Chronic vitamin A deficiency (VAD) leads to blindness, delayed growth, impaired immunity and is the leading cause of preventable childhood blindness. In contrast, VAD in flies does not result in developmental defects or lethality. But similar to mammals, flies deprived of vitamin A have defects in the visual system, like damaged photoreceptors and loss of light-sensing pigments. However, a gaping hole remains in our understanding of the molecular response to VAD. To identify genes and signaling pathways that respond to VAD, we performed RNA sequencing using Drosophila heads.
We identified 68 differentially expressed genes between vitamin A-rich and deprived conditions. Out of these, 50 genes were upregulated, and 18 genes were downregulated on VAD. Among these are the genes that are responsible for the synthesis of the retinal chromophore (ninaB, ninaG, Pdh) and the termination of the phototransduction pathway (Arr1, Arr2, inaC, stops). We also detected significant changes in the expression of genes that encode for specific aminoacyl-tRNA synthetases (GluProRS, IleRS, LeuRS, LysRS), major nutrient reservoir proteins (Lsp1alpha, Lsp1beta, and Lsp2), calcium buffers (Cpn, Cnx99a), and factors that mediate stress or immune responses (per, Cyp309a1, TotA, TotC, TotM, dnr1, Diedel).
A comparison between genes responding to VAD and previously identified blue light stress-responsive genes showed a largely nonoverlapping transcriptome response to these two types of environmental stresses. Only seven genes, with poorly understood functions, were similar between these two studies. Taken together, our study provides insights into the molecular mechanisms that respond to vitamin A deprivation.