Document Type

Honors Project

Publication Date

Spring 6-3-2015


Cilia are microtubule-based organelles that facilitate a variety of sensory and motility-specific processes. Mutations in genes that encode cilia-specific proteins can manifest as highly devastating diseases, such as polycystic kidney disease and Bardet-Biedl syndrome. In this study, a comparative genomics approach was used to identify ciliary genes that facilitate sensory-specific roles. One gene from this candidate list (encoded at the C05D10.2 locus in the C. elegans genome) was chosen for comprehensive characterization. We discovered that a mutant strain of C. elegans that possesses a deletion mutation within the C05D10.2 coding sequence exhibits a highly penetrant dye-filling defect in phasmid ciliated sensory neurons (CSNs). This phenotype was almost completely rescued by introducing a wild-type copy of the C05D10.2 gene into mutant animals. Additionally, we observed that a translational fusion of the full C05D10.2 coding sequence to green fluorescent protein (GFP) is expressed in anterior and posterior sensory neurons in C. elegans, and specifically localizes to the cilia at the tips of those neurons. Finally, preliminary data obtained from an automated worm-tracking system suggest that mutant worms that lack a functional copy of C05D10.2 roam more than wild-type animals. These combined data strongly suggest a sensory-specific role of C05D10.2 in C. elegans, and are corroborated by evidence that the human homolog of C05D10.2 may be associated with cilia function, as well.

Level of Honors

summa cum laude




Brian Piasecki