Figure 1.
Fungal and oomycete structures for effector secretion.
Left panel. Oomycete and fungal plant parasites differentiate infection structures such as extracellular hyphae, as well as invasive hyphae and haustoria that penetrate the host cell cavity and invaginate the plasma membrane. Haustoria (a) and hyphae (b) secrete effectors that are translocated into host cell cytoplasm by unknown mechanisms. Right panel. Effectors secreted from haustoria (a) and hyphae (b) cross different biological interfaces (extra-haustorial matrix [EHMx]/extra-haustorial membrane [EHM] for effectors secreted from haustoria, and apoplast/plant cell wall/plant plasma membrane for effectors secreted from hyphae).
Figure 2.
N-terminal effector domains proposed to mediate host-cell entry.
Effectors from fungal (left) and oomycete (right) pathogens. Divergent oomycete and fungal effectors carry a general secretion signal peptide followed by non-conserved N-terminal regions called “uptake” or “targeting/translocation” domains that have been proposed to mediate host-cell entry. In oomycetes, small conserved amino acids motifs (e.g., RXLR, CHXC, or LFLAK) have been identified within these regions, which help to define effector families with many members.
Table 1.
List of conflicting studies on filamentous pathogen effector translocation inside plant cells.
Figure 3.
Integrated process of effector translocation.
Effectors (blue) follow secretion routes (arrows) within a pathogen (orange), are secreted into host-parasite interfaces (grey), cross a membrane surrounding the host cell (green), and finally enter the host cell cytoplasm. Each translocation step is likely to be influenced by host- and parasite-derived mechanisms that need to be considered when studying effector trafficking.