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High mobility group nucleosome-binding protein 5 (HMGN5) is a chromatin architectural protein that binds specifically to nucleosomes and reduces the compaction of the chromatin fiber. The protein is present in most vertebrate tissues however the physiological function of this protein is unknown. To examine the function of HMGN5  in vivo , mice lacking the nucleosome-binding domain of HMGN5 were generated and characterized. Serological analysis revealed that compared to wild-type littermates ( Hmgn5 +/Y  ), mice with a targeted mutation in the HMGN5 gene ( Hmgn5 tm1/Y  ), had elevated serum albumin, non-HDL cholesterol, triglycerides, and alanine transaminase, suggesting mild hepatic abnormalities. Metabolomics analysis of liver extracts and urine revealed clear differences in metabolites between  Hmgn5 tm1/Y   and their  Hmgn5 +/Y   littermates.  Hmgn5 tm1/Y   mice had a significant increase in hepatic glutathione levels and decreased urinary concentrations of betaine, phenylacetylglycine, and creatine, all of which are metabolically related to the glutathione precursor glycine. Microarray and qPCR analysis revealed that expression of two genes affecting glutathione metabolism, glutathione peroxidase 6 ( Gpx6 ) and hexokinase 1 ( Hk1 ), was significantly decreased in  Hmgn5 tm1/Y   mouse liver tissue. Analysis of chromatin structure by DNase I digestion revealed alterations in the chromatin structure of these genes in the livers of  Hmgn5 tm1/Y   mice. Thus, functional loss of HMGN5 leads to changes in transcription of  Gpx6  and  Hk1  that alter glutathione metabolism.

Metabolomics Reveals a Role for the Chromatin-Binding Protein HMGN5 in Glutathione Metabolism