The Transcription Factor ztf-29 is Required for C. elegans Nervous System Development

In humans, Kallmann syndrome (KS) is classified by lack of sense of smell due to olfactory bulbs not forming to completion, resulting in delayed or absent puberty. It has been shown that this disease is x-linked and has the ability to be passed to offspring. The investigation of the cause of KS has proven difficult, as about half of present cases of Kallmann syndrome have no known specific cause, leading to the conclusion that there are multiple factors at play and not just one gene, protein, or transcription factor in particular. However, the model organism, nematode C. elegans, has an ortholog gene of the human gene KAL1, kal-1, that might be used to study the transcriptional regulation of kal-1 to provide a better understanding of KS. The kal-1 gene has a promoter driving GFP in the strain of C. elegans known as otIs33. It has been shown that a percentage of the double mutant strain, ztf-29;otIs33, contain a specific expression phenotype that shows a wider nerve ring than normal. The aim of this project is to determine how ztf-29 plays a role in the cell adhesion or axon guidance of kal-1 expressing neurons, as well as conclude why this widening of the nerve ring occurs, and which neuron specifically is responsible