Auxin Deprivation Induces Synchronous Golgi Differentiation in Suspension-Cultured Tobacco BY-2 Cells1

Winicur, Z. M.; Zhang, Guo Feng; Staehelin, L. Andrew

doi:10.1104/pp.117.2.501

Cited by 50 publications

(47 citation statements)

References 53 publications

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“…As shown in Fig. 5A, the addition of 2,4-D to auxin-starved cells induced division within 3 h, confirming the timing and the absolute values of increase in mitotic index as previously described (23). YkB (1 M) completely inhibited cell division induced by 2,4-D, and cells entered stasis (Fig.…”

Section: Ykb Inhibition Links Aux/iaa Stability To Auxin-regulated Cesupporting

confidence: 89%

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Yokonolide B, a Novel Inhibitor of Auxin Action, Blocks Degradation of AUX/IAA Factors

Hayashi

Jones

Ogino

et al. 2003

Journal of Biological Chemistry

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Yokonolide B (YkB; also known as A82548A), a spiroketal-macrolide, was isolated from Streptomyces diastatochromogenes B59 in a screen for inhibitors of ␤-glucoronidase expression under the control of an auxin-responsive promoter in Arabidopsis. YkB inhibits the expression of auxin-inducible genes as shown using native and synthetic auxin promoters as well as using expression profiling of 8,300 Arabidopsis gene probes but does not affect expression of an abscisic acid-and a gibberellin A 3 -inducible gene. The mechanism of action of YkB is to block AUX/IAA protein degradation; however, YkB is not a general proteasome inhibitor. YkB blocks auxin-dependent cell division and auxin-regulated epinastic growth mediated by auxin-binding protein 1. Gain of function mutants such as shy2-2, slr1, and axr2-1 encoding AUX/IAA transcriptional repressors and loss of function mutants encoding components of the ubiquitin-proteolytic pathway such as axr1-3 and tir1-1, which display increased AUX/IAAs protein stability, are less sensitive to YkB, although axr1 and tir1 mutants were sensitive to MG132, a general proteasome inhibitor, consistent with a site of action downstream of AXR1 and TIR. YkB-treated seedlings displayed similar phenotypes as dominant AUX/IAA mutants. Taken together, these results indicate that YkB acts to block AUX/IAA protein degradation upstream of AXR and TIR, links a shared element upstream of AUX/IAA protein stability to auxin-induced cell division/elongation and to auxin-binding protein 1, and provides a new tool to dissect auxin signal transduction.Auxin controls cell division, elongation, and differentiation and therefore, through its action at the level of the cell, exerts profound effects on growth and development throughout the life of the plant (1). Consistent with the diverse effects of auxin on growth and development is that the expression patterns of a number of genes are dramatically and rapidly altered by auxin application (2), suggesting that auxin ultimately regulates cell growth by controlling the profile of expressed genes. AUX/IAA genes comprise a 34-member gene family in Arabidopsis that is one of three known gene families that are regulated by auxin and implicated to play essential roles in auxin signaling (3, 4).The molecular and genetic studies on auxin signaling have revealed that auxin specifically enhances the transcription of many AUX/IAA genes within minutes without requiring de novo protein synthesis, suggesting that AUX/IAA genes are primary auxin-response genes (5, 6). AUX/IAA genes encode short lived nuclear proteins capable of heterodimerization with auxin-responsive factors (7) and are thought to act by negatively regulating the expression of early auxin-responsive genes including other members of the AUX/IAA family (3).Studies on Arabidopsis mutants with altered responses to auxin such as iaa3/shy2-2, iaa7/axr2-1, iaa17/axr3, iaa14/slr1, tir1, and axr1 revealed that the turnover rate of AUX/IAA proteins is in some way important in various developmental processes including ...

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Section: Ykb Inhibition Links Aux/iaa Stability To Auxin-regulated Cesupporting

confidence: 89%

“…Deprivation of auxin stops cell division and reveals the underlying cell elongation. Readdition of auxin stimulates division in a semisynchronous manner (23). As shown in Fig.…”

Section: Ykb Inhibition Links Aux/iaa Stability To Auxin-regulated Cementioning

confidence: 98%

Yokonolide B, a Novel Inhibitor of Auxin Action, Blocks Degradation of AUX/IAA Factors

