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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
2004-12-7
pubmed:abstractText
Overexpression in Leishmania amazonensis promastigotes of the GTPase-deficient small G protein LdARL-3A-Q70L specifically provokes the loss of the flagella without affecting cell viability and body size. However, motility is lost and, remarkably, cells do not survive in the insect vector Lutzomyia longipalpis gut, leading to interruption of parasite transmission. We report here that overexpression of the same protein in Leishmania major, Leishmania donovani, and Crithidia fasciculata also led to significant alterations of the flagella. Surprisingly, ablation of TbARL-3A expression by RNAi in Trypanosoma brucei brucei also provoked flagella shortening, revealing that overexpression of the GTPase-deficient protein seems functionally equivalent to a drastic reduction in its native counterpart abundance. This renders possible complementary studies of an essential pathway in related organisms. Potential significance for the protein function is discussed as well as future strategies for stopping the transmission of several neglected parasitic diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0014-4894
pubmed:author
pubmed:issnType
Print
pubmed:volume
108
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
126-33
pubmed:meshHeading
pubmed:articleTitle
Trypanosomatid flagellum biogenesis: ARL-3A is involved in several species.
pubmed:affiliation
Laboratoire de Génomique Fonctionnelle des Trypanosomatides, UMR CNRS 5162, Université Bordeaux 2, 146 Rue Léo Saignat, 33000 Bordeaux, France.
pubmed:publicationType
Journal Article