AI Article Synopsis
- PNPO and PDXK work together to create pyridoxal 5'-phosphate (PLP), the active form of vitamin B6, with PDXK phosphorylating various forms of B6 and PNPO oxidizing them into PLP.
- Research showed that reducing PDXK in Drosophila and human cells affects glucose metabolism and DNA integrity, while silencing the sgll gene, which is the Drosophila equivalent of PNPO, leads to chromosome abnormalities and diabetes-like symptoms.
- The study indicates that chromosome aberrations in sgll cells are largely caused by harmful effects from high glucose levels, highlighting the importance of maintaining proper PLP levels for glucose balance and DNA health.
Article Abstract
Pyridoxine/pyridoxamine 5'-phosphate oxidase (PNPO) and pyridoxal kinase (PDXK) cooperate to produce pyridoxal 5'-phosphate (PLP), the active form of vitamin B6. PDXK phosphorylates pyridoxine, pyridoxamine, and pyridoxal by producing PNP, PMP, and PLP, whereas PNPO oxidizes PNP, PMP, into PLP. We previously demonstrated that PDXK depletion in Drosophila and human cells impacts on glucose metabolism and DNA integrity. Here we characterized sgll, the Drosophila ortholog of PNPO gene, showing that its silencing by RNA interference elicits chromosome aberrations (CABs) in brains and induces diabetic hallmarks such as hyperglycemia and small body size. We showed that in sgll neuroblasts CABs are largely produced by the genotoxic effect of the advanced glycation end products triggered by high glucose. As in sgll cells, part of PLP is still produced by PDXK activity, these data suggest that PLP dosage need to be tightly regulated to guarantee glucose homeostasis and DNA integrity.
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| http://dx.doi.org/10.1002/jcp.28990 | DOI Listing |
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