Inhibition of Growth of Cultured Tobacco Cells at Low Concentrations of Lovastatin Is Reversed by Cytokinin

Crowell, Dring N.; Salaz, Michael S.

doi:10.1104/pp.100.4.2090

Cited by 73 publications

(75 citation statements)

References 29 publications

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“…Cytokinins were found to be necessary for the entry of tobacco mesophyll protoplasts into S phase [10] and for the G2/M transition of tobacco and Glycine max suspension cultures [9,11]. Crowell and Salaz [33] have shown that the growth of tobacco BY-2 cells is inhibited by low concentrations of lovastatin, which inhibits the isoprenoid pathway that leads to the biosynthesis of the cytokinin side chain. This inhibition could be reversed by supplying Z to the medium, These data support our suggestion that fluctuations in the levels of specific cytokinins at distinct stages of the:cell cycle reflect their essential role during these phases.…”

Section: Discussionmentioning

confidence: 99%

Levels of endogenous cytokinins, indole‐3‐acetic acid and abscisic acid during the cell cycle of synchronized tobacco BY‐2 cells

Redig¹,

et al. 1996

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Correlation between cell cycle progression and endogenous levels of plant hormones was studied in synchronized tobacco BY-2 cell suspension cultures. Sixteen different cytokinins, indole-3-acetic acid (IAA) and abscisic acid (ABA) were extracted using solid-phase anion exchange chromatography in combination with immunoaffinity purification, and quantified by mass spectrometry. No significant correlation could be identified for IAA and ABA. In contrast, there were sharp peaks in the levels of specific cytokinins (zeatin-and dihydrozeatin-type) at the end of the S phase and during mitosis. The levels of other cytokinins analyzed, including zeatins N-and O-glucosides, remained low, suggesting that the increased amounts of their corresponding non-glucosylated form resulted from de novo synthesis. These f'mdings suggest that zeatin-and dihydrozeatintype cytokinins might play a specific regulatory role in the progression of the plant cell cycle. One hypothesis to explain cytokinin action is based on a specific interaction with kinases that regulate cell cycle progression, as has been recently shown for the cytokinin analogue olomoucine.

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Section: Discussionmentioning

confidence: 99%

Levels of endogenous cytokinins, indole‐3‐acetic acid and abscisic acid during the cell cycle of synchronized tobacco BY‐2 cells

Redig¹,

et al. 1996

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“…As this latter compound is a precursor of essential constituents, pleiotropic effects can be expected. Mevinolin or its analogs such as compactin act as efficient inhibitors of plant cell proliferation (Ryder and Goad, 1980;Ceccarelli and Lorenzi, 1984;Dö ll et al, 1984;Bach and Lichtenthaler, 1987;Hata et al, 1987;Crowell and Salaz, 1992;Randall et al, 1993;Morehead et al, 1995), and analogous to early observations made with various animal and human cell lines, specific effects on progression through a cell cycle of plant cells have been predicted (Bach, 1987). Using tobacco (Nicotiana tabacum L. cv Bright Yellow-2 [TBY-2]) cells (Nagata et al, 1992), we recently demonstrated that mevinolin treatment leads to an arrest of a majority of cells in late G1 phase (Hemmerlin and Bach, 1998).…”

mentioning

confidence: 84%

Farnesol-Induced Cell Death and Stimulation of 3-Hydroxy-3-Methylglutaryl-Coenzyme A Reductase Activity in Tobacco cv Bright Yellow-2 Cells,

Hemmerlin

Bach

2000

Plant Physiology

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Growth inhibition of tobacco (Nicotiana tabacum L. cv Bright Yellow-2) cells by mevinolin, a specific inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGR) could be partially overcome by the addition of farnesol. However, farnesol alone inhibited cell division and growth as measured by determination of fresh weight increase. When 7-d-old tobacco cv Bright Yellow-2 cells were diluted 40-fold into fresh culture, the cells exhibited a dose-dependent sensitivity to farnesol, with 25 m sufficient to cause 100% cell death, as measured by different staining techniques, cytometry, and monitoring of fragmentation of genomic DNA. Cells were less sensitive to the effects of farnesol when diluted only 4-fold. Farnesol was absorbed by the cells, as examined by [1-3 H]farnesol uptake, with a greater relative enrichment by the more diluted cells. Both mevinolin and farnesol treatments stimulated apparent HMGR activity. The stimulation by farnesol was also reflected in corresponding changes in the steady-state levels of HMGR mRNA and enzyme protein with respect to HMGR gene expression and enzyme protein accumulation.

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“…LVS when used at 1 mM or at a lower concentration is known to act in blocking specifically the synthesis of the CK precursor from the mevalonate pathway (Alberts, 1988;Crowell and Salaz, 1992;Hartig and Beck, 2005). PI-55 and LGR-991 are inhibitors of CK perception, acting, respectively, as competitors of the CK receptors Arabidopsis His kinase AHK4 and AHK3/4 (Spíchal et al, 2009;Nisler et al, 2010).…”

Section: Exogenous Applications Of Chemicals and Growth Measurementsmentioning

confidence: 99%

Cytokinins Are Initial Targets of Light in the Control of Bud Outgrowth

et al. 2016

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Bud outgrowth is controlled by environmental and endogenous factors. Through the use of the photosynthesis inhibitor norflurazon and of masking experiments, evidence is given here that light acts mainly as a morphogenic signal in the triggering of bud outgrowth and that initial steps in the light signaling pathway involve cytokinins (CKs). Indeed, in rose (Rosa hybrida), inhibition of bud outgrowth by darkness is suppressed solely by the application of CKs. In contrast, application of sugars has a limited effect. Exposure of plants to white light (WL) induces a rapid (after 3-6 h of WL exposure) up-regulation of CK synthesis (RhIPT3 and RhIPT5), of CK activation (RhLOG8), and of CK putative transporter RhPUP5 genes and to the repression of the CK degradation RhCKX1 gene in the node. This leads to the accumulation of CKs in the node within 6 h and in the bud at 24 h and to the triggering of bud outgrowth. Molecular analysis of genes involved in major mechanisms of bud outgrowth (strigolactone signaling [RwMAX2], metabolism and transport of auxin [RhPIN1, RhYUC1, and RhTAR1], regulation of sugar sink strength [RhVI, RhSUSY, RhSUC2, and RhSWEET10], and cell division and expansion [RhEXP and RhPCNA]) reveal that, when supplied in darkness, CKs up-regulate their expression as rapidly and as intensely as WL. Additionally, up-regulation of CKs by WL promotes xylem flux toward the bud, as evidenced by Methylene Blue accumulation in the bud after CK treatment in the dark. Altogether, these results suggest that CKs are initial components of the light signaling pathway that controls the initiation of bud outgrowth.

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Inhibition of Growth of Cultured Tobacco Cells at Low Concentrations of Lovastatin Is Reversed by Cytokinin

Cited by 73 publications

References 29 publications

Levels of endogenous cytokinins, indole‐3‐acetic acid and abscisic acid during the cell cycle of synchronized tobacco BY‐2 cells

Levels of endogenous cytokinins, indole‐3‐acetic acid and abscisic acid during the cell cycle of synchronized tobacco BY‐2 cells

Farnesol-Induced Cell Death and Stimulation of 3-Hydroxy-3-Methylglutaryl-Coenzyme A Reductase Activity in Tobacco cv Bright Yellow-2 Cells,

Cytokinins Are Initial Targets of Light in the Control of Bud Outgrowth

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