Branch point control at malonyl-CoA node: A computational framework to uncover the design principles of an ideal genetic-metabolic switch
Living organism is an intelligent system coded by hierarchically-organized information to perform precisely-controlled biological functions. Biophysical models are important tools to uncover the design rules underlying complex genetic-metabolic circuit interactions. Based on a previously engineered...
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| Published in | Metabolic engineering communications Vol. 10; p. e00127 |
|---|---|
| Main Author | |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.06.2020
Elsevier |
| Subjects | |
| Online Access | Get full text |
| ISSN | 2214-0301 2214-0301 |
| DOI | 10.1016/j.mec.2020.e00127 |
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| Abstract | Living organism is an intelligent system coded by hierarchically-organized information to perform precisely-controlled biological functions. Biophysical models are important tools to uncover the design rules underlying complex genetic-metabolic circuit interactions. Based on a previously engineered synthetic malonyl-CoA switch (Xu et al., PNAS, 2014), we have formulated nine differential equations to unravel the design principles underlying an ideal metabolic switch to improve fatty acids production in E. coli. By interrogating the physiologically accessible parameter space, we have determined the optimal controller architecture to configure both the metabolic source pathway and metabolic sink pathway. We determined that low protein degradation rate, medium strength of metabolic inhibitory constant, high metabolic source pathway induction rate, strong binding affinity of the transcriptional activator toward the metabolic source pathway, weak binding affinity of the transcriptional repressor toward the metabolic sink pathway, and a strong cooperative interaction of transcriptional repressor toward metabolic sink pathway benefit the accumulation of the target molecule (fatty acids). The target molecule (fatty acid) production is increased from 50% to 10-folds upon application of the autonomous metabolic switch. With strong metabolic inhibitory constant, the system displays multiple steady states. Stable oscillation of metabolic intermediate is the driving force to allow the system deviate from its equilibrium state and permits bidirectional ON-OFF gene expression control, which autonomously compensates enzyme level for both the metabolic source and metabolic sink pathways. The computational framework may facilitate us to design and engineer predictable genetic-metabolic switches, quest for the optimal controller architecture of the metabolic source/sink pathways, as well as leverage autonomous oscillation as a powerful tool to engineer cell function.
•Metabolic engineer can engineer both the chemistry and control modules in the cell.•9 differential equations used to define a previously engineered malonyl-CoA switch.•Optimal control architecture of metabolic source and sink pathways were determined.•Models were used to unravel the design principles underlying an ideal metabolic switch.•Stable oscillation of metabolic intermediates permits alternating ON-OFF genetic control. |
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| AbstractList | Living organism is an intelligent system coded by hierarchically-organized information to perform precisely-controlled biological functions. Biophysical models are important tools to uncover the design rules underlying complex genetic-metabolic circuit interactions. Based on a previously engineered synthetic malonyl-CoA switch (Xu et al., PNAS, 2014), we have formulated nine differential equations to unravel the design principles underlying an ideal metabolic switch to improve fatty acids production in
. By interrogating the physiologically accessible parameter space, we have determined the optimal controller architecture to configure both the metabolic source pathway and metabolic sink pathway. We determined that low protein degradation rate, medium strength of metabolic inhibitory constant, high metabolic source pathway induction rate, strong binding affinity of the transcriptional activator toward the metabolic source pathway, weak binding affinity of the transcriptional repressor toward the metabolic sink pathway, and a strong cooperative interaction of transcriptional repressor toward metabolic sink pathway benefit the accumulation of the target molecule (fatty acids). The target molecule (fatty acid) production is increased from 50% to 10-folds upon application of the autonomous metabolic switch. With strong metabolic inhibitory constant, the system displays multiple steady states. Stable oscillation of metabolic intermediate is the driving force to allow the system deviate from its equilibrium state and permits bidirectional ON-OFF gene expression