| Summary: | In response to pathogen infection, plants typically use RESISTANCE (R) proteins to recognize and induce a strong defence response. SNC1 belongs to a class of R-proteins, and the gain of function snc1 mutant has constitutively active immune responses. MOS4 has been identified through a snc1 suppressor screen. MOS4 interacts in a complex called the mos4-associated complex (MAC) which is homologous to splicing-related complexes in yeast and humans. However, no splicing defects have been observed in any MAC single mutants. Two MAC proteins, AtCDC5 (a transcription factor) and MAC3A/3B (an E3 ubiquitin ligase) could be responsible for defence signalling downstream of the MAC. Since mos4-1 has the same defence phenotype as both atcdc5 and mac3a/3b, mutations to any of these genes probably has the same effect on perturbing the MAC. We performed a mos4-1 snc1 suppressor screen to identify signalling components downstream of the MAC.
The suppressor screen identified 31 dwarf mutants that all had either high PR2 defence gene expression or resistance to a virulent pathogen, H.a. Noco2, suggesting that the mutations affect defence signalling. Three mutants, 60B-1, 83-2 and 39-1, were characterized in greater detail and each of their respective mutations were mapped. 60B-1 carries a mutation to a known negative regulator of defence signalling, BON1. 83-2 carries a further gain of function mutation to snc1, however, unlike snc1 which causes snc1 protein accumulation, snc1 protein accumulation in 83-2 does not appear to be affected, suggesting that the protein is converted into a more active form. The molecular lesion in 39-1 was mapped near the southern telomere of chromosome 1, its exact location awaits discovery.
We have shown that a mos4 snc1 suppressor screen can successfully identify both recessive negative regulators of defence and dominant positive regulators of defence.
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