TY  - GEN
T1  - The Caenorhabditis elegans and Haemonchus contortus beta-tubulin genes cannot substitute for loss of the Saccharomyces cerevisiae beta-tubulin gene
AU  - Gibson, Sophia B
AU  - Harper, Clare S
AU  - Lackner, Laura L
AU  - Andersen, Erik C
DO  - 10.17912/micropub.biology.000411
UR  - http://beta.micropublication.org/journals/biology/micropub-biology-000411/
AB  - Parasitic nematode infections continue to have an enormous impact on human and livestock health worldwide (Hotez et al., 2014; Kaplan & Vidyashankar, 2012). A limited arsenal of anthelmintic drugs are available to combat these infections. One of the most widely used classes is benzimidazoles (BZ), and resistance against this class is widespread (Kaplan & Vidyashankar, 2012). Previous studies to understand parasitic nematode resistance using the free-living model organism Caenorhabditis elegans showed that variation in the C. elegans beta-tubulin gene ben-1, an ortholog of beta-tubulins in parasitic nematodes, confers resistance to BZ drugs (Dilks et al., 2020; Driscoll et al., 1989; Hahnel et al., 2018). The most common missense mutation resistance alleles are F167Y, E198A, and F200Y (Avramenko et al., 2019; Mohammedsalih et al., 2020). Although computational models have predicted that these amino acids are involved in the binding of BZ compounds to beta-tubulins, the binding remains to be investigated empirically at the structural level because nematode-specific beta-tubulin structures have not been created (Aguayo-Ortiz et al., 2013; Hahnel et al., 2018). To better understand the mechanisms of resistance, we sought to obtain those crystallographic structures.
PY  - 2021
JO  - microPublication Biology
ER  -