High impact information on PBS2

• RAR1 and NDR1 contribute quantitatively to disease resistance in Arabidopsis, and their relative contributions are dependent on the R gene assayed [1].
• We have identified the Arabidopsis ortholog of barley RAR1 as a component of resistance specified by multiple nucleotide binding/Leu-rich repeat resistance (R) genes recognizing different bacterial and oomycete pathogen isolates [2].
• Characterization of partially and fully defective rar1 mutations revealed that wild-type RAR1 acts as a rate-limiting regulator of early R gene-triggered defenses, determining the extent of pathogen containment, hypersensitive plant cell death, and an oxidative burst at primary infection sites [2].
• The pbs mutations are recessive and have been mapped to chromosomes I (pbs2) and V (pbs1 and pbs3) [3].
• Silencing of NDR1, RAR1 and HSP90, known to be required for the RPS2-mediated resistance, resulted in loss of the resistance, while silencing of EDS1 and SGT1b, which are not required for the RPS2-mediated resistance, caused no change of the resistance [4].

Biological context of PBS2

• These data indicate that the PBS2 protein functions in a pathway that is important only to a subset of disease-resistance genes [3].
• We demonstrate that Arabidopsis SGT1b has two distinct, genetically separable functions in the plant immune system: SGT1b antagonizes RAR1 to negatively regulate R protein accumulation before infection, and SGT1b has a RAR1-independent function that regulates programmed cell death during infection [5].
• These data imply both operationally distinct and cooperative functions of SGT1 and RAR1 in plant disease resistance [6].

References