These data suggest that P. capsici expresses some genes in common with other Phytophthora pathogens, but the timing may differ. Our RXLR dataset includes several predicted orthologs to known avirulence genes such as P. sojae Avr1b and P. infestans Avr3a. For instance, the predicted protein Pc22053 showed 33% identity with P. sojae Avr1b. Epimedoside-A However, Pc22053 can not cause cell death in N. benthamiana during the transient expression assays. This is not surprising as data from P. sojae indicate that Avr1b induced cell death occurs only on soybean plants carrying Rps1b. To explore this further, we tested for transcripts of Pc22053 by RT-PCR and observed its highly expression during the host infection. Furthermore, we observed that Pc22053 can suppress the HR induced by all 8 different effectors. Similarly, selected RXLR effectors and the RXLR-like SNE1 protein from other Phytophthora species have demonstrated their ability to suppress cell death and defense. We demonstrated that one P. capsici CRN gene Pc506611 does not cause plant cell death when transiently expressed in N. benthamiana. This is not a rare case because recent studies show that cell death induction is not a universal feature of CRN proteins. Over-expression of Phytophthora CRN domains only induce necrosis in a few cases. Intriguingly, when the putative Pc506611 CRN protein sequence was compared against NCBI Nr database, a ubiquitin-like domain was detected in this protein. The family of proteins containing UBL and ubiquitin-associated domains has been implicated in proteasomal degradation. Whether the protein contributed to the pathogenicity through ubiquitin pathway during the host-oomycete interaction is yet to be 
determined. Furthermore, the high expression of Pc506611 during the GC and early infection stages leads us to suspect that it contributes positively to the pathogen’s virulence. Ectopic expression showed that this gene can suppress plant cell death caused by all tested cell death inducers but R3a/Avr3a. Data from a recent study on P. sojae CRNs indicate that one CRN, PsCRN115, also suppresses cell death elicited by e.g. PsojNIP and PsCRN63. The similar results indicated that this family of effectors also has similar abilities to RXLR effectors in suppressing plant defense. Host cell death or the HR is an effective and ultimate defense mechanism against obligate biotrophic and hemibiotrophic pathogens. However, delayed HR could be counterproductive and benefit hemibiotrophic pathogens in necrotrophic growth stages. P. capsici is a hemibiotroph and switches from biotrophic to necrotrophic growth 18 to 42 h following the invasion of N. benthamiana leaves. Therefore, the ability of P. capsici to suppress or delay the HR of host tissue is likely a major component of its D-Pantothenic acid sodium pathogenic strategy, as is for P. sojae. We observed a small number of NLPs and elicitins with differential expression. DEG analysis showed that three NLPs showed increased expression at GC compared with MY. RT-PCR analysis demonstrated that they are highly expressed during the infection stages. Similarly, a study on P. sojae NLPs found that most NLP are highly expressed during cyst germination and infection stages. Ectopic expression showed that one of our P. capsici NLP genes triggered cell death in N. benthamiana. Although it is accepted that NLPs can contribute to virulence as toxins, it has been reported that many members of this family do not possess obvious toxic activity.