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Publikationen - Molekulare Signalverarbeitung

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Publikation

Gasperini, D., Chauvin, A., Acosta, I.F., Kurenda, A., Stolz, S., Chétalat, A., Wolfender J.-L. & Farmer, E.E. Axial and Radial Oxylipin Transport. Plant Physiol. 169, 2244-2254, (2015) DOI: 10.1104/pp.15.01104

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Publikation

Gasperini, D., Chételat, A., Acosta, I.F., Goossens, J., Pauwels, L., Goossens, A., Dreos, R., Alonso, E. & Farmer, E.E. Multilayered Organization of Jasmonate Signalling in the Regulation of Root Growth PLoS Genet. 11 (6), e1005300, (2015) DOI: 10.1371/journal.pgen.1005300

Physical damage can strongly affect plant growth, reducing the biomass of developing organs situated at a distance from wounds. These effects, previously studied in leaves, require the activation of jasmonate (JA) signalling. Using a novel assay involving repetitive cotyledon wounding in Arabidopsis seedlings, we uncovered a function of JA in suppressing cell division and elongation in roots. Regulatory JA signalling components were then manipulated to delineate their relative impacts on root growth. The new transcription factor mutant myc2-322B was isolated. In vitro transcription assays and whole-plant approaches revealed that myc2-322B is a dosage-dependent gain-of-function mutant that can amplify JA growth responses. Moreover, myc2-322B displayed extreme hypersensitivity to JA that totally suppressed root elongation. The mutation weakly reduced root growth in undamaged plants but, when the upstream negative regulator NINJA was genetically removed, myc2-322B powerfully repressed root growth through its effects on cell division and cell elongation. Furthermore, in a JA-deficient mutant background, ninja1 myc2-322B still repressed root elongation, indicating that it is possible to generate JA-responses in the absence of JA. We show that NINJA forms a broadly expressed regulatory layer that is required to inhibit JA signalling in the apex of roots grown under basal conditions. By contrast, MYC2, MYC3 and MYC4 displayed cell layer-specific localisations and MYC3 and MYC4 were expressed in mutually exclusive regions. In nature, growing roots are likely subjected to constant mechanical stress during soil penetration that could lead to JA production and subsequent detrimental effects on growth. Our data reveal how distinct negative regulatory layers, including both NINJA-dependent and -independent mechanisms, restrain JA responses to allow normal root growth. Mechanistic insights from this work underline the importance of mapping JA signalling components to specific cell types in order to understand and potentially engineer the growth reduction that follows physical damage.

Publikation

Acosta, I.F., Gasperini, D., Chételat, A., Stolz, S., Santuari, L. & Farmer, E.E. Role of NINJA in root jasmonate signaling. In: PNAS 110 (38), 15473-15478, (2013) DOI: 10.1073/pnas.1307910110

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Bücher und Buchkapitel

Yamaguchi, I., Cohen, J.D., Culler, A.H., Quint, M., Slovin, J.P., Nakajima, M., Sakakibara, H., Kuroha, T., Hirai, N., Yokota, T., Ohta, H., Kabayashi, Y., Mori, H. & Sakagami, Y. Plant Hormones. In: Comprehensive Natural Products II (Lew Mander and Hung-Wen (Ben) Liu). Comprehensive Natural Products II, Elsevier, Oxford 9-125, (2010)

The definition of a plant hormone has not been clearly established, so the compounds classified as plant hormones often vary depending on which definition is considered. In this chapter, auxins, gibberellins (GAs), cytokinins, abscisic acid, brassinosteroids, jasmonic acid-related compounds, and ethylene are described as established plant hormones, while polyamines and phenolic compounds are not included. On the other hand, several peptides that have been proven to play a clear physiological role(s) in plant growth and development, similar to the established plant hormones, are referred. This chapter will focus primarily on the more recent discoveries of plant hormones and their impact on our current understanding of their biological role. In some cases, however, it is critical to place recent work in a proper historical context.

Publikation

Ludwig-Müller, J., Denk, K., Cohen, J.D. & Quint, M. An inhibitor of tryptophan-dependent biosynthesis of indole-3-acetic acid alters seedling development in Arabidopsis J Plant Growth Regul 29, 242-248, (2010)

Although polar transport and the TIR1-dependent signaling pathway of the plant hormone auxin/indole-3-acetic acid (IAA) are well characterized, understanding of the biosynthetic pathway(s) leading to the production of IAA is still limited. Genetic dissection of IAA biosynthetic pathways has been complicated by the metabolic redundancy caused by the apparent existence of several parallel biosynthetic routes leading to IAA production. Valuable complementary tools for genetic as well as biochemical analysis of auxin biosynthesis would be molecular inhibitors capable of acting in vivo on specific or general components of the pathway(s), which unfortunately have been lacking. Several indole derivatives have been previously identified to inhibit tryptophan-dependent IAA biosynthesis in an in vitro system from maize endosperm. We examined the effect of one of them, 6-fluoroindole, on seedling development of Arabidopsis thaliana and tested its ability to inhibit IAA biosynthesis in feeding experiments in vivo. We demonstrated a correlation of severe developmental defects or growth retardation caused by 6-fluoroindole with significant downregulation of de novo synthesized IAA levels, derived from the stable isotope-labeled tryptophan pool, upon treatment. Hence, 6-fluoroindole shows important features of an inhibitor of tryptophan-dependent IAA biosynthesis both in vitro and in vivo and thus may find use as a promising molecular tool for the identification of novel components of the auxin biosynthetic pathway(s).

Publikation

Quint, M., Barkawi, L.S., Fan, K.T., Cohen, J.D. & Gray, W.M. Arabidopsis IAR4 modulates auxin response by regulating auxin homeostasis Plant Physiol 150, 748-758, (2009)

In a screen for enhancers of tir1-1 auxin resistance, we identified two novel alleles of the putative mitochondrial pyruvate dehydrogenase E1α-subunit, IAA-Alanine Resistant4 (IAR4). In addition to enhancing the auxin response defects of tir1-1, iar4 single mutants exhibit numerous auxin-related phenotypes including auxin-resistant root growth and reduced lateral root development, as well as defects in primary root growth, root hair initiation, and root hair elongation. Remarkably, all of these iar4 mutant phenotypes were rescued when endogenous indole-3-acetic acid (IAA) levels were increased by growth at high temperature or overexpression of the YUCCA1 IAA biosynthetic enzyme, suggesting that iar4 mutations may alter IAA homeostasis rather than auxin response. Consistent with this possibility, iar4 mutants exhibit increased Aux/IAA stability compared to wild type under basal conditions, but not in response to an auxin treatment. Measurements of free IAA levels detected no significant difference between iar4-3 and wild-type controls. However, we consistently observed significantly higher levels of IAA-amino acid conjugates in the iar4-3 mutant. Furthermore, using stable isotope-labeled IAA precursors, we observed a significant increase in the relative utilization of the Trp-independent IAA biosynthetic pathway in iar4-3. We therefore suggest that the auxin phenotypes of iar4 mutants are the result of altered IAA homeostasis.

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