control, which autonomously compensates enzyme level for both the metabolic source and metabolic sink pathways. The computational framework may facilitate us to design and engineer predictable genetic-metabolic switches, quest for the optimal controller architecture of the metabolic source/sink pathways, as well as leverage autonomous oscillation as a powerful tool to engineer cell function. Living organism is an intelligent system coded by hierarchically-organized information to perform precisely-controlled biological functions. Biophysical models are important tools to uncover the design rules underlying complex genetic-metabolic circuit interactions. Based on a previously engineered synthetic malonyl-CoA switch (Xu et al., PNAS, 2014), we have formulated nine differential equations to unravel the design principles underlying an ideal metabolic switch to improve fatty acids production in E. coli. By interrogating the physiologically accessible parameter space, we have determined the optimal controller architecture to configure both the metabolic source pathway and metabolic sink pathway. We determined that low protein degradation rate, medium strength of metabolic inhibitory constant, high metabolic source pathway induction rate, strong binding affinity of the transcriptional activator toward the metabolic source pathway, weak binding affinity of the transcriptional repressor toward the metabolic sink pathway, and a strong cooperative interaction of transcriptional repressor toward metabolic sink pathway benefit the accumulation of the target molecule (fatty acids). The target molecule (fatty acid) production is increased from 50% to 10-folds upon application of the autonomous metabolic switch. With strong metabolic inhibitory constant, the system displays multiple steady states. Stable oscillation of metabolic intermediate is the driving force to allow the system deviate from its equilibrium state and permits bidirectional ON-OFF gene expression control, which autonomously compensates enzyme level for both the metabolic source and metabolic sink pathways. The computational framework may facilitate us to design and engineer predictable genetic-metabolic switches, quest for the optimal controller architecture of the metabolic source/sink pathways, as well as leverage autonomous oscillation as a powerful tool to engineer cell function. Living organism is an intelligent system coded by hierarchically-organized information to perform precisely-controlled biological functions. Biophysical models are important tools to uncover the design rules underlying complex genetic-metabolic circuit interactions. Based on a previously engineered synthetic malonyl-CoA switch (Xu et al., PNAS, 2014), we have formulated nine differential equations to unravel the design principles underlying an ideal metabolic switch to improve fatty acids production in E. coli. By interrogating the physiologically accessible parameter space, we have determined the optimal controller architecture to configure both the metabolic source pathway and metabolic sink pathway. We determined that low protein degradation rate, medium strength of metabolic inhibitory constant, high metabolic source pathway induction rate, strong binding affinity of the transcriptional activator toward the metabolic source pathway, weak binding affinity of the transcriptional repressor toward the metabolic sink pathway, and a strong cooperative interaction of transcriptional repressor toward metabolic sink pathway benefit the accumulation of the target molecule (fatty acids). The target molecule (fatty acid) production is increased from 50% to 10-folds upon application of the autonomous metabolic switch. With strong metabolic inhibitory constant, the system displays multiple steady states. Stable oscillation of metabolic intermediate is the driving force to allow the system deviate from its equilibrium state and permits bidirectional ON-OFF gene expression control, which autonomously compensates enzyme level for both the metabolic source and metabolic sink pathways. The computational framework may facilitate us to design and engineer predictable genetic-metabolic switches, quest for the optimal controller architecture of the metabolic source/sink pathways, as well as leverage autonomous oscillation as a powerful tool to engineer cell function. •Metabolic engineer can engineer both the chemistry and control modules in the cell.•9 differential equations used to define a previously engineered malonyl-CoA switch.•Optimal control architecture of metabolic source and sink pathways were determined.•Models were used to unravel the design principles underlying an ideal metabolic switch.