The second site modifier, Sympathy for the ligule, encodes a homolog of Arabidopsis enhanced disease resistance4 and rescues the liguleless narrow maize mutant

Authors: ANDERSON, ALYSSA - University Of California; ST. AUBIN, BRIAN - University Of California; ABRAHAM-JUAREZ, MARIA - Potosino Institute Of Scientific & Technological Researh; LEIBOFF, SAMUEL - University Of California; SHEN, ZHOUXIN - University Of California, San Diego; BRIGGS, STEVEN - University Of California, San Diego; BRUNKARD, JACOB - University Of California; Hake, Sarah

Submitted to: The Plant Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/13/2019
Publication Date: 6/21/2019
Citation: Anderson, A.A., St. Aubin, B., Abraham-Juarez, M.J., Leiboff, S., Shen, Z., Briggs, S.P., Brunkard, J.O., Hake, S.C. 2019. The second site modifier, Sympathy for the ligule, encodes a homolog of Arabidopsis enhanced disease resistance4 and rescues the liguleless narrow maize mutant. The Plant Cell. 31:1829-1844. https://doi.org/10.1105/tpc.18.00840.
DOI: https://doi.org/10.1105/tpc.18.00840

Interpretive Summary: The expressivity of a mutant phenotype is often dependent on other genes. These second site modifiers have been identified through mutagenesis screens and crosses to different backgrounds. Maize (Zea mays) is particularly rich for identification of modifiers because of the high genetic variation among maize inbred lines. Liguleless narrow-R has striking developmental phenotypes caused by an EMS-induced point mutation that eliminates protein kinase activity. As a heterozygote in the inbred line B73, Lgn-R plants are short with narrow leaves and reduced inflorescences. Mutants die when the plants are grown in hot temperatures. The expressivity of the Lgn-R phenotype is background-dependent. Plant height, leaf width, inflorescence and ligule development are all restored to near wild-type in Mo17. We identified the modifier that is responsible for the difference of the Lgn-R phenotype between Mo17 and B73.

Technical Abstract: liguleless narrow1 encodes a plasma membrane-localized receptor-like kinase required for normal maize development. The semi-dominant Lgn-R mutation lacks kinase activity and severity depends on inbred background. We created near isogenic lines and assayed the phenotype in multiple environments. Lgn-R plants that carry the B73 version of Sympathy for the ligule die in hot conditions but those with the Mo17 version (Sol-M) survive and are taller at cool temperatures. To identify Sol, we used recombinant mapping and analyzed the Lgn-R phenotype in additional inbreds. We identified sequence variations in GRMZM2G075262 that segregate with the Lgn-R phenotypes. Gene expression is high in Lgn-R B73 but not with one copy of Sol-M. An EMS mutation confirmed SOL as a homolog of Arabidopsis ENHANCED DISEASE RESISTANCE4 (EDR4). SOL, like EDR4, is induced in response to pathogen associated molecular patterns. Integrated transcriptomic and phosphoproteomic analyses suggest that Lgn-R plants constitutively activate a MAP kinase signaling cascade that induces temperature-sensitive immune responses. We propose that the severe Lgn-R phenotypes result from constitutive defense induction and that SOL 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.