SAR was established in more than half of the moss samples by 22h post-induction, but 34h post-induction provided the additional time necessary to ensure the highest level of Gomisin-D systemic protection in our experiments. It is important to note that Ergosterol plants did not achieve 100% protection against plant death at 34 h post-induction, suggesting that the putative SAR signal was not transmitted past the cut point within 10 h of induction in all samples. Lack of signal transmission would prevent the distal ends from undergoing appropriate changes in PR gene expression, rendering the distal ends susceptible to challenge. Possible explanations for observed variability may include differences in the viability and initial health of both the moss samples and pathogen. Despite the variability, the trends strongly support the occurrence of SAR in this non-vascular plant. Physical wounding experiments did not induce SAR in A. serpens, a finding consistent with data showing that physical wounding is incapable of inducing SAR in vascular plants. Therefore, we conclude that rather than simply responding to a physical wound, the moss must be able to sense some specific feature of the pathogen itself. In addition, results of the wounding experiments suggest that simply cutting the moss plants, as part of our method, would not be sufficient to cause induction of the SAR by itself. The b-1,3 glucan experiments demonstrate that this common oomycete cell wall component can act as a defense elicitor and induce a nearly identical increase in resistance when compared with induction by the pathogen itself. The similar response by moss to both b-1,3 glucan and P. irregulare itself suggests that this cell wall component may be detected by the plant during infection by P. irregulare. Previous studies implicate the involvement of b-1,3 glucans in SAR in vascular plants. Our results suggest that the moss may possess components of a conserved sensory mechanism for oomycete cell wall material similar to that found in the vascular plants. While our results collectively indicate the existence of a SARlike mechanism in A. serpens, it remains to be seen whether this SAR mechanism, and its components, are conserved relative to those in vascular plants. Three possible evolutionary histories exist for this defense response. One possibility is that SAR arose prior to the divergence of non-vascular and vascular plants, approximately 470 million yr ago. In this scenario, much of the molecular machinery for SAR should be conserved in nearly all land plants. This evolutionary model is supported by findings that both moss and vascular plants have several conserved genes as well as two plant hormones, SA and JA. Alternately, SAR might have evolved independently in non-vascular and vascular plants, either before or after the divergence of the pteridophytes. More work is necessary to confirm its presence or absence in pteridophytes and to examine the degree of similarity between the SAR mechanisms of all types of plants. Now that a reliable moss-pathogen culture system has been developed and the existence of SAR has been documented in a non-vascular plant, it will be necessary to identify genes in A. serpens that are orthologous to PR genes and other SAR-associated genes in vascular plants. Researchers previously detected the induction of four 
plant defense genesin P. patens in response to a pathogen. However, the expression of these genes, and additional PR genes, must be studied to determine if they are induced throughout the plant.