Significant change observed in carbohydrate levels with an induced defense response
prompted a further study to determine if the presence of these carbohydrates would affect
growth of P. capsici. To our knowledge, these data provide the first evidence that the carbohydrate
galactose can directly inhibit growth of P. capsici. While it is unknown if the increased
concentration of galactose observed in induced plants is sufficient to inhibit growth of P. capsici
after infection, several reports indicate that galactose metabolism may play an important role
in infection by Phytophthora spp. A late blight resistant hybrid potato line (Solanum phureja X
Solanum tuberosum) was shown to differentially overexpress a gene encoding for α-galactosidase
upon infection by P. infestans [23]. The α-galactosidase gene, also known as melibiase,
cleaves the polysacharide melibiose to produce galactose and glucose. While the role of α-galactosidase
in plant resistance is unknown, its over-expression during infection by P. infestans
indicates that sugar metabolism is involved in plant-pathogen interactions. In P. sojae, a putative
UDP-glucose 4-epimerase open reading frame (ORF) was identified in close proximity to a
necrosis inducing protein and was shown to be actively expressed in zoospores and during
pathogenesis [24]. Interconversion of UDP-galactose to UDP-glucose by UDP-glucose 4-epimerase
is an essential step during galactose catabolism and its expression during early infection
indicates that limiting galactose accumulation in Phytophthora spp. may be important for pathogenicity.
In Saccharomyces cerevisiae, mutant lines with increased uptake of galactose accumulated
galactitol and had a lower maximum growth rate compared to wild type cells [25].
Our results indicate that galactose is an inhibitor of P. capsici under in-vitro growth conditions,
and could enable novel strategies for Phytophthora disease control.