TY - JOUR
T1 - Glyoxalase 2 Coordinates de Novo Serine Metabolism
AU - Trujillo, Marissa N.
AU - Jennings, Erin Q.
AU - Farrera, Dominique O.
AU - Kitamura, Naoya
AU - Anderson, Colin C.
AU - Gehrke, Sarah
AU - Reisz, Julie A.
AU - Johannsen, Mogens
AU - Roede, James R.
AU - D'Alessandro, Angelo
AU - Galligan, James J.
N1 - Publisher Copyright:
© 2025 Wiley-VCH GmbH.
PY - 2025/4/1
Y1 - 2025/4/1
N2 - Phosphoglycerate dehydrogenase (PHGDH) is the first enzyme in de novo Ser biosynthesis. Numerous metabolic pathways rely on Ser as a precursor, most notably one-carbon metabolism, glutathione biosynthesis, and de novo nucleotide biosynthesis. To facilitate proliferation, many cancer cells shunt glycolytic flux through this pathway, placing PHGDH as a metabolic liability and feasible therapeutic target for the treatment of cancer. Herein, we demonstrate the post-translational modification (PTM) of PHGDH by lactoylLys. These PTMs are generated through a non-enzymatic acyl transfer from the glyoxalase cycle intermediate, lactoylglutathione (LGSH). Knockout of the primary LGSH regulatory enzyme, glyoxalase 2 (GLO2), results in increased LGSH and resulting lactoylLys modification of PHGDH. These PTMs reduce enzymatic activity, resulting in a marked reduction in intracellular Ser. Using stable isotope tracing, we demonstrate reduced flux through the de novo Ser biosynthetic pathway. Collectively, these data identify PHGDH as a target for modification by lactoylLys, resulting in reduced enzymatic activity and reduced intracellular Ser.
AB - Phosphoglycerate dehydrogenase (PHGDH) is the first enzyme in de novo Ser biosynthesis. Numerous metabolic pathways rely on Ser as a precursor, most notably one-carbon metabolism, glutathione biosynthesis, and de novo nucleotide biosynthesis. To facilitate proliferation, many cancer cells shunt glycolytic flux through this pathway, placing PHGDH as a metabolic liability and feasible therapeutic target for the treatment of cancer. Herein, we demonstrate the post-translational modification (PTM) of PHGDH by lactoylLys. These PTMs are generated through a non-enzymatic acyl transfer from the glyoxalase cycle intermediate, lactoylglutathione (LGSH). Knockout of the primary LGSH regulatory enzyme, glyoxalase 2 (GLO2), results in increased LGSH and resulting lactoylLys modification of PHGDH. These PTMs reduce enzymatic activity, resulting in a marked reduction in intracellular Ser. Using stable isotope tracing, we demonstrate reduced flux through the de novo Ser biosynthetic pathway. Collectively, these data identify PHGDH as a target for modification by lactoylLys, resulting in reduced enzymatic activity and reduced intracellular Ser.
KW - 3-phosphoglycerate dehydrogenase (PHGDH)
KW - cell metabolism
KW - glycolysis
KW - glyoxalase 2 (GLO2)
KW - lactoylation
KW - post-translational modification (PTM)
KW - serine
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U2 - 10.1002/cbic.202401086
DO - 10.1002/cbic.202401086
M3 - Article
AN - SCOPUS:85219427400
SN - 1439-4227
VL - 26
JO - ChemBioChem
JF - ChemBioChem
IS - 7
M1 - e202401086
ER -