The CASPs are believed to be the core effectors of apoptosis.
We identified the 26 core effectors of TRAIL-mediated apoptosis signaling from the literature and determined whether the inter-relationships between these genes using the RF model would predict TRAIL-sensitivity.
It is notable that only the RxL part of the RxLR seems to be highly conserved within potential core effectors of Phytophthora and downy mildews, similar to the situation in Plasmodium [ 90], in which the same residues seem to play a vital role for delivering its effectors to the host cytoplasm [ 90– 92].
Comparisons of these have led to the identification of core effector gene sets and to explain some of the differences in host-specificity between pathovars.
In the present study, we identified SKRP proteins as pathogen virulence targets and novel regulators in plant pre-mRNA splicing machinery by screening for host clients of the Phytophthora sojae core effector PsAvr3c.
Interestingly, 5 out of 9 T3E genes families showing a strong signal of diversifying selection also belong to the core effector group.
It is now well documented that while 21 core effector genes are conserved in all EPEC and EHEC strains, the distribution of the non-conserved, accessory, effector genes varies from strain to strains (Iguchi et al., 2009).
We note that while the core effector-binding region of CED-10 is 100% conserved with human Rac1, Rac2 and Rac3 (YIPTVFDNY), RAC-2 has nonconservative variants in two residues (YI LTVFD TY), and mutation of many of these residues in human Rac1 disrupt binding of Pak and other effectors (Westwick et al. 1997).
However, there might be some core effectors that are the hallmark of an entire group of pathogens and which are crucial for pathogenicity (Sharma et al. 2014).
A group of 21 core effectors, including all those encoded within LEE and a number of non-LEE effectors, are shared by all A/E pathogens [ 79, 80].
