Perinatal Protein Deprivation Impacts Nuclear O-GalNAc Glycosylation in Rat Pup Cells

GARAY, YOHANA CAMILA; CEJAS, ROMINA BEATRIZ; PERONDI, MARIA CECILIA; GUTIÉRREZ, MARIA CECILIA; PARODI, PEDRO; FERRERO, FRANCO ALEJANDRO; LARDONE, RICARDO DANTE; VALDOMERO, ANALÍA; CUADRA, GABRIEL RICARDO; IRAZOQUI, FERNANDO JOSÉ

Congreso; Congreso SAIB SAMIGE 2021; 2021

SAIB

Post-translational modifications are key factors in the modulation of nuclear protein function controlling cell physiology and individual health. We study the influence of early under-nutrition on the nuclear O-GalNAc glycosylation of rat pup cells. Pregnant rats were fed with well-nourished and protein deprived diets, and after weaning at 30 days, pups were studied. Perinatal protein deficit exerted a direct consequence on offspring development, reducing the progeny weight. In different offspring tissues, we analyzed for the presence in nucleus of all the factors involved in the beginning of O-GalNAc glycan biosynthesis: the substrate donor (UDP-GalNAc), the enzyme activity (ppGalNAc-T) and the glycosylation product (O-GalNAc glycans). Here we observed that UDP-GalNAc levels available in cytoplasm and nucleus were not affected in cells from liver, cerebral cortex, cerebellum and hippocampus. However, perinatal protein deficiency affected the total activity of ppGalNAc-T localized in liver nucleus, thus reducing the “writing” ppGalNAc-T activity of nuclear O-GalNAc glycans. In addition, liver nucleoplasm of protein-deprived pups reported a significant reduction in expression of nuclear O-GalNAc glycan level. Our results suggest that limited availability of essential amino acids during early life stages (gestation and lactation) can modulate nuclear O-GalNAc glycosylation, which might ultimately regulate nuclear protein functions.