation of the cell cycle in post-mitotic neurons is sufficient to induce neuronal death. Multiple lines of evidence suggest that abortive cell cycle activation is a consequence of pathogenic forms of tau, a protein that drives neurodegeneration in Alzheimer’s disease and related “tauopathies.” We have combined network analysis of human Alzheimer’s disease and mouse tauopathy with mechanistic studies in Drosophila to discover that pathogenic forms of tau drive abortive cell cycle activation by disrupting the cellular program that maintains neuronal identity. Mechanistically, we identify Moesin, a prognostic biomarker for cancer and mediator of the epithelial-mesenchymal transition (EMT), as a major effector of tau-induced neurotoxicity. We find that aberrant activation of Moesin in neurons acts through the actin cytoskeleton to dysregulate the cellular program that maintains neuronal identity. Our study identifies mechanistic parallels between tauopathy and cancer and sets the stage for novel therapeutic approaches.

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