Our Collaboratory Fellows have published papers on a variety of research topics, stemming from Collaboratory-supported collaborations across campus.
Find us on Google Scholar: https://scholar.google.com/citations?user=XN6DdggAAAAJ&hl=en
1. | Pontrelli Sammy, ; Riley C. B. Fricke and Shao Thing Teoh, ; Walter A. Laviña, ; Sastia Prama Putri, ; Sorel Fitz-Gibbon, ; Matthew Chung, ; Matteo Pellegrini, ; Eiichiro Fukusaki, ; Liao, James C: Metabolic repair through emergence of new pathways in Escherichia coli. In: Nature Chemical Biology, 14 (11), pp. 1005–1009, 2018. (Type: Journal Article | Abstract | Links | BibTeX) @article{Pontrelli2018Metabolic, title = {Metabolic repair through emergence of new pathways in Escherichia coli}, author = {Pontrelli, Sammy, and Riley C. B. Fricke,and Shao Thing Teoh, and Walter A. Laviña, and Sastia Prama Putri, and Sorel Fitz-Gibbon, and Matthew Chung, and Matteo Pellegrini, and Eiichiro Fukusaki, and James C. Liao}, doi = {https://doi.org/10.1038/s41589-018-0149-6}, year = {2018}, date = {2018-10-16}, journal = {Nature Chemical Biology}, volume = {14}, number = {11}, pages = {1005–1009}, abstract = {Escherichia coli can derive all essential metabolites and cofactors through a highly evolved metabolic system. Damage of pathways may affect cell growth and physiology, but the strategies by which damaged metabolic pathways can be circumvented remain intriguing. Here, we use a ΔpanD (encoding for aspartate 1-decarboxylase) strain of E. coli that is unable to produce the β-alanine required for CoA biosynthesis to demonstrate that metabolic systems can overcome pathway damage by extensively rerouting metabolic pathways and modifying existing enzymes for unnatural functions. Using directed cell evolution, rewiring and repurposing of uracil metabolism allowed formation of an alternative β-alanine biosynthetic pathway. After this pathway was deleted, a second was evolved that used a gain-of-function mutation on ornithine decarboxylase (SpeC) to alter reaction and substrate specificity toward an oxidative decarboxylation–deamination reaction. After deletion of both pathways, yet another independent pathway emerged using polyamine biosynthesis, demonstrating the vast capacity of metabolic repair. }, keywords = {}, pubstate = {published}, tppubtype = {article} } Escherichia coli can derive all essential metabolites and cofactors through a highly evolved metabolic system. Damage of pathways may affect cell growth and physiology, but the strategies by which damaged metabolic pathways can be circumvented remain intriguing. Here, we use a ΔpanD (encoding for aspartate 1-decarboxylase) strain of E. coli that is unable to produce the β-alanine required for CoA biosynthesis to demonstrate that metabolic systems can overcome pathway damage by extensively rerouting metabolic pathways and modifying existing enzymes for unnatural functions. Using directed cell evolution, rewiring and repurposing of uracil metabolism allowed formation of an alternative β-alanine biosynthetic pathway. After this pathway was deleted, a second was evolved that used a gain-of-function mutation on ornithine decarboxylase (SpeC) to alter reaction and substrate specificity toward an oxidative decarboxylation–deamination reaction. After deletion of both pathways, yet another independent pathway emerged using polyamine biosynthesis, demonstrating the vast capacity of metabolic repair. |
2018 |
Pontrelli Sammy, ; Riley C. B. Fricke and Shao Thing Teoh, ; Walter A. Laviña, ; Sastia Prama Putri, ; Sorel Fitz-Gibbon, ; Matthew Chung, ; Matteo Pellegrini, ; Eiichiro Fukusaki, ; Liao, James C Metabolic repair through emergence of new pathways in Escherichia coli Journal Article Nature Chemical Biology, 14 (11), pp. 1005–1009, 2018. Abstract | Links | BibTeX | Tags: e.coli, metabolic repair @article{Pontrelli2018Metabolic, title = {Metabolic repair through emergence of new pathways in Escherichia coli}, author = {Pontrelli, Sammy, and Riley C. B. Fricke,and Shao Thing Teoh, and Walter A. Laviña, and Sastia Prama Putri, and Sorel Fitz-Gibbon, and Matthew Chung, and Matteo Pellegrini, and Eiichiro Fukusaki, and James C. Liao}, doi = {https://doi.org/10.1038/s41589-018-0149-6}, year = {2018}, date = {2018-10-16}, journal = {Nature Chemical Biology}, volume = {14}, number = {11}, pages = {1005–1009}, abstract = {Escherichia coli can derive all essential metabolites and cofactors through a highly evolved metabolic system. Damage of pathways may affect cell growth and physiology, but the strategies by which damaged metabolic pathways can be circumvented remain intriguing. Here, we use a ΔpanD (encoding for aspartate 1-decarboxylase) strain of E. coli that is unable to produce the β-alanine required for CoA biosynthesis to demonstrate that metabolic systems can overcome pathway damage by extensively rerouting metabolic pathways and modifying existing enzymes for unnatural functions. Using directed cell evolution, rewiring and repurposing of uracil metabolism allowed formation of an alternative β-alanine biosynthetic pathway. After this pathway was deleted, a second was evolved that used a gain-of-function mutation on ornithine decarboxylase (SpeC) to alter reaction and substrate specificity toward an oxidative decarboxylation–deamination reaction. After deletion of both pathways, yet another independent pathway emerged using polyamine biosynthesis, demonstrating the vast capacity of metabolic repair. }, keywords = {e.coli, metabolic repair}, pubstate = {published}, tppubtype = {article} } Escherichia coli can derive all essential metabolites and cofactors through a highly evolved metabolic system. Damage of pathways may affect cell growth and physiology, but the strategies by which damaged metabolic pathways can be circumvented remain intriguing. Here, we use a ΔpanD (encoding for aspartate 1-decarboxylase) strain of E. coli that is unable to produce the β-alanine required for CoA biosynthesis to demonstrate that metabolic systems can overcome pathway damage by extensively rerouting metabolic pathways and modifying existing enzymes for unnatural functions. Using directed cell evolution, rewiring and repurposing of uracil metabolism allowed formation of an alternative β-alanine biosynthetic pathway. After this pathway was deleted, a second was evolved that used a gain-of-function mutation on ornithine decarboxylase (SpeC) to alter reaction and substrate specificity toward an oxidative decarboxylation–deamination reaction. After deletion of both pathways, yet another independent pathway emerged using polyamine biosynthesis, demonstrating the vast capacity of metabolic repair. |