•Stable oscillation of metabolic intermediates permits alternating ON-OFF genetic control. Living organism is an intelligent system coded by hierarchically-organized information to perform precisely-controlled biological functions. Biophysical models are important tools to uncover the design rules underlying complex genetic-metabolic circuit interactions. Based on a previously engineered synthetic malonyl-CoA switch (Xu et al., PNAS, 2014), we have formulated nine differential equations to unravel the design principles underlying an ideal metabolic switch to improve fatty acids production in E. coli . By interrogating the physiologically accessible parameter space, we have determined the optimal controller architecture to configure both the metabolic source pathway and metabolic sink pathway. We determined that low protein degradation rate, medium strength of metabolic inhibitory constant, high metabolic source pathway induction rate, strong binding affinity of the transcriptional activator toward the metabolic source pathway, weak binding affinity of the transcriptional repressor toward the metabolic sink pathway, and a strong cooperative interaction of transcriptional repressor toward metabolic sink pathway benefit the accumulation of the target molecule (fatty acids). The target molecule (fatty acid) production is increased from 50% to 10-folds upon application of the autonomous metabolic switch. With strong metabolic inhibitory constant, the system displays multiple steady states. Stable oscillation of metabolic intermediate is the driving force to allow the system deviate from its equilibrium state and permits bidirectional ON-OFF gene expression control, which autonomously compensates enzyme level for both the metabolic source and metabolic sink pathways. The computational framework may facilitate us to design and engineer predictable genetic-metabolic switches, quest for the optimal controller architecture of the metabolic source/sink pathways, as well as leverage autonomous oscillation as a powerful tool to engineer cell function. • Metabolic engineer can engineer both the chemistry and control modules in the cell. • 9 differential equations used to define a previously engineered malonyl-CoA switch. • Optimal control architecture of metabolic source and sink pathways were determined. • Models were used to unravel the design principles underlying an ideal metabolic switch. • Stable oscillation of metabolic intermediates permits alternating ON-OFF genetic control. Living organism is an intelligent system coded by hierarchically-organized information to perform precisely-controlled biological functions. Biophysical models are important tools to uncover the design rules underlying complex genetic-metabolic circuit interactions. Based on a previously engineered synthetic malonyl-CoA switch (Xu et al., PNAS, 2014), we have formulated nine differential equations to unravel the design principles underlying an ideal metabolic switch to improve fatty acids production in E. coli. By interrogating the physiologically accessible parameter space, we have determined the optimal controller architecture to configure both the metabolic source pathway and metabolic sink pathway. We determined that low protein degradation rate, medium strength of metabolic inhibitory constant, high metabolic source pathway induction rate, strong binding affinity of the transcriptional activator toward the metabolic source pathway, weak binding affinity of the transcriptional repressor toward the metabolic sink pathway, and a strong cooperative interaction of transcriptional repressor toward metabolic sink pathway benefit the accumulation of the target molecule (fatty acids). The target molecule (fatty acid) production is increased from 50% to 10-folds upon application of the autonomous metabolic switch. With strong metabolic inhibitory constant, the system displays multiple steady states. Stable oscillation of metabolic intermediate is the driving force to allow the system deviate from its equilibrium state and permits bidirectional ON-OFF gene expression control, which autonomously compensates enzyme level for both the metabolic source and metabolic sink pathways. The computational framework may facilitate us to design and engineer predictable genetic-metabolic switches, quest for the optimal controller architecture of the metabolic source/sink pathways, as well as leverage autonomous oscillation as a powerful tool to engineer cell function. Living organism is an intelligent system coded by hierarchically-organized information to perform precisely-controlled biological functions. Biophysical models are important tools to uncover the design rules underlying complex genetic-metabolic circuit interactions. Based on a previously engineered synthetic malonyl-CoA switch (Xu et al., PNAS, 2014), we have formulated nine differential equations to unravel the design principles underlying an ideal metabolic switch to improve fatty acids production in E. coli. By interrogating the physiologically accessible parameter space, we have determined the optimal controller