UC Berkeley

Plants adapt to a variety of harsh environments with built-in resilience. Be it pathogen attacks or temperature stress, integrating these environmental signals is key for proper growth and development. liguleless narrow1 (lgn) encodes a plasma membrane-localized receptor-like kinase that is required for normal maize development including leaf shape, internode elongation, and fertility. The semi-dominant mutation (Lgn-R) lacks kinase activity. We assayed the phenotype in multiple environments and genetic backgrounds and found dramatic variations in expressivity. Analysis using a subset of the NAM founder lines revealed five inbred lines, including B73, that exhibit increased death rates in hot conditions and severe phenotypes in cool conditions. Four additional inbred lines, including Mo17, survive to exhibit severe phenotypes in hot conditions but are nearly indistinguishable from their non-mutant siblings at cool temperatures. A QTL analysis combined with additional mapping techniques identified one of the second site modifiers between these two lines, Sympathy for the ligule (Sol). Inbred lines that have the most severe phenotypes for Lgn-R show constitutive induction of Sol in the mutant background as well as a predilection for a particular set of indels and SNPs within the coding sequence. Rescuing lines do not show an induction of this gene in the mutant background. An EMS mutation further confirmed the identity of Sol to be this gene, a maize homolog of Arabidopsis ENHANCED DISEASE RESISTANCE4 (EDR4).

Sol, like EDR4, is induced in response to pathogen associated molecular patterns such as flg22. Integrated transcriptomic and phosphoproteomic analyses suggest that Lgn-R plants constitutively activate an immune response. We propose that the severe Lgn-R developmental phenotypes are the result of constitutive defense induction and that SOL potentially functions in repressing this response in Mo17 but not B73. Identification of LGN and SOL provide insight into the integration of developmental control and immunity.