Abstract
The genome of the protozoan parasite Toxoplasma gondii was found to contain two genes encoding tyrosine hydroxylase; that produces l-DOPA. The encoded enzymes metabolize phenylalanine as well as tyrosine with substrate preference for tyrosine. Thus the enzymes catabolize phenylalanine to tyrosine and tyrosine to l-DOPA. The catalytic domain descriptive of this class of enzymes is conserved with the parasite enzyme and exhibits similar kinetic properties to metazoan tyrosine hydroxylases, but contains a unique N-terminal extension with a signal sequence motif. One of the genes, TgAaaH1, is constitutively expressed while the other gene, TgAaaH2, is induced during formation of the bradyzoites of the cyst stages of the life cycle. This is the first description of an aromatic amino acid hydroxylase in an apicomplexan parasite. Extensive searching of apicomplexan genome sequences revealed an ortholog in Neospora caninum but not in Eimeria, Cryptosporidium, Theileria, or Plasmodium. Possible role(s) of these bi-functional enzymes during host infection are discussed.
Highlights
Toxoplasma gondii is among the most successful of parasites with the potential to infect all warm blooded animals and with an estimated prevalence of 30% in the world’s human population [1,2]
To identify metabolic enzymes that may be secreted from T. gondii into its host cell, we compared the enzyme set resulting from applying the SHARKhunt search algorithm to the T. gondii genome to the set of proteins at ToxoDB with predicted signal peptides (www.toxodb.org [18,19]
Among the remainders we focused on an unexpected metabolic enzyme with a predicted signal peptide but no predicted transmembrane helix; a predicted tyrosine hydroxylase
Summary
Toxoplasma gondii is among the most successful of parasites with the potential to infect all warm blooded animals and with an estimated prevalence of 30% in the world’s human population [1,2]. Infection normally consists of an acute stage in which the rapidly growing tachyzoites infect a range of tissues, followed by a latent stage during which slowly replicating bradyzoites form tissue cysts in muscle and brain [3,4]. The tropism of parasites for brain tissue is intriguing and has been linked with specific behavioural changes. In rodents infection with T. gondii has been shown to modify aversion to predators that might facilitate transmission of parasites [5,6]. There are reports indicating infection may lead to psychological sequelae in humans. The mechanism responsible for the behavioural changes remains unclear
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