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txt Introduction The liver exclusively synthesizes bile acids from cholesterol via two biosynthetic pathways.
Herein, c was defined as the unit vector in the direction of the growth flux, and the growth flux was defined in terms of the biosynthetic requirements: (Equation 4) where d m is the biomas ... modeled as a single reaction that converts all the biosynthetic precursors into biomass.
For each in silico deletion strain, the optimal production of the twelve biosynthetic precursors and the metabolic cofactors was also calculated to identify auxotrophic requirements and impaired functions in the metabolic network (Table 1).
The optimal production of the biosynthetic precursors was calculated by setting the objective function to the drain of a single metabolite (i.
Additionally, the optimal production of the 12 biosynthetic precursors, high-energy phosphate bonds, and redox potential was calculated for each in silico deletion strain (Table 1) to determine the specific effect of the gene deletion on the metabolic capabilities.
The optimal biomass yield and biosynthetic precursor production capabilities were calculated for each E.
Specifically, the gltA -, icdA -, and acnAB - in silico deletion strains were unable to produce one biosynthetic precursor (?
-ketoglutarate, Table 1), and ... etained the capability to synthesize the remaining biosynthetic precursors and cofactors nearly equivalent to the wild-type.
Furthermore, the essential glycolytic gene products ( pgk, gapAC ) were required for the synthesis of oxaloacetate, succinyl-CoA, ?
-ketoglutarate, pyruvate, phosphoenolpyruvate (PEP), and 3-phosphoglycerate within all conditions, and were unable to synthesize all biosynthetic precursors under anaerobic growth conditions.
The fba -, pfkAB -, and tpiA - in silico deletion strains had a limited capability to synthesize glyceraldehyde 3-phosphate, 3-phosphoglycerate, phosphoenolpyruvate, pyruvate, acetyl-CoA, ?
-ketoglutarate, succinyl-CoA, oxaloacetate, and high-energy phosphate bonds in all phases, and were completely unable to synthesize many of the biosynthetic precursors in phases 46 (Table 1) ( tpi - in silico strain discussed below).
However, the eno -and gpmAB - in silico deletion strains were limited in their production capability of high-energy phosphate bonds under all conditions, and were unable to produce any of the biosynthetic precursors in phase 6 even with the serine degradation pathway.
Finally, the ppc gene product was required for the anaerobic synthesis of oxaloacetate and ?
-ketoglutarate, but the in silico analysis suggests that this gene product is not essential for growth in aerobic conditions where the glyoxylate by-pass has the potential to replenish the biosynthetic precursors [ 29].
The production capabilities of the fumABC - in silico deletion strain was not limited with respect to the biosynthetic precursors shown in the table (other than a slight limitation of ATP production in P1 glucose, oxygen ).
The in silico pgi deletion strain had a reduced capacity to produce all the biosynthetic precursors under oxygen limitation, and this resulted in a decreased normalized growth yield of this in silico deletion strain.
28 more results not shown.
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