Pleiotropic regulatory locus 2 exhibits unequal genetic redundancy with its homolog PRL1.
In plants, signaling leading to resistance against biotrophic pathogens is complex. Perception of pathogenic microbes by resistance (R) proteins is relayed though successive activities of downstream components, in a network that is not well understood. PLEIOTROPIC REGULATORY LOCUS 1 (PRL1) and >20 other proteins are members of the MOS4-associated complex (MAC), a regulatory node in defense signaling. Of all characterized MAC members, mutations in PRL1 cause the most severe susceptibility towards both virulent and avirulent microbial pathogens. Genetic suppressors of prl1 represent new signaling elements and may aid in further unraveling of defense mechanisms. Our identification and characterization of a dominant suppressor of prl1 revealed a regulatory, gain-of-function mutation in PLEIOTROPIC REGULATORY LOCUS 2 (PRL2), a close homolog of PRL1. Loss-of-function mutants of PRL2 do not exhibit altered phenotypes; however, prl1 prl2 double mutants exhibit enhanced morphological defects consistent with unequal genetic redundancy between the homologs. Up-regulated gene expression mediated by the dominant prl2-1D allele completely suppresses disease susceptibility in the prl1 mutant background and also restores wild-type appearance, further supporting functional equivalence between the two PRL proteins.
Michael Smith Laboratories, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.
Tabea
T
Weihmann
Kristoffer
K
Palma
Yukino
Y
Nitta
Xin
X
Li
D048868:Adaptor Proteins, Signal Transducing / Q000737:chemistry / Q000235:genetics* / Q000378:metabolism; D000483:Alleles; D000595:Amino Acid Sequence; D017360:Arabidopsis / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D029681:Arabidopsis Proteins / Q000737:chemistry / Q000235:genetics* / Q000378:metabolism; D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D002874:Chromosome Mapping; D003001:Cloning, Molecular; D060467:Disease Resistance / Q000235:genetics; D005799:Genes, Dominant / Q000235:genetics; D016153:Genes, Suppressor; D005816:Genetic Complementation Test; D008969:Molecular Sequence Data; D009154:Mutation / Q000235:genetics; D009687:Nuclear Proteins / Q000235:genetics* / Q000378:metabolism; D010641:Phenotype; D010935:Plant Diseases / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D057865:Plant Immunity / Q000235:genetics; D017386:Sequence Homology, Amino Acid; D013489:Suppression, Genetic / Q000235:genetics
D048868:Adaptor Proteins, Signal Transducing; D029681:Arabidopsis Proteins; D002352:Carrier Proteins; D009687:Nuclear Proteins; C492005:PRL1 protein, Arabidopsis; C581964:PRL2 protein, Arabidopsis