Abstract
SummaryAn understanding of the cell biology underlying the burgeoning molecular genetic and genomic knowledge of oomycete pathogenicity is essential to gain the full context of how these pathogens cause disease on plants. An intense research focus on secreted Phytophthora effector proteins, especially those containing a conserved N‐terminal RXLR motif, has meant that most cell biological studies into Phytophthora diseases have focussed on the effectors and their host target proteins. While these effector studies have provided novel insights into effector secretion and host defence mechanisms, there remain many unanswered questions about fundamental processes involved in spore biology, host penetration and haustorium formation and function.
Highlights
The progression of infectionIf the infection is successfully established, hyphae subsequently grow intercellularly (Fig. 2)
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Penetration of the host may occur through natural openings such as stomata (e.g. P. palmivora; Sarria et al, 2016) or lenticels (e.g. P. infestans entry into potato tubers; Judelson & Ah Fong, 2019, P. ramorum entry into stems; Oßwald et al, 2014), directly between anticlinal walls of surface cells without appressorium formation (e.g. P. cinnamomi; Hardham, 2005, O’Gara et al, 2015; Fig. 2) or through wounds
Summary
If the infection is successfully established, hyphae subsequently grow intercellularly (Fig. 2). Judelson & Ah Fong (2019) suggest, that haustoria are not the major sites of nutrient acquisition for the hemibiotrophic Phytophthora species due to a lack of nutrient transporters specific to haustorium-forming species, the lack of haustorial neckbands and that haustoria only represent about 2% of the pathogen surface area. Their primary role may be defence suppression. Sporangiophore emergence on leaves generally occurs at night, this strategy has the advantage that the sporangia have reduced exposure to UV radiation This must involve manipulation of stomatal regulation (Judelson & Ah Fong, 2019), presumably by pathogenicity factors produced later in the infection time course. Pseudomonas syringae is known to produce the toxin coronatine, which mimics conjugated jasmonic acid and induces stomatal opening (Melotto et al, 2006) but there are other pathways a pathogen could manipulate to achieve this end (reviewed by McLachlan et al, 2014)
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