View source for Effector

The evolution of [[PAMPs/MAMPs |PAMP]]-triggered immune system enabling the detection of [[PAMPs/MAMPs |PAMPs]] has led to the development of pathogen ability to evade this type of resistance. Emerging evidence report that, during infection, pathogens actively suppress the plant’s [[PAMPs/MAMPs |PAMP]]-triggered defenses. 
It is likely that all pathogenic microbes encode [[Effector |effectors]] that suppress [[PAMPs/MAMPs |PAMP]]-triggered defenses.

* Animal '''bacterial''' pathogens are known to secrete only a small number of effectors into host cells, while plant pathogens can secrete approximately 20 to 30 effectors during infection. The simultaneous action of different effectors is reported to induce variations in host cell physiology, resulting in the promotion of pathogen growth and development. Type III secretion system (TTSS) represents an essential component of bacterial pathogenic system. Bacterial and fungal effectors are reported to have enzyme activity that modify host proteins resulting in increased pathogen virulence and allowing the evasion of plant pathogen detection; moreover, bacterial effectors have also been demonstrated to be involved in activating plant transcription. Bacterial effectors contribute to pathogen virulence, often by mimicking or inhibiting eukaryotic cellular functions.

(Jones JD, Dangl JL. The plant immune system. Nature. 2006 Nov 16;444(7117):323-9.[http://www.ncbi.nlm.nih.gov/pubmed/17108957 PMID: 17108957])

* Pathogenic '''fungi''' form the haustorium, that is a specialized infection structure (no TTSS has been discovered for fungal pathogens); fungal effectors) may be delivered from haustoria into the plant intercellular space (apoplast). The activity of fungal effectors is enzymatic in some cases, but most of the  effectors have a still unknown mechanism of action. So, most fungal effectors are small proteins of unknown function containing a signal for secretion into the apoplast.

* '''Viral''' virulence determinants (correspondent to the previously discussed effectors) lead to the suppression of the host viral infection response. RNA silencing represent the principal mechanism by which plant promote resistance to viral pathogens, preferentially recognizing viral double strand RNA (dsRNA). The success of a virus’ silencing suppressor may be a major factor determining the host range of the specific virus. Different suppressors are reported to interfere with unique components of the host-silencing machinery, suggesting that many viruses independently developed the means to suppress silencing.
Morevoer, specific R proteins recognize viral components – either silencing suppressors or other proteins –
that accumulate following successful viral replication and translation.


(Chisholm ST, Coaker G, Day B, Staskawicz BJ. Host-microbe interactions: shaping the evolution of the plant immune response. Cell. 2006 Feb 24;124(4):803-14. [http://www.ncbi.nlm.nih.gov/pubmed/16497589 PMID: 16497589])

[[Category:Biology]]