Dataset Information

Liu2010_Hormonal_Crosstalk_Arabidopsis

ABSTRACT: This is the single cell model for analysis of hormonal crosstalk in Arabidopsis described in the article: Modelling and experimental analysis of hormonal crosstalk in Arabidopsis. Liu J, Mehdi S, Topping J, Tarkowski P and Lindsey K. Mol Syst Biol. 2010 Jun 8;6:373; PmID: 20531403 , DOI: 10.1038/msb.2010.26 Abstract: An important question in plant biology is how genes influence the crosstalk between hormones to regulate growth. In this study, we model POLARIS (PLS) gene function and crosstalk between auxin, ethylene and cytokinin in Arabidopsis. Experimental evidence suggests that PLS acts on or close to the ethylene receptor ETR1, and a mathematical model describing possible PLS-ethylene pathway interactions is developed, and used to make quantitative predictions about PLS-hormone interactions. Modelling correctly predicts experimental results for the effect of the pls gene mutation on endogenous cytokinin concentration. Modelling also reveals a role for PLS in auxin biosynthesis in addition to a role in auxin transport. The model reproduces available mutants, and with new experimental data provides new insights into how PLS regulates auxin concentration, by controlling the relative contribution of auxin transport and biosynthesis and by integrating auxin, ethylene and cytokinin signalling. Modelling further reveals that a bell-shaped dose-response relationship between endogenous auxin and root length is established via PLS. This combined modelling and experimental analysis provides new insights into the integration of hormonal signals in plants. This model was originally created using Copasi and taken from the supplementary materials of the MSB article. It uses equation 5 for the auxin biosynthesis and was altered to also contain the reactions for ACC, IAA and cytokinine import. Different from the supplementary material, the parameters for the auxin synthesis, v2, are set to k2c = 0.01 uM and k2=0.2 uM_per_sec and for the WT PLS transcription k6=0.3 . To obtain the model described in the first table of the supplementary materials, set k2c=k2=0 and k6=0.9 . For the pls and PLSox mutants, k6 should be set to 0 and 0.45, respectively. This model originates from BioModels Database: A Database of Annotated Published Models. It is copyright (c) 2005-2010 The BioModels Team. For more information see the terms of use . To cite BioModels Database, please use Le Novère N., Bornstein B., Broicher A., Courtot M., Donizelli M., Dharuri H., Li L., Sauro H., Schilstra M., Shapiro B., Snoep J.L., Hucka M. (2006) BioModels Database: A Free, Centralized Database of Curated, Published, Quantitative Kinetic Models of Biochemical and Cellular Systems Nucleic Acids Res., 34: D689-D691.

SUBMITTER: Lukas Endler

PROVIDER: BIOMD0000000269 | BioModels | 2024-09-02

REPOSITORIES: BioModels

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	BIOMD0000000269?filename=BIOMD0000000269-biopax2.owl	Owl
	BIOMD0000000269?filename=BIOMD0000000269-biopax3.owl	Owl
	BIOMD0000000269?filename=BIOMD0000000269-matlab.m	Other
	BIOMD0000000269?filename=BIOMD0000000269-octave.m	Other
	BIOMD0000000269?filename=BIOMD0000000269.m	Other

Items per page:

1 - 5 of 14

Publications

Modelling and experimental analysis of hormonal crosstalk in Arabidopsis.

Liu Junli J Mehdi Saher S Topping Jennifer J Tarkowski Petr P Lindsey Keith K

Molecular systems biology 20100601

An important question in plant biology is how genes influence the crosstalk between hormones to regulate growth. In this study, we model POLARIS (PLS) gene function and crosstalk between auxin, ethylene and cytokinin in Arabidopsis. Experimental evidence suggests that PLS acts on or close to the ethylene receptor ETR1, and a mathematical model describing possible PLS-ethylene pathway interactions is developed, and used to make quantitative predictions about PLS-hormone interactions. Modelling co ...[more]

PMID: 20531403

Similar Datasets

Project description:This model is from the article: The influence of cytokinin-auxin cross-regulation on cell-fate determination in Arabidopsis thaliana root development Muraro D, Byrne H, King J, Voss U, Kieber J, Bennett M. J Theor Biol.2011 Aug 21;283(1):152-67. PMID: 21640126, Abstract: Root growth and development in Arabidopsis thaliana are sustained by a specialised zone termed the meristem, which contains a population of dividing and differentiating cells that are functionally analogous to a stem cell niche in animals. The hormones auxin and cytokinin control meristem size antagonistically. Local accumulation of auxin promotes cell division and the initiation of a lateral root primordium. By contrast, high cytokinin concentrations disrupt the regular pattern of divisions that characterises lateral root development, and promote differentiation. The way in which the hormones interact is controlled by a genetic regulatory network. In this paper, we propose a deterministic mathematical model to describe this network and present model simulations that reproduce the experimentally observed effects of cytokinin on the expression of auxin regulated genes. We show how auxin response genes and auxin efflux transporters may be affected by the presence of cytokinin. We also analyse and compare the responses of the hormones auxin and cytokinin to changes in their supply with the responses obtained by genetic mutations of SHY2, which encodes a protein that plays a key role in balancing cytokinin and auxin regulation of meristem size. We show that although shy2 mutations can qualitatively reproduce the effect of varying auxin and cytokinin supply on their response genes, some elements of the network respond differently to changes in hormonal supply and to genetic mutations, implying a different, general response of the network. We conclude that an analysis based on the ratio between these two hormones may be misleading and that a mathematical model can serve as a useful tool for stimulate further experimental work by predicting the response of the network to changes in hormone levels and to other genetic mutations.