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A kinetic model describes metabolic response to perturbations and distribution of flux control in the benzenoid network of Petunia hybrida
Author(s) -
Colón Amy Marshall,
Sengupta Neelanjan,
Rhodes David,
Dudareva Natalia,
Morgan John
Publication year - 2010
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2010.04127.x
Subject(s) - petunia , kinetic energy , flux (metallurgy) , biological system , metabolic network , metabolic control analysis , chemistry , biochemistry , biology , physics , gene , organic chemistry , quantum mechanics , insulin , endocrinology
Summary In recent years there has been much interest in the genetic enhancement of plant metabolism; however, attempts at genetic modification are often unsuccessful due to an incomplete understanding of network dynamics and their regulatory properties. Kinetic modeling of plant metabolic networks can provide predictive information on network control and response to genetic perturbations, which allow estimation of flux at any concentration of intermediate or enzyme in the system. In this research, a kinetic model of the benzenoid network was developed to simulate whole network responses to different concentrations of supplied phenylalanine (Phe) in petunia flowers and capture flux redistributions caused by genetic manipulations. Kinetic parameters were obtained by network decomposition and non‐linear least squares optimization of data from petunia flowers supplied with either 75 or 150 m m 2 H 5 ‐Phe. A single set of kinetic parameters simultaneously accommodated labeling and pool size data obtained for all endogenous and emitted volatiles at the two concentrations of supplied 2 H 5 ‐Phe. The generated kinetic model was validated using flowers from transgenic petunia plants in which benzyl CoA:benzyl alcohol/phenylethanol benzoyltransferase ( BPBT ) was down‐regulated via RNAi. The determined in vivo kinetic parameters were used for metabolic control analysis, in which flux control coefficients were calculated for fluxes around the key branch point at Phe and revealed that phenylacetaldehyde synthase activity is the primary controlling factor for the phenylacetaldehyde branch of the benzenoid network. In contrast, control of flux through the β‐oxidative and non‐β‐oxidative pathways is highly distributed.