SUMMARYPhytophthora cinnamomi Rands was first isolated from cinnamon trees in Sumatra in 1922. The pathogen is believed to have originated near Papua New Guinea but now has a worldwide distribution. P. cinnamomi is heterothallic with A1 and A2 mating types; however, even in areas in which both mating types are present, it appears that genetic diversity arises asexually rather than as a result of sexual recombination. P. cinnamomi can grow saprophytically in the soil for long periods, rapidly capitalizing on the advent of favourable conditions to sporulate and produce vast numbers of asexual, biflagellate zoospores. The motile zoospores are attracted to suitable infection sites, where they attach and invade the plant. Within a few days, hyphae ramify throughout the tissues of susceptible plants, forming sporangia on the plant surface and rapidly amplifying the disease inoculum. Over the last 10 -15 years, molecular analyses have clarified details of the phylogeny of P. cinnamomi and other Oomycetes. Research on P. cinnamomi has given rise to a more comprehensive understanding of the structure and function of the motile zoospores. New methods have been developed for P. cinnamomi identification and diagnosis. Long-term studies of diseased sites, particular those in southern Australia, have produced a better understanding of the epidemiology of P. cinnamomi diseases. Research has also increased our knowledge of the mode of action and efficacy of inhibitors of P. cinnamomi diseases, especially the phosphonates. This review will present an overview of the advances these studies have made in our understanding of P. cinnamomi pathogenicity, epidemiology and control.Taxonomy: Phytophthora cinnamomi Rands; kingdom Chromista; phylum Oomycota; order Peronosporales; family Peronosporaceae; genus Phytophthora .Host range: Likely to infect in excess of 3000 species of plants including over 2500 Australian native species, and crops such as avocado, pineapple, peach, chestnut and macadamia.Disease symptoms: A root pathogen which usually causes rotting of fine and fibrous roots but which can also cause stem cankers. Often causes dieback of young shoots and is thought to do so as a result of interference with transpiration from roots to shoots.

SummaryCytoplasmic aggregation, the rapid translocation of cytoplasm and subcellular components to the site of pathogen penetration, is one of the earliest reactions of plant cells against attack by microorganisms. We have investigated cytoplasmic aggregation during Arabidopsis-oomycete interactions. Infection by nonpathogenic Phytophthora sojae was prevented in the plant epidermal cell layer, whereas Peronospora parasitica isolates Cala2 (avirulent) and Noks1 (virulent) could both penetrate into the mesophyll cell layer. Epidermal cell responses to penetration by these oomycetes were examined cytologically with a range of transgenic Arabidopsis plants expressing Green Fluorescent Protein (GFP)-tagged cell components. These included plants containing GFP-TUA6 for visualizing microtubules, GFP-hTalin for actin microfilaments, GFP-tm-KKXX for endoplasmic reticulum (ER), and STtmd-GFP for the Golgi apparatus. In all interactions, actin microfilaments were actively re-arranged and formed large bundles in cytoplasmic strands focused on the penetration site. Aggregation of ER membrane and accumulation of Golgi bodies at the infection site were observed, suggesting that production and secretion of plant materials were activated around the penetration site. Microtubules did not become focused on the penetration site. No difference was evident between the responses of epidermal cells in the non-host, incompatible and compatible interactions. This result indicates that the induction of cytoplasmic aggregation in Arabidopsis epidermal cells was neither suppressed by the virulent strain of Peronospora, nor effective in stopping infection.

Translocation of pathogen effector proteins into the host cell cytoplasm is a key determinant for the pathogenicity of many bacterial and oomycete plant pathogens. A number of secreted fungal avirulence (Avr) proteins are also inferred to be delivered into host cells, based on their intracellular recognition by host resistance proteins, including those of flax rust (Melampsora lini). Here, we show by immunolocalization that the flax rust AvrM protein is secreted from haustoria during infection and accumulates in the haustorial wall. Five days after inoculation, the AvrM protein was also detected within the cytoplasm of a proportion of plant cells containing haustoria, confirming its delivery into host cells during infection. Transient expression of secreted AvrL567 and AvrM proteins fused to cerulean fluorescent protein in tobacco (Nicotiana tabacum) and flax cells resulted in intracellular accumulation of the fusion proteins. The rust Avr protein signal peptides were functional in plants and efficiently directed fused cerulean into the secretory pathway. Thus, these secreted effectors are internalized into the plant cell cytosol in the absence of the pathogen, suggesting that they do not require a pathogenencoded transport mechanism. Uptake of these proteins is dependent on signals in their N-terminal regions, but the primary sequence features of these uptake regions are not conserved between different rust effectors.

A root pathogen which causes rotting of fine and fibrous roots, but which can also cause stem cankers. Root damage may inhibit water movement from roots to shoots, leading to dieback of young shoots. USEFUL WEBSITES: http://fungidb.org/fungidb/; http://genome.jgi.doe.gov/Phyci1/Phyci1.home.html; http://www.ncbi.nlm.nih.gov/assembly/GCA_001314365.1; http://www.ncbi.nlm.nih.gov/assembly/GCA_001314505.1.

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