The spring barley (Hordeum vulgare L.) was modified to alter nitrogen-use efficiency and leaf senescence through targeted mutagenesis of the endogenous abnormal reproductive organ development 1 (ARE1) gene. The ARE1 gene encodes a regulator involved in nitrogen metabolism, nutrient remobilization and the progression of leaf senescence. To achieve this modification, a single-nucleotide deletion was introduced into the coding sequence of the endogenous barley ARE1 gene, generating a loss-of-function allele. The mutation disrupts the normal reading frame of the gene and introduces a premature termination codon, resulting in the absence of a functional ARE1 protein. Disruption of ARE1 function has been associated with altered nitrogen utilization, delayed senescence and improved nitrogen-use efficiency under nitrogen-limiting conditions.