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The mitogen activated protein kinase (MAPK) gene family functions as a cohort during the Glycine max defense response to Heterodera glycines
- McNeece, Brant T., Sharma, Keshav, Lawrence, Gary W., Lawrence, Kathy S., Klink, Vincent P.
- Plant physiology and biochemistry 2019 v.137 pp. 25-41
- Arabidopsis thaliana, Glycine max, Heterodera glycines, allotetraploidy, biosynthesis, carbon metabolism, gene expression, genes, glycosides, hemicellulose, immunity, membrane fusion, mitogen-activated protein kinase, mitogens, pathogenesis, pathogens, secretion, signal transduction, transcription (genetics), transcriptomics
- Mitogen activated protein kinases (MAPKs) play important signal transduction roles. However, little is known regarding how they influence the gene expression of other family members and the relationship to a biological process, including the Glycine max defense response to Heterodera glycines. Transcriptomics have identified MAPK gene expression occurring within root cells undergoing a defense response to a pathogenic event initiated by H. glycines in the allotetraploid Glycine max. Functional analyses are presented for its 32 MAPKs revealing 9 have a defense role, including homologs of Arabidopsis thaliana MAPK (MPK) MPK2, MPK3, MPK4, MPK5, MPK6, MPK13, MPK16 and MPK20. Defense signaling occurring through pathogen activated molecular pattern (PAMP) triggered immunity (PTI) and effector triggered immunity (ETI) have been determined in relation to these MAPKs. Five different types of gene expression relate to MAPK expression, influencing PTI and ETI gene expression and proven defense genes including an ABC-G transporter, 20S membrane fusion particle components, glycoside biosynthesis, carbon metabolism, hemicellulose modification, transcription and secretion. The experiments show MAPKs broadly influence defense MAPK gene expression, including the co-regulation of parologous MAPKs and reveal its relationship to proven defense genes. The experiments reveal each defense MAPK induces the expression of a G. max homolog of a PATHOGENESIS RELATED1 (PR1), itself shown to function in defense in the studied pathosystem.