Auxin-Induced Epinasty of Tobacco Leaf Tissues (A Nonethylene-Mediated Response)

Keller, Christopher P.; Volkenburgh, Elizabeth Van

doi:10.1104/pp.113.2.603

Cited by 55 publications

(68 citation statements)

References 21 publications

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“…This process cannot explain directly the phenomenon of leaf epinasty, but indicates the tight relationship between light, auxin metabolism and differential growth. Next to that, the suggestion that auxin is involved is supported by findings that application of auxins exogenously could induce leaf epinasty (Keller and VanVolkenburgh, 1997;Jones et al, 1998;Keller and Van Volkenburgh, 1998;Keller, 2007) and that auxin-overproducing plants show a similar type of same leaf epinasty (Klee et al, 1987;Romano et al, 1993;Romano et al, 1995;Kim et al, 2007).…”

Section: Involvement Of Phytohormonessupporting

confidence: 48%

Leaf Epinasty in Chrysanthemum: Enabling Breeding Against an Adverse Trait by Physiological Research

Geest¹,

Ieperen²,

Post³

et al. 2012

Acta Hortic.

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Breeding for a certain trait is only possible when the phenotypic variation that is caused by genotypic variation can be estimated. For traits that strongly depend on environmental conditions, this can be extremely difficult and knowledge and collaboration with experts from other disciplines becomes essential. A wellknown example is breeding for disease resistance. Here, we describe a similar approach to assist breeding against adverse leaf deformations that severely reduce the ornamental value of some chrysanthemum (Dendranthema × grandiflora) genotypes during greenhouse cultivation in winter. These leaf deformations occur rather unpredictably, but seem to be related to the increased use of assimilation light. To breed against this trait knowledge is needed (i) about inductive environments in which sensitive and insensitive genotypes are distinguishable, and (ii) about the physiological background associated with leaf epinasty. In this paper hypothetical physiological factors and mechanisms are discussed, which may mediate effects of light spectrum and greenhouse climate on leaf epinasty. One factor involved could be starch accumulation, since leaf epinasty usually aggravates after disbudding -a practice that most probably alters the sink-source balance. Additionally, light spectra can affect the circadian clock and thereby disturb starch synthesis and breakdown resulting in accumulation. Both within and independent of this process, plant hormones such as auxin and ethylene may play a role in leaf epinasty. This theoretical framework will be used to further investigate the physiological background of leaf epinasty and to come up with a test in which susceptibility for leaf epinasty can be assessed.

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Section: Involvement Of Phytohormonessupporting

confidence: 48%

Leaf Epinasty in Chrysanthemum: Enabling Breeding Against an Adverse Trait by Physiological Research

Geest¹,

Ieperen²,

Post³

et al. 2012

Acta Hortic.

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“…One attractive hypothesis is thus that they could modulate the activity of proteins directly involved in auxin transport. Importantly, AUX1 and members of its family of auxin influx carriers have recently been shown to control leaf flatness (Keller and Van Volkenburgh, 1997;Li et al, 2007;Bainbridge et al, 2008). However, while in aux1 mesophyll protoplasts auxin accumulation was reduced, the opposite was found in pks1pks2 protoplasts.…”

Section: Discussionmentioning

confidence: 71%

“…Auxin transport by PGP19, PIN3, and AUX1 as well as auxin-dependent transcription are required for normal phototropism (Friml et al, 2002;Tatematsu et al, 2004;Stone et al, 2008). Although in the case of leaf flattening a direct connection between phototropin and auxin signaling has not yet been established, several genetic and pharmacological experiments provide evidence that leaf flattening is also regulated by auxin homeostasis and signaling (Keller and Van Volkenburgh, 1997;Li et al, 2007;Bainbridge et al, 2008). Analogous scenarios can be envisaged where in hypocotyls the phototropins coordinate asymmetric growth while in leaves the same photoreceptors coordinate symmetric growth of the lamina to ensure its flatness (Poethig, 1997;Whippo and Hangarter, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, phototropic responses and leaf flattening are slower symmetric growth processes coordinated by cell expansion and division. Such growth coordination is under tight hormonal regulation, and the hormone auxin is a central regulator of phototropism (Holland et al, 2009), leaf flattening (Keller and Van Volkenburgh, 1997;Li et al, 2007;Bainbridge et al, 2008;Braun et al, 2008), and leaf positioning (Tao et al, 2008;Millenaar et al, 2009). An important task is to identify points of convergence between phototropin signaling and auxin signaling.…”

