Trypanosomatid flagellum biogenesis: ARL-3A is involved in several species.
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.
Sahin
Annelise
A
Laboratoire de Génomique Fonctionnelle des Trypanosomatides, UMR CNRS 5162, Université Bordeaux 2, 146 Rue Léo Saignat, 33000 Bordeaux, France.
Lemercier
Guillaume
G
Tetaud
Emmanuel
E
Espiau
Benoît
B
Myler
Peter
P
Stuart
Kenneth
K
Bakalara
Norbert
N
Merlin
Gilles
G
D000595:Amino Acid Sequence; D000818:Animals; D015153:Blotting, Western; D005407:Flagella / Q000502:physiology*; D015870:Gene Expression; D008969:Molecular Sequence Data; D009068:Movement; D015800:Protozoan Proteins / Q000737:chemistry / Q000235:genetics / Q000502:physiology*; D016415:Sequence Alignment; D014351:Trypanosomatina / Q000235:genetics / Q000502:physiology*
D015800:Protozoan Proteins