The pathogenesis‐related (PR) proteins of plants have originally been identified as proteins that are strongly induced upon biotic and abiotic stress. These proteins fall into 17 distinct classes (PR1–PR17). The mode of action of most of these PR proteins has been well characterized, except for PR1, which belongs to a widespread superfamily of proteins that share a common CAP domain. Proteins of this family are not only expressed in plants but also in humans and in many different pathogens, including phytopathogenic nematodes and fungi. These proteins are associated with a diverse range of physiological functions. However, their precise mode of action has remained elusive. The importance of these proteins in immune defence is illustrated by the fact that PR1 overexpression in plants results in increased resistance against pathogens. However, PR1‐like CAP proteins are also produced by pathogens and deletion of these genes results in reduced virulence, suggesting that CAP proteins can exert both defensive and offensive functions. Recent progress has revealed that plant PR1 is proteolytically cleaved to release a C‐terminal CAPE1 peptide, which is sufficient to activate an immune response. The release of this signalling peptide is blocked by pathogenic effectors to evade immune defence. Moreover, plant PR1 forms complexes with other PR family members, including PR5, also known as thaumatin, and PR14, a lipid transfer protein, to enhance the host's immune response. Here, we discuss possible functions of PR1 proteins and their interactors, particularly in light of the fact that these proteins can bind lipids, which have important immune signalling functions.

Background: Verticillium dahliae is a soil-borne fungus that causes vascular wilt diseases in a wide range of plant hosts. V. dahliae produces multicelled, melanized resting bodies, also known as microsclerotia (MS) that can survive for years in the soil. The MS are the primary source of infection of the Verticillium disease cycle. Thus, MS formation marks an important event in the disease cycle of V. dahliae. Results: In this study, next generation sequencing technology of RNA-Seq was employed to investigate the global transcriptomic dynamics of MS development to identify differential gene expression at several stages of MS formation in strain XS11 of V. dahliae, isolated from smoke tree. We observed large-scale changes in gene expression during MS formation, such as increased expression of genes involved in protein metabolism and carbohydrate metabolism. Genes involved in glycolytic pathway and melanin biosynthesis were dramatically up-regulated in MS. Cluster analyses revealed increased expression of genes encoding products involved in primary metabolism and stress responses throughout MS development. Differential expression of ubiquitin-dependent protein catabolism and cell death-associated genes during MS development were revealed. Homologs of genes located in the lineage-specific (LS) regions of V. dahliae strain VdLs.17, were either not expressed or showed low expression. Furthermore, alternative splicing (AS) events were analyzed, revealing that over 95.0% AS events involve retention of introns (RI). Conclusions: These data reveal the dynamics of transcriptional regulation during MS formation and were used to construct a comprehensive high-resolution gene expression map. This map provides a key resource for understanding the biology and molecular basis of MS development of V. dahliae.

The data presented in this study provide a key resource for understanding the biology and molecular basis of necrotrophic pathogen responses to Nicotiana benthamiana resistance utilizing effector proteins, and CcCAP1 may be used in future studies to understand effector-triggered susceptibility processes in the Cytospora chrysosperma -poplar interaction system.

Fus3/Kss1, also known as Pmk1 in several pathogenic fungi, is a component of the mitogen‐activated protein kinase (MAPK) signalling pathway that functions as a regulator in fungal development, stress response, mating, and pathogenicity. Cytospora chrysosperma, a notorious woody plant‐pathogenic fungus, causes canker disease in many species, and its Pmk1 homolog, CcPmk1, is required for fungal development and pathogenicity. However, the global regulation network of CcPmk1 is still unclear. In this study, we compared transcriptional analysis between a CcPmk1 deletion mutant and the wild type during the simulated infection process. A subset of transcription factor genes and putative effector genes were significantly down‐regulated in the CcPmk1 deletion mutant, which might be important for fungal pathogenicity. Additionally, many tandem genes were found to be regulated by CcPmk1. Eleven out of 68 core secondary metabolism biosynthesis genes and several gene clusters were significantly down‐regulated in the CcPmk1 deletion mutant. GO annotation of down‐regulated genes showed that the ribosome biosynthesis‐related processes were over‐represented in the CcPmk1 deletion mutant. Comparison of the CcPmk1‐regulated genes with the Pmk1‐regulated genes from Magnaporthe oryzae revealed only a few overlapping regulated genes in both CcPmk1 and Pmk1, while the enrichment GO terms in the ribosome biosynthesis‐related processes were also found. Subsequently, we calculated that in vitro feeding artificial small interference RNAs of CcPmk1 could silence the target gene, resulting in inhibited fungal growth. Furthermore, silencing of BcPmk1 in Botrytis cinerea with conserved CcPmk1 and BcPmk1 fragments could significantly compromise fungal virulence using the virus‐induced gene silencing system in Nicotiana benthamiana. These results suggest that CcPmk1 functions as a regulator of pathogenicity and can potentially be designed as a target for broad‐spectrum disease control, but unintended effects on nonpathogenic fungi need to be avoided.