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confidence: 99%

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The Arabidopsis PHYTOCHROME KINASE SUBSTRATE2 Protein Is a Phototropin Signaling Element That Regulates Leaf Flattening and Leaf Positioning

et al. 2010

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In Arabidopsis (Arabidopsis thaliana), the blue light photoreceptor phototropins (phot1 and phot2) fine-tune the photosynthetic status of the plant by controlling several important adaptive processes in response to environmental light variations. These processes include stem and petiole phototropism (leaf positioning), leaf flattening, stomatal opening, and chloroplast movements. The PHYTOCHROME KINASE SUBSTRATE (PKS) protein family comprises four members in Arabidopsis (PKS1-PKS4). PKS1 is a novel phot1 signaling element during phototropism, as it interacts with phot1 and the important signaling element NONPHOTOTROPIC HYPOCOTYL3 (NPH3) and is required for normal phot1-mediated phototropism. In this study, we have analyzed more globally the role of three PKS members (PKS1, PKS2, and PKS4). Systematic analysis of mutants reveals that PKS2 (and to a lesser extent PKS1) act in the same subset of phototropin-controlled responses as NPH3, namely leaf flattening and positioning. PKS1, PKS2, and NPH3 coimmunoprecipitate with both phot1-green fluorescent protein and phot2-green fluorescent protein in leaf extracts. Genetic experiments position PKS2 within phot1 and phot2 pathways controlling leaf positioning and leaf flattening, respectively. NPH3 can act in both phot1 and phot2 pathways, and synergistic interactions observed between pks2 and nph3 mutants suggest complementary roles of PKS2 and NPH3 during phototropin signaling. Finally, several observations further suggest that PKS2 may regulate leaf flattening and positioning by controlling auxin homeostasis. Together with previous findings, our results indicate that the PKS proteins represent an important family of phototropin signaling proteins.

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“…Differential expansion of tissue layers in cylindrical organs, such as stems and roots, results in tissue tension, often redirecting growth, as in the case of shoot phototropism and root gravitropic curvature (Liscum and StoweEvans, 2000;Swarup et al, 2005). Leaf epinasty is also the consequence of differential growth of the abaxial and adaxial sides (Keller and Van Volkenburgh, 1997). Within one single tissue layer of a flat tissue structure, such as the abaxial leaf epidermis, tension is more difficult to translate into motion to release pressure.…”

Section: Differential Cell Expansion Within the Leaf Epidermismentioning

confidence: 99%

Model-Based Analysis of Arabidopsis Leaf Epidermal Cells Reveals Distinct Division and Expansion Patterns for Pavement and Guard Cells

et al. 2011

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To efficiently capture sunlight for photosynthesis, leaves typically develop into a flat and thin structure. This development is driven by cell division and expansion, but the individual contribution of these processes is currently unknown, mainly because of the experimental difficulties to disentangle them in a developing organ, due to their tight interconnection. To circumvent this problem, we built a mathematic model that describes the possible division patterns and expansion rates for individual epidermal cells. This model was used to fit experimental data on cell numbers and sizes obtained over time intervals of 1 d throughout the development of the first leaf pair of Arabidopsis (Arabidopsis thaliana). The parameters were obtained by a derivative-free optimization method that minimizes the differences between the predicted and experimentally observed cell size distributions. The model allowed us to calculate probabilities for a cell to divide into guard or pavement cells, the maximum size at which it can divide, and its average cell division and expansion rates at each point during the leaf developmental process. Surprisingly, average cell cycle duration remained constant throughout leaf development, whereas no evidence for a maximum cell size threshold for cell division of pavement cells was found. Furthermore, the model predicted that neighboring cells of different sizes within the epidermis expand at distinctly different relative rates, which could be verified by direct observations. We conclude that cell division seems to occur independently from the status of cell expansion, whereas the cell cycle might act as a timer rather than as a size-regulated machinery.

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Auxin-Induced Epinasty of Tobacco Leaf Tissues (A Nonethylene-Mediated Response)

Cited by 55 publications

References 21 publications

Leaf Epinasty in Chrysanthemum: Enabling Breeding Against an Adverse Trait by Physiological Research

Leaf Epinasty in Chrysanthemum: Enabling Breeding Against an Adverse Trait by Physiological Research

The Arabidopsis PHYTOCHROME KINASE SUBSTRATE2 Protein Is a Phototropin Signaling Element That Regulates Leaf Flattening and Leaf Positioning

Model-Based Analysis of Arabidopsis Leaf Epidermal Cells Reveals Distinct Division and Expansion Patterns for Pavement and Guard Cells

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