Salt stress activates tyrosine metabolism and dhurrin-associated SbCYP79A1 in sorghum.

Potential toxicity to livestock limits the widespread adoption of forage sorghum as a higher-yielding, more nutritious, and more climate-resilient alternative to maize. Although low-dhurrin cultivars are available, their safety under saline conditions remain insufficiently understood. Here, we investigated the salt-stress molecular basis of dhurrin-associated toxicity in sorghum, with emphasis on tyrosine metabolism and the dhurrin-pathway genomics. We demonstrate that exposure to medium salt stress enriches 56 genes in the tyrosine metabolism pathway, including the dhurrin-specific cytochrome SbCYP79A1 that encodes an upstream tyrosine N-monooxygenase, in the inbred line RTx430. We show that SbCYP79A1 activates toxicity potential through dhurrin accumulation and imposes a growth penalty. Comparative genomic analysis of cis promoter elements at the coding DNA sequences using enriched motif elicitation revealed highly conserved G-rich regions interspersed with thymine residues across the broader tyrosine metabolism genes, characterized by enrichment in TATA-box and CAAT-box cis-regulatory elements. In contrast, the dhurrin-specific motif maintains the G-rich backbone typical of tyrosine background but is further enriched in cytosine residues, displays repositioned thymine bases, and shows strong enrichment of ABREH and G-box cis-regulatory elements. Together, these findings link salt stress to activation of tyrosine metabolism and dhurrin-associated cyanogenic potential in sorghum and identify promoter features that may guide future strategies to reduce forage toxicity in saline environments.