Expression of nicotinic acetylcholine receptor subunits from parasitic nematodes in Caenorhabditis elegans

被引:14
|
作者
Sloan, Megan A.
Reaves, Barbara J.
Maclean, Mary J.
Storey, Bob E.
Wolstenholme, Adrian J.
机构
[1] Univ Georgia, Dept Infect Dis, Athens, GA 30602 USA
[2] Univ Georgia, Ctr Trop & Emerging Global Dis, Athens, GA 30602 USA
基金
美国国家卫生研究院;
关键词
Caenorhabditis elegans; Haemonchus contortus; Ascaris suum; Nicotinic acetylcholine receptor; Levamisole; GATED CHLORIDE CHANNEL; HAEMONCHUS-CONTORTUS; FUNCTIONAL RECONSTITUTION; LEVAMISOLE RECEPTORS; MOLECULAR-CLONING; ENCODES; GENES;
D O I
10.1016/j.molbiopara.2015.12.006
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The levamisole-sensitive nicotinic acetylcholine receptor present at nematode neuromuscular junctions is composed of multiple different subunits, with the exact composition varying between species. We tested the ability of two well-conserved nicotinic receptor subunits, UNC-38 and UNC-29, from Haemonchus contortus and Ascaris suum to rescue the levamisole-resistance and locomotion defects of Caenorhabditis elegans strains with null deletion mutations in the unc-38 and unc-29 genes. The parasite cDNA5 were cloned downstream of the relevant C. elegans promoters and introduced into the mutant strains via biolistic transformation. The UNC-38 subunit of H. contortus was able to completely rescue both the locomotion defects and levamisole resistance of the null deletion mutant VC2937 (ok2896), but no C elegans expressing the A. suum UNC-38 could be detected. The H. contortus UNC-29.1 subunit partially rescued the levamisole resistance of a C. elegans null mutation in unc-29 VC1944 (ok2450), but did cause increased motility in a thrashing assay. In contrast, only a single line of worms containing the A. suum UNC-29 subunit showed a partial rescue of levamisole resistance, with no effect on thrashing. (C) 2015 The Authors. Published by Elsevier B.V.
引用
收藏
页码:44 / 50
页数:7
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