TIR signaling promotes the interactions between lipase-like proteins EDS1/PAD4 and ADR1-L1 immune receptor, and oligomerization of ADR1-L1.

Both plants and animals utilize nucleotide-binding leucine-rich repeat immune receptors (NLRs) to perceive the presence of pathogen-derived molecules and induce immune responses. NLR genes are far more abundant and diverse in vascular plants than in animals. Truncated NLRs, which lack one or more of the canonical domains, are also commonly encoded in plant genomes. However, little is known about their functions, especially the N-terminally truncated ones. Here, we show that the Arabidopsis thaliana N-terminally truncated helper NLR (hNLR) gene N REQUIREMENT GENE1 (NRG1C) is highly induced upon pathogen infection and in autoimmune mutants. The immune response and cell death conferred by some Toll/interleukin-1 receptor-type NLRs (TNLs) were compromised in Arabidopsis NRG1C overexpression lines. Detailed genetic analysis revealed that NRG1C antagonizes the immunity mediated by its full-length neighbors NRG1A and NRG1B. Biochemical tests suggested that NRG1C might interfere with the EDS1–SAG101 complex, which functions in immunity signaling together with NRG1A/1B. Interestingly, Brassicaceae NRG1Cs are functionally exchangeable and that the Nicotiana benthamiana N-terminally truncated hNLR NRG2 also antagonizes NRG1 activity. Together, our study uncovers an unexpected negative role of N-terminally truncated hNLRs in immunity in different plant species.

Nuclei define eukaryotes, enabling macromolecular compartmentalization and cellular regulation. Each nucleus is believed to contain one or more haploid sets of chromosomes (1N). However, we discovered that haploid cells of the pathogenic fungi Sclerotinia sclerotiorum and Botrytis cinerea distribute their chromosomes such that each of their nuclei contains only a subset of the haploid chromosomes (≤½N). The unusual chromosomal distribution was confirmed by cellular and molecular methods including chromosome counting, fluorescence in situ hybridization, flow cytometry–based DNA measurements, and single-nucleus polymerase chain reaction experiments. This phenomenon challenges fundamental assumptions about nuclear organization and opens fresh avenues in chromosome biology.

Arabidopsis thaliana TIR-type immune receptor SNC1 (Suppressor of npr1-1, constitutive 1) requires NADase, but not the 2′,3′-cAMP/cGMP synthetase activity to trigger in planta immune responses.

Sclerotinia sclerotiorum is a phytopathogenic soilborne fungus that damages diverse crops worldwide. It has recently been discovered that this fungus distributes its 16 chromosomes irregularly between two nuclei within each haploid ascospore. Here, we study the meiotic process by tracking phenotypic segregation and recombination events in the progeny of a strain resulting from the fusion of two morphologically distinct mutants. We show that, despite the unusual chromosomal distribution into two nuclei, chromosome segregation and genetic recombination occur normally in S. sclerotiorum, likely due to a tight coordination between the two complementing nuclei during meiosis. Consistently, an atypical ascospore development process deviating from the conventional model was observed. Furthermore, we show that our co-segregation analyses method can be used to identify causal mutations in uncharacterized mutants, uncovering a role for deubiquitination in fungal development and virulence.

Sclerotinia sclerotiorum causes white mold or stem rot in a broad range of economically important plants, bringing significant yield losses worldwide. Host-induced gene silencing (HIGS) has been showing promising effects in controlling many fungal pathogens, including S. sclerotiorum . However, molecular genetic understanding of signaling pathways involved in its development and pathogenicity is needed to provide effective host-induced gene silencing (HIGS) targets for disease control. Here, by employing a forward genetic screen, we characterized an evolutionarily conserved mitogen-activated protein kinase (MAPK) cascade in S. sclerotiorum , consisting of SsSte50-SsSte11-SsSte7-Smk1, controlling mycelial growth, sclerotia development, compound appressoria formation, virulence, and hyphal fusion. Moreover, disruption of the putative downstream transcription factor SsSte12 led to normal sclerotia but aberrant appressoria formation and host penetration defects, suggestive of diverged regulation downstream of the MAPK cascade. Most importantly, targeting of SsSte50 using host-expressed HIGS double stranded RNA resulted in largely reduced virulence of S. sclerotiorum on Nicotiana benthamiana leaves. Therefore, this MAPK signaling cascade is generally needed for its growth, development, and pathogenesis, and is an ideal HIGS target for mitigating economic damages caused by S. sclerotiorum infection.