Abstract
It is known that the expression of AtMAPR3 (membrane associated progesterone receptor 3 in Arabidopsis thaliana), a novel heme binding protein, is induced by exogenesis hydrogen peroxide and jasmonate. As revealed from public microarray database, the expression of AtMAPR3 is upregulated under various biotic stresses, such as infection by Botrytis cinerea and Phytophthora infestans. To further understand whether the physiological role of AtMAPR3 is related to ROS generating stresses, this study compare the phenotypic difference between wild type and a knock out mutant of AtMAPR3, atmapr3-1. It was found that the lesion area of atmapr3-1 mutant was larger than wild type by 1.7 fold when infected with B. cinerea. Also, the expression of AtMAPR3 in wild type was increased to 11 fold when infected for two days, indicate AtMAPR3 is responsive to the B. cinerea infection. To clarify if the presence of AtMAPR3 affects ROS responsive genes, the expression of these genes were examined in wild type or atmapr3-1 with B. cinerea infection. The expression of two pathogen responsive genes, PR5 (pathogenesis-related gene 5) and PDF1.2b (plant defensin 1.2b) in wild type infected with B. cinerea increased by 5 and 3.5 folds respectively after 24 hours and 36 hours. However, in atmapr3-1 mutants, the induced expression of those two genes were hypersensitive (reach to 11 and 15 folds respectively) to. Moreover, the expression of two ROS related genes TAT3 (tyrosine aminotransferase 3) and ZAT10 (salt tolerance zinc finger 10) in response to B. cinerea infection showed different expression patterns between wild type and atmapr3-1 mutant. The expression of TAT3 in wild type infected by B. cinerea increased along time and reached to its peak at 48 hours (about 14 folds). However in the atmapr3-1 mutant, the expression of those genes reached to its peak at 24 hours (about 9 folds). The ZAT gene response to B. cinerea infection showed similar expression pattern. These results implied the presence of AtMAPR3 affected the expression of some ROS responsive genes. I proposed that when plant infected by pathogens, the triggered ROS signaling pathway might induce the expression of AtMAP3, and the physiological role of AtMAPR3 might relate to this stress.
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