architecture to configure both the metabolic source pathway and metabolic sink pathway. We determined that low protein degradation rate, medium strength of metabolic inhibitory constant, high metabolic source pathway induction rate, strong binding affinity of the transcriptional activator toward the metabolic source pathway, weak binding affinity of the transcriptional repressor toward the metabolic sink pathway, and a strong cooperative interaction of transcriptional repressor toward metabolic sink pathway benefit the accumulation of the target molecule (fatty acids). The target molecule (fatty acid) production is increased from 50% to 10-folds upon application of the autonomous metabolic switch. With strong metabolic inhibitory constant, the system displays multiple steady states. Stable oscillation of metabolic intermediate is the driving force to allow the system deviate from its equilibrium state and permits bidirectional ON-OFF gene expression control, which autonomously compensates enzyme level for both the metabolic source and metabolic sink pathways. The computational framework may facilitate us to design and engineer predictable genetic-metabolic switches, quest for the optimal controller architecture of the metabolic source/sink pathways, as well as leverage autonomous oscillation as a powerful tool to engineer cell function.Living organism is an intelligent system coded by hierarchically-organized information to perform precisely-controlled biological functions. Biophysical models are important tools to uncover the design rules underlying complex genetic-metabolic circuit interactions. Based on a previously engineered synthetic malonyl-CoA switch (Xu et al., PNAS, 2014), we have formulated nine differential equations to unravel the design principles underlying an ideal metabolic switch to improve fatty acids production in E. coli. By interrogating the physiologically accessible parameter space, we have determined the optimal controller architecture to configure both the metabolic source pathway and metabolic sink pathway. We determined that low protein degradation rate, medium strength of metabolic inhibitory constant, high metabolic source pathway induction rate, strong binding affinity of the transcriptional activator toward the metabolic source pathway, weak binding affinity of the transcriptional repressor toward the metabolic sink pathway, and a strong cooperative interaction of transcriptional repressor toward metabolic sink pathway benefit the accumulation of the target molecule (fatty acids). The target molecule (fatty acid) production is increased from 50% to 10-folds upon application of the autonomous metabolic switch. With strong metabolic inhibitory constant, the system displays multiple steady states. Stable oscillation of metabolic intermediate is the driving force to allow the system deviate from its equilibrium state and permits bidirectional ON-OFF gene expression control, which autonomously compensates enzyme level for both the metabolic source and metabolic sink pathways. The computational framework may facilitate us to design and engineer predictable genetic-metabolic switches, quest for the optimal controller architecture of the metabolic source/sink pathways, as well as leverage autonomous oscillation as a powerful tool to engineer cell function. |
| ArticleNumber | e00127 |
| Author | Xu, Peng |
| Author_xml | – sequence: 1 givenname: Peng surname: Xu fullname: Xu, Peng email: pengxu@umbc.edu organization: Department of Chemical, Biochemical and Environmental Engineering, University of Maryland Baltimore County, Baltimore, MD 21250, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32455112$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1021_acssynbio_1c00391 crossref_primary_10_1021_acs_jafc_3c06528 crossref_primary_10_1016_j_copbio_2020_06_006 crossref_primary_10_1002_bit_27562 crossref_primary_10_1038_s41598_024_76029_1 crossref_primary_10_1016_j_synbio_2020_07_003 crossref_primary_10_1016_j_ymben_2020_08_015 |
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| Keywords | Metabolic switches Metabolic engineering Synthetic biology Autonomous oscillation Biophysical models Controller architecture |
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| SubjectTerms | artificial intelligence Autonomous oscillation binding capacity Biophysical models Controller architecture differential equation enzymes Escherichia coli fatty acids gene expression malonyl coenzyme A Metabolic engineering Metabolic switches protein degradation repressor proteins Special issue on The Natural Product Issue edited by Greg Stephanopoulos, Anthony Sinskey and Kang Zhou Synthetic biology transactivators |
| Title | Branch point control at malonyl-CoA node: A computational framework to uncover the design principles of an ideal genetic-metabolic switch |
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