Project Title

Does Neurogenin regulate vab-1 during neurogenesis?

Presenters

Academic department under which the project should be listed

CSM - Molecular and Cellular Biology

Faculty Sponsor Name

Dr. Martin Hudson

Abstract (300 words maximum)

Schizophrenia is a mental disorder that roughly affects 1% of the world population and disrupts a person’s emotional, cognitive and social actions in life that can lead to other psychotic symptoms. A previous study has linked schizophrenia to certain mutations found in chromosome 5 in humans. Neurogenin-1, a basic helix-loop-helix transcription factor gene also found on chromosome 5, is a key regulator of neural differentiation. Neurogenin-1 has been implicated in some schizophrenia cases, although how this occurs at the molecular level is not well understood.

To further understand the role of Neurogenin-1 during human neuronal development, we are looking at an ortholog gene, ngn-1, in a much simpler organism, the nematode Caenorhabditis elegans. This 1mm-long roundworm is a powerful model organism for studying neuronal differentiation, due to its short life cycle, transparent body morphology, and its fully sequenced genome. Our preliminary data reveals that ngn-1 regulates multiple aspects of axon guidance during neural development. Based on the phenotypes seen in ngn-1 mutants, we hypothesize that ngn-1 may regulate transcription of axon guidance genes including the Eph receptor tyrosine kinase vab-1.

To address this question, we have created strains that contain the following mutations; vab-1 alone, ngn-1 alone, and both vab-1 and ngn-1. These strains also contain a GFP reporter gene that drives GFP expression in just one pair of interneurons in the head. These strains will allow us to compare any differences in location or displacement of the AIY neurons in the double mutant when compared to each single mutant alone. If vab-1 functions in the same genetic pathway as ngn-1, then the double mutant should not be significantly different when compared to each single mutant alone.

Project Type

Poster

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Does Neurogenin regulate vab-1 during neurogenesis?

Schizophrenia is a mental disorder that roughly affects 1% of the world population and disrupts a person’s emotional, cognitive and social actions in life that can lead to other psychotic symptoms. A previous study has linked schizophrenia to certain mutations found in chromosome 5 in humans. Neurogenin-1, a basic helix-loop-helix transcription factor gene also found on chromosome 5, is a key regulator of neural differentiation. Neurogenin-1 has been implicated in some schizophrenia cases, although how this occurs at the molecular level is not well understood.

To further understand the role of Neurogenin-1 during human neuronal development, we are looking at an ortholog gene, ngn-1, in a much simpler organism, the nematode Caenorhabditis elegans. This 1mm-long roundworm is a powerful model organism for studying neuronal differentiation, due to its short life cycle, transparent body morphology, and its fully sequenced genome. Our preliminary data reveals that ngn-1 regulates multiple aspects of axon guidance during neural development. Based on the phenotypes seen in ngn-1 mutants, we hypothesize that ngn-1 may regulate transcription of axon guidance genes including the Eph receptor tyrosine kinase vab-1.

To address this question, we have created strains that contain the following mutations; vab-1 alone, ngn-1 alone, and both vab-1 and ngn-1. These strains also contain a GFP reporter gene that drives GFP expression in just one pair of interneurons in the head. These strains will allow us to compare any differences in location or displacement of the AIY neurons in the double mutant when compared to each single mutant alone. If vab-1 functions in the same genetic pathway as ngn-1, then the double mutant should not be significantly different when compared to each single mutant alone.