Hayashi

Jones

Ogino

et al. 2003

Journal of Biological Chemistry

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“…Moreover, it was found that the amyloplast formation in BY-2 cells was always accompanied by a reduction in cell multiplication rate, increase in cell volume , shorter lifetime, weaker cell-cell adhesion (Sakai et al 2004a), and alterations in the secretion properties (unpublished result). The changes observed under amyloplst-inducing conditions resembles to what observed during differentiation of root cap cells, as has been suggested from the study of Golgi differentiation (Staehelin et al 1990, Winicur et al 1998. Thus, the behavior of BY-2 cells under amyloplast-inducing conditions (in the absence of auxin) might mimic the process of differentiation of the cells in the root cap, whereas the behavior under normal culture condition (in the presence of auxin) might mimic the process of cell proliferation in the meristem (Sakai et al 2004a).…”

Section: Amyloplast Differentiation In By-2 Cells: Similarity To Rootsupporting

confidence: 67%

Cytological Studies on Proliferation, Differentiation, and Death of BY-2 Cultured Tobacco Cells

et al. 2015

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Summary A procedure for the simultaneous isolation of mitochondrial and plastid nucleoids was first established in BY-2 cells. Biochemical analysis suggested the presence of nucleosome-like repetitive structural units in both of the plant organelle nucleoids. The isolated organelle nucleoids were also used for establishment of in vitro transcription/DNA synthesis systems, with which regulation of organelle genomes during proliferation and differentiation was investigated. The results revealed that transient and synchronous activation of DNA synthesis occurred in mitochondria and plastids in the initial phase of cell proliferation, which was caused by a transient activation of dually-targeted organelle DNA polymerase genes. Another series of investigations revealed a drastic difference in the transcription activity between BY-2 proplastids and leaf chloroplasts, which was brought about by differential use of bacterial-and phage-type plastid RNA polymerases. To investigate regulation of plastid gene expression further, a procedure to induce amyloplast formation in BY-2 cells was established. Various changes observed during this process were collectively similar to those observed during root cap cell differentiation. BY-2 cells were also used to develop a novel model system for programmed cell death during hypersensitive reaction (HR), in which we have succeeded in inducing programmed cell death with 100% efficiency by application of an elicitor. This system revealed that the HR cells activated anti-microbial defense mechanism by themselves and transmitted signal(s) to establish acquired resistance in neighboring cells, while executing cell-death program. Thus, BY-2 cells have taught us a lot about proliferation, differentiation, and death of plant cells.

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“…Readdition of auxin stimulates division in a semisynchronous manner (Winicur et al, 1998). As shown in Figure 4A, the cell division in auxin-starved cells was initiated by the addition of 2,4-D within 3 h as described previously (Winicur et al, 1998). Application of 20 mM TrfA completely inhibited cell division induced by 2,4-D and cells entered stasis (Fig.…”

Section: Trfa Inhibits Auxin-dependent Cell Divisionmentioning

confidence: 60%

“…Cell division of BY2 cultured cells is critically dependent on auxin and is interrupted by auxin deprivation. Readdition of auxin stimulates division in a semisynchronous manner (Winicur et al, 1998). As shown in Figure 4A, the cell division in auxin-starved cells was initiated by the addition of 2,4-D within 3 h as described previously (Winicur et al, 1998).…”

Section: Trfa Inhibits Auxin-dependent Cell Divisionmentioning

confidence: 94%

Characterization of Terfestatin A, a New Specific Inhibitor for Auxin Signaling

et al. 2005

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Terfestatin A (TrfA), terphenyl-β-glucoside, was isolated from Streptomyces sp. F40 in a forward screen for compounds that inhibit the expression of auxin-inducible genes in Arabidopsis (Arabidopsis thaliana). TrfA specifically and competitively inhibited the expression of primary auxin-inducible genes in Arabidopsis roots, but did not affect the expression of genes regulated by other plant hormones such as abscisic acid and cytokinin. TrfA also blocked the auxin-enhanced degradation of auxin/indole-3-acetic acid (Aux/IAA) repressor proteins without affecting the auxin-stimulated interaction between Aux/IAAs and the F-box protein TIR1. TrfA treatment antagonized auxin responses in roots, including primary root inhibition, lateral root initiation, root hair promotion, and root gravitropism, but had only limited effects on shoot auxin responses. Taken together, these results indicate that TrfA acts as a modulator of Aux/IAA stability and thus provides a new tool for dissecting auxin signaling.

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Auxin Deprivation Induces Synchronous Golgi Differentiation in Suspension-Cultured Tobacco BY-2 Cells1

Cited by 50 publications

References 53 publications

Yokonolide B, a Novel Inhibitor of Auxin Action, Blocks Degradation of AUX/IAA Factors

Yokonolide B, a Novel Inhibitor of Auxin Action, Blocks Degradation of AUX/IAA Factors

Cytological Studies on Proliferation, Differentiation, and Death of BY-2 Cultured Tobacco Cells

Characterization of Terfestatin A, a New Specific Inhibitor for Auxin Signaling

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