The oomycete Phytophthora infestans, causal agent of the tomato and potato late blight, generates important economic and environmental losses worldwide. As current control strategies are becoming less effective, there is a need for studies on oomycete metabolism to help identify promising and more effective targets for chemical control. The
pyrimidine pathways are attractive metabolic targets to combat
tumors, virus and
parasitic diseases but have not yet been studied in Phytophthora.
Pyrimidines are involved in several critical cellular processes and play structural, metabolic and regulatory functions. Here, we used genomic and transcriptomic information to survey the
pyrimidine metabolism during the P. infestans life cycle. After assessing the putative gene machinery for
pyrimidine salvage and de novo synthesis, we inferred genealogies for each enzymatic domain in the latter pathway, which displayed a mosaic origin. The last two
enzymes of the pathway,
orotate phosphoribosyltransferase and orotidine-5-monophosphate
decarboxylase, are fused in a multi-domain
enzyme and are duplicated in some P. infestans strains. Two splice variants of the third gene (
dihydroorotase) were identified, one of them encoding a
premature stop codon generating a non-functional truncated
protein. Relative expression profiles of
pyrimidine biosynthesis genes were evaluated by qRT-PCR during
infection in Solanum phureja. The third and fifth genes involved in this pathway showed high up-regulation during biotrophic stages and down-regulation during necrotrophy, whereas the
uracil phosphoribosyl
transferase gene involved in
pyrimidine salvage showed the inverse behavior. These findings suggest the importance of de novo
pyrimidine biosynthesis during the fast replicative early
infection stages and highlight the dynamics of the metabolism associated with the hemibiotrophic life style of pathogen.