A polymorphic inframe deletion in the ODR-10 extracellular loop 2 abolishes diacetyl sensing

Area of Science:

• Neuroscience
• Genetics
• Molecular Biology

Background:

• The nematode Caenorhabditis elegans (C. elegans) utilizes olfactory receptors to detect environmental odorants.
• The ODR-10 protein functions as a specific olfactory receptor for diacetyl in C. elegans.

Purpose of the Study:

• To investigate the causal relationship between an in-frame deletion in the odr-10 gene and impaired diacetyl attraction in C. elegans.
• To determine the specific impact of the deletion on the diacetyl olfactory receptor's structure and function.

Main Methods:

• Utilized genome editing techniques in the N2 background of C. elegans.
• Phenotypic analysis of mutant strains to assess olfactory attraction to diacetyl and pyrrole.
• Bioinformatic analysis to predict the structural consequences of the deletion on the ODR-10 protein.

Main Results:

• Confirmed that a 30 bp in-frame deletion in the odr-10 gene is directly responsible for the diacetyl sensing defect.
• Demonstrated that the DL226 strain, carrying this deletion, exhibits defective attraction to diacetyl but retains attraction to pyrrole.
• Showed that the deletion precisely removes the predicted ligand-binding extracellular loop 2 (ECL2) of the ODR-10 receptor.

Conclusions:

• The identified in-frame deletion in the odr-10 gene is the causative mutation for impaired diacetyl olfaction in C. elegans.
• Extracellular loop 2 (ECL2) of the ODR-10 receptor is critical for diacetyl ligand binding and subsequent behavioral responses.