Loss of complex-type N-linked glycans attenuates maximum cell density and susceptibility to human serum of Trypanosoma brucei brucei.
Parasitol Int
; 101: 102874, 2024 Aug.
Article
em En
| MEDLINE
| ID: mdl-38417735
ABSTRACT
Trypanosoma brucei brucei is a parasitic protist that expresses cell surface proteins modified with complex-type N-linked glycan (NLG), like multicellular organisms. However, little is known about the role of complex-type NLG. In T. b. brucei, it has been shown that either one of the glycosyltransferases, TbGT11 or TbGT15, is sufficient to initiate the synthesis of complex-type NLG. To clarify the role of complex-type NLG, it is necessary to generate cells lacking both enzymes. Therefore, we deleted TbGT11 and TbGT15 from the genome of T. b. brucei for the phenotypic examination. The mutant strain grew in culture, with reduced maximum cell density; showed decreased susceptibility to normal human serum, which contains trypanolytic factors; and lacked uptake of the haptoglobin-hemoglobin complex. These data indicate that protein modification by complex-type NLG is not essential but is required for receptor function.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Polissacarídeos
/
Trypanosoma brucei brucei
Limite:
Humans
Idioma:
En
Revista:
Parasitol Int
/
Parasitol. int
/
Parasitology international
Assunto da revista:
PARASITOLOGIA
Ano de publicação:
2024
Tipo de documento:
Article