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. 2014 Feb 26;9(2):e88072. doi: 10.1371/journal.pone.0088072

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© 2014 Harper et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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The strain requires additional oxaloacetate to grow. Growth is achieved through direct synthesis of oxaloacetate by alternative pathways such as the glyoxylate shunt or pck, or through an increase of PEP levels, which drives flux through these pathways. The top seven mutated pathways identified by pathway phenotype sequencing are shown in red. It has been shown that Ppc knockouts cause increased flux through the glyoxylate shunt [60], consistent with our observed mutations in AceK and IclR. Mutations in PtsI have previously been observed in response to a growth-based selection for increased succinate production, in a scenario where Pck overexpression was also observed [27]. Similarly, deletion of ptsH, which also deactivates the PTS system and increases the intracellular PEP pool, has also been shown to increase succinate yields [48].

Inline graphic — The strain requires additional oxaloacetate to grow. Growth is achieved through direct synthesis of oxaloacetate by alternative pathways such as the glyoxylate shunt or pck, or through an increase of PEP levels, which drives flux through these pathways. The top seven mutated pathways identified by pathway phenotype sequencing are shown in red. It has been shown that Ppc knockouts cause increased flux through the glyoxylate shunt [60], consistent with our observed mutations in AceK and IclR. Mutations in PtsI have previously been observed in response to a growth-based selection for increased succinate production, in a scenario where Pck overexpression was also observed [27]. Similarly, deletion of ptsH, which also deactivates the PTS system and increases the intracellular PEP pool, has also been shown to increase succinate yields [48].